Myckola Yabluchansky
My principle of the disease optimality
For doctors indeed
Yabluchansky M. My principle of the disease optimality. For doctors indeed. 2002.
The principle of disease optimality defines its norm, the optimal variant when a patient pays a little payment by his/her health for a qualitative recovery. “Whales” of the principle disease optimality are philosophy of health and disease, theory of optimal processes, and a principle of optimality in biology. The principle of disease optimality proves a strategy and a tactic of a treatment of a patient through its normalization by bringing to the conditions of an optimal variant. New clinic could be established on the principle of disease optimality.
This book writes for physicians and their patients and for everybody who care of the private health.
©Yabluchansky M.
Instead of introduction
It is the beginning of the century. Expectations for the changes are being justified.
For me, as for a doctor, the most important part is a professional part. There are a lot of new things here. They are not in the trifles, but in the philosophy of the subject.
I became the participant of a doctor’s perception his/her role in medicine and the role of medicine in the society. It gave us a lot of useful things. The example, which I use not for the first time, is intervention of the ideas of the optimality to the clinics. I was lucky to summarize them as the “principle of the disease optimality”. The principle is the local application of one of the most fundamental natural phenomena, which is known in different spheres of natural sciences.
In the references one can find an incomplete summary of publications on this theme. The main works of the author in this important for me sphere are included there.
In spite of the locality of the principle, its sequences for the medicine I see as revolutionary in the real understanding of this word.
The principle intuitionally justifies corrected by the time and recognized by the medical society philosophy which is build on the trust to the nature, effective use of its constructive motive forces.
For me, the century we entered is the century of optimality.
In the furious pace of life there is a time deficiency. There is lack of it for the “other’s” ideas. Especially there are a lot of them in the thick books which are like anachronism on the stage of effused to the endlessness medical science. That is why it appeared an idea of my small book – distillation of my own thoughts on the topic of disease optimality.
The way how the philosophy of disease optimality is accepted is a question for me, its author, but not for the philosophy by itself. It already exists according to its own independent laws. I know many doctors, professionals, who not only like this philosophy, but this philosophy also helps them in their routine work.
Probably there are doctors who didn’t accept this philosophy because they didn’t understand it. However, there are more doctors who didn’t come across it.
I wrote this little book to promote faster dissemination of the philosophy.
You, not me, can judge this publication, but I did my best.
I will be grateful for your criticism and suggestions.
The theme of the disease optimality is important for me, and I will not leave your reaction without the answer.
You can write on one of the emails: mydoctorlife@gmail.com, myabl@mail.ru.
Sincerely,
Myckola Yabluchansky.
Prehistory of the principle
A clinic is in crisis.
The crisis is conditioned by many reasons. In the list there are economic, social, ecological, and, naturally, medical problems.
For me, the medical problems are concentrated in incorrect understanding of diseases. This incorrect understanding being out of the reality of modern life, leads to the false diagnosis and treatment decisions.
According to the faulty philosophy dominating in a modern clinic diseases are opposed to the norms of health, and the condition of a patient is evaluated by deflection from the norms of a healthy person.
By this philosophy the actions of a doctor are directed to the “normalization” of functions and structures of a patient in the sense of bringing to the norms of a healthy person. It doesn’t mean what a price is and if it is possible.
Endless line of tests and mistakes in the patient management proves that this philosophy is dead-end and defines the crisis of the clinic.
The example is the acute myocardial infarction. Its history is in “insistent” refusals from every time appearing new “promising” treatment methods.
We needed years to become sure that:
• Steroids limit the infarction zone but complicate its recovering
• Indirect anticoagulants (out of thrombolitic therapy as a compound link) increase the risk of thrombo-embolic complications.
• Non-steroid anti-inflammation means lead to the development of post infarction heart aneurism in a case of a wrong prescription.
• Coronaroactive remedies in systematic use “rob” the infarction zone.
As a result a prognosis and outcome of the disease becomes worse.
In majority we continue thinking that a disease is not a natural condition of a human life; and that only the norms of a healthy person have a right for existence in the world which we created.
I see a crisis of a modern clinic in this approach.
A Disease should be Normal
The reason of a clinics crisis is in wrong understanding of health. The sequence of these misunderstandings is a wrong approach to a patient, disappointment in the basis of a clinic.
Let’s analyze a formula “sanos-patos”. Everything is correct in it. Two measures are opposed – the measures of disease and health.
There is a trouble with the formula “norm-pathology”. Health is reduced to the norm. A disease is opposed to the norm.
I will explain my idea; it is clear.
In philosophy a measure – a category and a norm- is an idea connected with the measure. If we have a measure, we should have a norm as it goes without saying.
The norm is one of the parts of the measure which is rather limited defined by the aim function. Under the aim function we understand a norm. One aim is one norm. Unlimited number of aims leads to unlimited number of norms in the same measure. Moreover, every norm is concrete.
Let’s take an example from an engendering. A bulb. It can be used beginning from a part of a second until some years. There is a norm – a bulb is ok if it can be used during a certain period of time. There are a lot of bulbs. They are different. Even I know few dozens: from the torch bulbs to usual lamp ones. Each of them has its own norm.
Let’s take an example from sport. Sportsmen’s achievements are different in sprint, football and baseball,… if we make a champion in sprint to lift a weight, and a champion in swimming or chess… the result is not too difficult to predict.
Another example is from education. There are different educational standards in economics, mathematics, and medicine. Every standard is a norm. Two young people, who are twins, differ because they graduated from different departments. They had different educational standards. Everyone confirms his/her own standard, his/her norm of education. In all the examples the norms are connected with the aim functions. A bulb should work not less then…; sportsmen should run not more then…; a certain student should have an exact amount of courses, have a definite number of exams according to his/her specialty.
A measure of a disease cannot exist without norms even inductively; the same as a measure of health; the same as any measure. I formulate a norm of a disease as a variant when a patient pays a minimum payment by his/her health resources.
The idea of a norm of a disease is much wider then the idea of a norm of health.
There can be a variant of a particular disease with its particular characteristics in a certain patient, with concrete geno- and phenotypic determinants, with social, ecological and other conditions. These exacting diagnostic and other characteristics are typical for this moment of a disease development.
The aim here is a variant when a patient pays a minimum payment by his/her health recourses for a disease under certain conditions.
I want to stress that a local root of a mistaken approach of a clinic is partly in a fact that correct construction “sanos-patos” is opposed to the incorrect one “norm-disease”.
A strategy when parameters of a patient are brought to the norms of a healthy person is mistaken.
“Normalization” of a heart output and frequency of heart contractions in understanding of the norms of a healthy person in the case of a heart failure damages a heart and shortens a life.
Reasonable decrease heart output and increase of contraction frequency is one of the mechanisms of compensation of heart pump dysfunction.
Hyperthermic syndrome in a case of an acute pneumonia corresponding it severeness is necessary condition of a qualitative recovery of a patient.
Gastroenterology again got into trouble: now it is anti-helicobacter pillory therapy of a ulcer disease. I don’t know if it is good or not but the risk of oesophagus tumors and other complications increases. The world is excited. Not so long time ago it was inspired to forget everything that was worked out in its treatment before.
There is numerous numbers of examples.
I admire how the ancients understood health and disease: “health is natural in human under certain conditions; under other conditions a disease is also natural…” (Golbah).
“Remedy” for a modern clinic
Philosophical analysis of health and analysis predetermines spread of optimality ideas on clinic.
The problem of patient treatment according to this idea is formulated as a strategy of optimal management which provides the most favorable (optimal) from all other variants flowing of a disease.
The strategy of optimal management is a subject of a research of mathematical theory of optimal processes which is the most common instrument of an optimal solving of management tasks.
In the frames of this theory a patient management can be considered as a particular task.
The theory was created because of engineering demands and it became one of the most perspective directions of modern mathematics.
It gives methodology and methods of finding of optimal management:
A) Optimality in a meaning of getting an aim of a process for the shortest period of time;
B) Optimality in a meaning of getting an aim of a process with the minimum inputs of resources.
The tasks which a doctor solves in his/her work with a patient are management.
Diagnostic and prognoses are intermediate stages.
There is only one aim – to help a patient; to do the best to make a treatment or, in the other words, to make management.
That is why a mathematical theory of optimal processes is a “remedy” for a modern clinic.
Through principle to a new clinic
Natural spread of the theory of optimal processes on a disease in its philosophical understanding leads to formulation of a principle of disease optimality.
The principle states – the only variant is optimal which needs the minimum payment by the resources of health.
The principle soared hovered for a long time; but it isn’t and wasn’t understood in a right way.
G. Selye wrote: “is it possible to improve a natural defending mechanism? A theory “nature knows better” is seems to be rather applicable to adjustments. It is considered that… a natural selection … gradually developed the best possible defending reactions. But it is not so. We often can improve nature by suppressing the reactions which were developed for a defense but not necessarily useful under all the circumstances”.
There is a mistake here. Violation of optimality of a mechanism selected by nature is considered as its non-optimality.
I like the ideas of I. Davydovsky: “biological expediency of inflammation as natural spontaneous act doesn’t mean that this act in individual conditions is always necessary or that it conducts an absolute defense and “targeted” on it… a doctor faces a necessity not only to see spontaneous automatically developing processes of inflammation, but also to interfere before it starts”.
Please note; according to I. Davydovsky a doctor should interfere to an inflammation process only in a case of violation its natural (spontaneous) progression.
I think that the basis of the principle is fastened genetically as a mechanism of recovering. This is the way how nature selected them.
The aim of a doctor is to help a patient to go through a disease with the minimum losses. This is a real philosophy of family doctors.
The principle makes basic changes into the methodology of patient management. Its main point is optimal management. The sphere of the use of optimal management in the sense of fast actions is mainly in urgent conditions and in the sense of losses minimization is in a whole clinic.
An optimal progression of a disease provides:
1) Qualitative recovering in a case of acute forms;
2) Stable remission, less often and not severe complications in chronic forms;
3) The best possible quality of a patient’s life.
“Arrow of time” and reversibility of a disease
Aspiration to improve is always present in the world.
G. Selye, whom I quote in the previous paragraph, is not the only one.
Our post soviet space in contrast to the others accumulated a lot of experiences of planetarium size. It is easy for us “to make a fairy tale a reality”. It doesn’t matter that it is a fairy tale. The problem is we have to pay for it. And sometimes it is too expensive.
Normalization of a patient’s condition in a sense of bringing his/her functions to the norms of a healthy person is equal to the nature improvement, because a priory is allowed, it is axiomatized that nature is not perfect.
I want to insure you that this theme is more serious then just thinking about imperfectness of nature. Our (western) philosophy was built under a pressure of deterministic ideas. Of course they have a lot of clever things, but the most important ones go from classical (Newton) mechanics.
Deterministic ideas which are realized according to abstract mathematical tools, which were fixed for this mechanics, allow the existence of reversibility of time.
A representative of an exact science who is based on a deterministic platform would say: “give me a law and a reference point and I will predict the future and the past”.
It is right. He will do it. But this prediction in our real world doesn’t worth a pin. Real world is not deterministic, but it could be. Deterministic world is a rude idealization of a real one. Deterministic world is not alive; it is dead, and it doesn’t allow development.
Human nature more then a real world despises deterministic per se. The same related to the reversibility as well as in a narrow medical understanding.
The ancients said that it was not possible to come into the same river. I understand it in a meaning of impossibility of reversibility.
It is not understandable how we could loose this divine philosophy. East is wiser. From the ancient times they accept nature as a spontaneous harmony and put it into the deterministic frames is the same with subordinating it to the external power. Get know the Chinese pulse diagnostics. The problem is if the characteristics of pulse are disharmonious with the health condition of a patient. It is a catastrophe when a sick person has a pulse of a health one.
Making a research about order and chaos, definiteness and indefiniteness I. Prigozhin comes indisputable conclusion about deterministic – probabilistic world organization and the existence of the “arrow of time”. In the other words he confirms one of the most ancient philosophies of the irreversibility of a developing world.
There is no place for reversibility of a disease in the “arrow of time”. It is a mystics. It is necessary to go through a disease.
As for the words of “family doctors” a doctor should “lead a patient through a disease”.
I want to add, it should be done by the best way, according to the principle.
Principle and diagnosis
A disease diagnosis of a patient is not full or even wrong if it doesn’t contain information about an optimality degree (a degree deviation from the optimal variant) of a disease.
Out of this a doctor doesn’t have enough information for planning and fulfilling a correct treatment.
A clinical diagnosis is an inwardly non-contradictory formalized conclusion about patient’s health.
A possible formula of a diagnosis:
1. Naming of a disease (in the terms of international classification);
2. Remoteness of a disease (for acute diseases it is necessary to have an exact data; for chronic disease a remoteness should be in years and it should be a date of a last exacerbation);
3. Etiology ( if it is defined and has and if it important);
4. A stage (phase) of a disease development;
5. A degree of a disease severity;
6. Progression of a disease (optimal, non-optimal and how it is expressed);
7. Main clinic syndromes;
8. Complications;
9. Health resources;
10. Prognosis (for a present disease, recovery, life quality of a patient).
The formula in points 1-8, 10 is taken to any disease a patient has.
Point 6 is a key-point in a light of a principle, in the meaning of a achieving the tasks of a clinic.
Diagnosis as a conclusion about a patient’s health corresponds to it and changes with it. It is not a frozen construction.
“Qui bene diagnoscirt, bene curat”, Ancients said.
Good diagnostics should follow a principle.
You would never use it in full measure if you didn’t learn to formulate a full diagnosis and didn’t make it a rule of your professional activity.
Incomplete (out of definition of trajectory of a disease progression) diagnosis is like an incorrect understanding of a disease: it is harmful and dangerous in the same measure.
I hope the examples are not needed.
There are no miracles
Diagnosis is based on the information got about a patient. There are at least four sources of it.
The first one is a result of cooperation with a patient (interviewing, examination, objective research) and with his/her environment.
The second one is information got from medical documentation.
The third one is a variety of results got by special (important and unimportant) examinations.
The fourth one is the use of the previous three methods in a patient’s management (in the prism of time).
There are no problems with the first method. If we are not right we blame ourselves for our mistakes. As for the others, it is necessary to be attentive. It is not known who, when and under what circumstances got them and how they were interpreted.
Unfortunately, it is natural for human being to make mistakes. It is bad when somebody’s mistake is taken as a truth. It can cost a lot. That is why we should be careful with those data.
It is a false practice to trust somebody’s information unconditionally.
We should remember there is only one convincing argument Its Majesty The Fact if it was got by a right way.
And also – there are no miracles.
A patient by himself and all variety of data about him/her should be in a so-called bijective (mutual – simple) accordance: a patient shouldn’t be added to a data, but a data should be added to a patient. If there is no accordance we should think about a data problem first.
There is an example from my practice:
-Professor, you have cor triloculare pateint.
-How old is he?
-48.
-Let’s see. We will be the first.
The heart had four chambers.
That was necessary to prove.
About a data quality
Objective data can be received only by objective methods. Different methods can be proposed for defining the same data.
Different methods have different accuracy. That is why data received on the basis of different methods cannot be absolutely identical. But in general they should be the same if they were taken in a right way. There should be naturally the same interpretation.
If you are not sure in data you should redefine them in a different place and what is better by the other methods. It should be done for conscience’ sake and you will have greater confidence in a diagnosis.
About a “cost” and data interpretation
Data is a fact, and facts are stubborn things.
A fact is a fact, not more. It should be interpreted. There is a variety of recommendations, but it doesn’t mean that the facts should be evaluated in such a way.
I remember a detailed lecture in the school of European Society of Cardiology on heart failure on the border of Millenniums. There was a criterion of the lecture: patients with the ejection fraction of the left ventricle more then 25% have higher survival and patients with ejection fraction less then 25% have lower survival. There is no doubt that the criterion is comfortable if it is used correctly.
There is an example. The ejection fraction is 50%, but 30% goes back to the left atrium and only 20 % goes forward to the aorta. Is it really an ejection fraction? What is the chance to survive?
Every index, as an iceberg, has two parts: “under-water” and “above-water”.
“Above-water” part is a part which we oriented on and which we interpret.
“Under-water” part is not “under lock and key” but it is difficult to see it.
If you don’t remember about an “under-water” part, as in the example with the ejection fraction, you should be ready to have troubles.
You will have them in the diagnosis first, then in a patient’s management. There is no optimal patient’s management here.
It is just not more then good advice.
Nature is miserly
There is a tradition that we think that it is bad if data changes. It is right that it is bad, but we should remember that it changes because of bad circumstances.
One should remember that nature is miserly. Every structure has many functions, participates in many of them, as well as every function is associated with many structures and their changes. It is not necessary that the functions are associated with circumstances which are good for our hypothesis.
Also we should remember that there are the same mechanisms for pathological and physiological processes.
Nature doesn’t have special tools for pathological processes. It is miserly!
Do you want an example?
There are a lot of them.
According to my natural stinginess I’m giving you only one example: a patient with atherothrombosis has a hyperfibrinogenemia.
Is it bad or good?
According to everything it can be bad, because of risk of thrombosis and thrombo-embolytic…
On the other hand, in the case of atherosclerosis or erosion plagues is there another way for recovery as not through the primary “patching up” by thrombus on the basis of which the conjunctive tissue will form?
Nature has not created any other mechanisms!
So, should we interfere into these selected by nature mechanisms of “patching up” of plaques?
Is it good to interfere?
Are you afraid of risk of thromboemboli? Of course, there is such a risk.
But who knows statistics? Is it greater when interfere or do not interfere into the system of coagulation?
Wait, how many factors of coagulation are there? Is it just for a word to speak about dynamic balance in the coagulation system?
So, hyperfibrinogenemia in atherothrombosis is not for thrombosis and thromboembolisms, but as an effect of complicated atherosclerosis, which can be a result of…
Yes, you understand correctly. I didn’t finish, which can be the result of thoughtless medical actions.
Let’s remember, nature is not just “miserly”, but it is wise and we should take it into the consideration.
We should learn from it.
Stinginess is not a very bad quality. It is much better then wastefulness.
Not to go to far
Necessity and adequacy is a double condition which allows building a complete clinic diagnosis as a basis of a qualitative medical management.
Satisfaction of necessity is the minimum for the required amount of an examination.
Satisfaction of adequacy is the maximum.
Under-defining and under-fulfilling lead to the incomplete diagnosis. Over-defining and over-fulfilling lead to incredible expenses of a diagnosis, from financial losses to physical and moral detriments.
Moreover, every new examination increases a risk of non - qualitative data with the following results (because of different reasons).
The principle of disease optimality is a result, special case of optimality tasks, where optimality of a diagnostic process with thoughtfully planed procedures of a patient’s examinations takes place.
Careful optimal planning is in the basis of all doctor’s work/
There are no miracles
Medical management, especially on the basis of the philosophy of disease optimality, is good advice if there are problems with getting and interpreting facts and diagnosis construction.
Let’s remember, there are no miracles in reality!
Principle of patient’s management
The principle doesn’t contradict to the existing methodology of patient’s management. It restricts the most qualitative and full patient’s recovery.
Beginning treatment a real, in my understanding, doctor evaluates how duration, severity and organization of system and local patho- sanogenetic mechanisms of a disease correspond to or differ from an optimal variant with the aim to make a right decision about an amount, quality and consistency of interfering.
Medical actions should correspond to patient’s health and its changes.
Mental sphere
A person is a single whole in his mental and physical features. Mental features dominate. It should be given the biggest attention. We should help to form an adequate personal aims of patient in understanding his disease and getting control over it.
It is difficult to overestimate the role of psychology and good psychotherapy in the solving the tasks of recovery, the best movement through the disease and quality of life in general.
A word can heal.
A word must heal.
Give more attention to a patient.
Physical health
The formula – healthy spirit is in a healthy body – is a gold one. Physical activity prevents distress, chronic tiredness, early ageing, and increases resistance to diseases. It is important for health, but for recovery and favorable disease progression it is even more then important. We speak only about its characteristics. It should be balanced with health and should be determined by it.
In recommendation on physical activity doctors should take into the consideration a patient’s life style and his stereotypes.
Nutritional culture
There cannot be health without nutrition culture, especially when we speak about a sick person. The first rule here is moderation. Overweight predisposes to diseases.
There should be a special attention to quality and quantity of food.
We should stress the accordance of nutrition ration to a phase of a disease.
There is no appetite during the pick of acute and exacerbation of chronic diseases. It is normal. The appetite will return later.
Correctly organized nutrition as well as physical activities is the first medicine. In its absence any other actions don’t get a wished result.
Detoxification
Intoxication slows and changes of metabolism, complicates management, and worsens a disease progression. In making detoxification the priority should given to the natural ways: water regime and other cleaning procedures. Medical starvation is useful. It is used in a wide diapason, beginning from a part starvation to the full one. Parenteral interventions may be used as components of intensive therapy. But it solves its own tasks.
Influence on etiological and risk factors
In a case of a chronic disease the first reason of it has a historical meaning and that is why there is no necessity in etiotropic therapy. It is more important in acute and lingering forms of diseases. But even in this case an etiological factor is important if it is present with the interaction with patient’s organism. By itself this therapy is not effective enough. We should take into consideration how useful or harmful is it. Very often it is enough make impacts which increase reactivity of patient’s organism and optimizes his recovery.
We always should pay attention to risk factors.
Optimization of a disease
Optimization of a disease is realized via intervention into its (patho- and sanogenetic) mechanisms. These mechanisms are rehabilitative on their nature if there is no damage. They are directed on the recovery in the case of acute and sub-acute disease or at the end of a phase of exacerbation of a chronic disease. Moreover, the price is always minimal.
The aim of an intervention is to bring a disease to uncomplicated conditions and in no way to the norms of a healthy person!
Optimization assumes thoughtful control of a disease progression.
We always should be in a hurry with optimization because the basis of uncomplicated or complicated disease progression is formed during the first hours and days.
If we begin optimization late its effectiveness would be smaller.
Syndrome therapy
Syndrome therapy is directional on syndromes and is not connected with the mechanisms of a main disease. In the other words syndrome is a manifestation of a disease and its mechanisms. Intervention should be done in dangerous conditions and during periods of its overcoming. In the other cases the priority should be given to patho- and sanogenetic therapy, which also solves syndrome tasks.
General approach to use of medicines
Medicines are not prescribed forever on the same scheme. Therapies should evolution according to a disease. It is enough only to help a patient in difficult time. Sometimes we don’t realize that out treatment is not effective. Sometimes disease self organize and we are just witnesses of their (right or wrong) progression.
Polypragmasy is a difficult problem. We always want to predict everything. We should limit the amount of medicines to the minimum.
Drugs work not only in peace but also during stereotype activities. It is important not only to give doses but also intervals of taking medicines.
Peculiarities of a disease and a patient are put on pharmacokinetics of medicines. Base on optimality of a human organism and his wish to live when you prescribe drugs.
It will never let you down!
Principle of surgery patients’ management
Surgery clinic is not an exception. If there is time, pre-surgery preparation includes mobilization of mental, functional, and structural reserves of a patient’s organism for the surgery. During the intervention the priority is given to the methods which minimize functional and structural consequences of the organ under operation and the access to it.
Post-surgery period is a strategy of a patient’s management when his norms are not the norms of a healthy person.
Consequences of wrong directed therapy
A therapy which goes against the principle out of the optimization of patho – sanogenetic mechanisms of a disease, especially when it breaks them, has unfavorable consequences for its outcome. It is wrong.
Festine lente
This ancient wisdom is one of the strongest. Human health is a very important value to deal with it non-thoughtfully. The actions should be considered! Look before you leap. May be there is no need to leap.
The most important aim
A norm, an optimal variant of a disease is the first question we have when we choose a strategy for a patient’s management.
Is it a reasonable question that a suitable criterion here is the fastest recovery?
The answer is that a recovery date cannot be the criterion. A disease is figuratively like pregnancy. Is it good if it is premature? What about a prolonged one? Everyone knows that pregnancy is good when a baby is born on time.
The principle allows only one criteria of optimality: minimum losses of health for a disease.
The mistakes which were concentrated in a clinic are associated mostly with our distrust to a patient’s organism, perfection of his rehabilitation mechanisms, forgetting about a strategic aim of treatment with its substitution by absolute separate tasks.
It is still painful for me that the main thing for us is in shortening of the hospitalization periods, limitation of the myocardial infarction zone, suppression of an inflammation process in lungs, fastening cicatrisation of an ulcer. Only now the highest double criterion of treatment quality comes with many difficulties. This criterion is increasing of health quality and life span of a patient. It is interesting is there any other alternative philosophy to the principle which provides achieving this high criterion?
Secretly, for me disease optimality is a mean to increase health quality and life span of a patient.
The principle allows the existence of one global aim of treatment. This aim is achievement of the most qualitative patient’s recovery with the minimum price for his health. Depending on a disease the recovery can be complete or incomplete.
The other aims are local and they must obey to the global one. If the local aims are absolute the patient’s management would be ineffective. Be careful, all of them are ersatz!
Formalization of the principle application
It should be formalized. It can give a bigger chance that there would be less mistakes.
I see the application in such a way:
• Identification of an optimal variant for a patient;
• Patient’s diagnosis before a deviation of a disease from an optimal variant (including);
• Defining a degree and a character of deviation of a disease from an optimal variant;
• Establishing a (global) aim of a disease optimality in a patient;
• Patient’s management by the optimization of a disease progression;
• Solving local aims in cases of changes in a health condition of patients by the methods which don’t contradict to the aim of disease optimality.
The principle and new directions of science
The principle opens new directions in science which base on reexamination, addition to a clinic by formalized knowledge by optimal and non-optimal disease’s variants.
We need data that would allow us to differentiate an optimal and nonoptimal varients of a deasease on the all stages of its clinical course.
In the other case a doctor has only one criterion – deviation degree of index data (gender, age and other) from norms of a healthy person. Then a doctor has one approach to a patient’s management – to bring a patient to the norms of a healthy person by any means.
An old disease.
A dangerous disease!
Become supporters
Practical use of the principle requires professionalism and responsibility before a patient in the same measure.
It is necessary not only regulate a disease progression but also to optimize it.
It is much easier to evaluate syndromes as something pathological, suppress them and in the case of worsening of a patient’s health, if it happens, explain everything by imperfectness of a modern medicine.
There are a lot of examples when patients overcome not only their diseases but also bad treatment.
I’m sure that a doctor is a person who accepted human optimality and base on it helps his patients, a person who sees and treats a patient but not disease.
M. Mudrov said:”I’m going to announce you a new truth which can be unbelievable and which would be difficult to accept for many of you: “treatment is not overcoming a disease. It is in healing of a patient”.
I would like to add: “on the basis of the principle”.
Instead of conclusion
Dear colleague, I hope you accepted a philosophy of a patient’s management which is built on the principle of disease optimality.
I hope that those who red previous publications and got familiar with this third one of my principle also liked it, as well as its changes and additions.
Disease optimality is one of the fundamental laws of human nature. It created this law, put and continues to put it through the millstones of evolution, making it more filigree and perfect. I have a deep feeling of confidence that nature makes it according to a will of the wisest intellect – the creator.
Shouldn’t we trust nature? Shouldn’t we coordinate our actions with its wisdom?
Not bringing a patient to the norms of a healthy person, but his treatment according to the norms of optimal variant of a disease provides the best possible recovery. Even if he can’t overcome his disease.
The principle of disease optimality is the philosophy, a general approach to a disease but also it is an individual patient’s management.
It is also a new clinic.
We are establishing this clinic.
Join us!
References
1. Avtandilov G.G, Yabluchansky M.I., Salbiev K.D. at al. Quontitative morphology and mathematical modeling of the myocardial infarction. -Novosibirsk: Science, 1984.
2. Bobrov V.A., Yabluchansky M.I. Heart arrhythmia: The problem state and new approaches to the treatment. – Ukrainian Journal of cardiology. - № 1, 1996.
3. Vojno-Yasenetsky M.I. Biology and pathology of infectious processes. Leningrad, 1981.
4. Davydodsky I.V. The common pathology of the man. Мoskau.:Medicina, 1969.
5. Davydodsky I.V. The causality problem in the medicine. Мoskau.:Medicina ,1987.
6. Malaya L.T., Yabluchansky M.I., Vlasenko M.V. Non-complicated and complicated myocardial infarction healing forms, Кiev.:Health, 1992.
7. Marchuk G.I. Mathematical models in the immunology. Мoskau: Science, 1980.
8. Pontryagin L.S., Boltyansky V.G., Gamkrelidze R.V. at al. Mathematical theiry of the optimal processes. Мoskau: Science, 1983.
9. Prigogine I., Stengers I. Order from chaos. – Мoskau: Progress, 1986.
10. Prigogine I. The end of the distinctness. - Мoskau: Science, 1999.
11. Rashevsky N. Some medical aspects of the mathematical biology. Мoskau: World, 1966.
12. Rosen R. The optimality principle in biology. Мoskau: World, 1969.
13. Selye G. On the level of the entire organism. Мoskau: World, 1972.
14. Selye G. The stress without the distress. Мoskau: Progress, 1982.
15. Khvorostinka V.N., Yabluchansky M.I., Panchuk S.N. at al. Therapeutic gastroenterology. Guidance for the practical doctors. – Kharkov, Basis, 1999.
16. Yabluchansky M.I., Vasilyeva L.G., Volyansky Yu. L. The disease optimality principle. - Kharkov: Basis, 1992.
17. Yabluchansky M.I., Vecherko V.N., Panchuk S.N. at al. The optimal diagnostic and medical structures in the gastroenterological clinic. - Kharkov: Basis, 1993.
18. Yabluchansky M.I., Каntor B.Ya., Маrtynenko A.V. The functional investigations data interpretation of the cardiovascular system. - Kharkov: Basis, 1993.
19. Yabluchansky M.I. The somatic patients’ optimal menedgment (the general approach). — Kharkov: Basis, 1995.
20. Yabluchansky M.I., Маrtynenko A.V, Isaeva A.S. The basis of the practical using of the circulation system variability technolpgy. – Kharkov: Basis, 2000.
21. Yabluchansky M.I. The acute myocardial infarction strategy (for doctors indeed). – Kharkov: Basis, 2000.
22. Yabluchansky M.I., Маrtynenko A.V, Vakulenko I.P. at al. The interpretation in the clinical physiology.– Kharkov: University edition, 2002.
23. Yabluchansky M.I. Carefully, the ejection fraction.– Kharkov: University edition, 2002.
The principle of disease optimality defines its norm, the optimal variant when a patient pays a little payment by his/her health for a qualitative recovery.
“Whales” of the principle disease optimality are philosophy of health and disease, (mathematical) theory of optimal processes, and a principle of optimality in biology.
The opposition of “norm – pathology” is incorrect; the correct opposition is “sanology-pathology” and “health-disease”.
In health and disease, as in any other measure, norms are defined; for the norms of a disease, naturally, we should consider its optimal progression.
The principle of a disease optimality requires an additional information about a degree of optimality (non-optimality) of its progression to a diagnosis.
The principle of disease optimality proves a strategy and a tactic of a treatment of a patient through its normalization by bringing to the conditions of an optimal variant. Solving of separate tasks shouldn’t, at least, deviate from an optimal variant.
New clinic could be established on the principle of disease optimality.
понедельник, 29 декабря 2008 г.
среда, 24 декабря 2008 г.
Диагноз, под которым готов подписаться
Качка, що кульгає на обидві ноги
Все, до чого він доторкається, перетворюється в … попіл.
Жив у VII столітті до н.е. такий собі грецький цар Мідас, який, згідно міфології, мав унікальний дар: все, до чого він торкався, перетворювалось на золото. Спершу, коли в нього з'явився такий дар, жадібний цар дуже зрадів: він ходив своєю рідною країною, торкався до всього, що траплялося на очі, і підраховував прибутки.
Але пізніше виявився і інший бік медалі: цар Мідас мало не вмер з голоду, тому що їжа, до якої він торкався, теж перетворювалася в золото. Зрештою розум переміг жадобу: цар звернувся до бога Діоніса, щоб той позбавив його надприродного дару.
Час "царювання" Ющенка дуже нагадує події цього древньогрецького міфу: те, що спершу здавалося політичним золотом, виявилось м'яко кажучи попелом.
В хронічних поразках держави Україна та нинішнього українського істеблішменту можна звинувачувати кого завгодно і що завгодно.
Але головна відповідальність за всі політичні та економічні негаразди в країні повинна лежати на першій особі держави – президентові цієї держави. Інакше навіщо було брати на себе відповідальність за долю держави на цілих п'ять років?
Новини ТаблоID
Черновецький заспівав, як через нього не доспали. АУДІО
Мексиканську королеву краси затримали з партією наркотиків
Еротична фотосесія Астаф‘євої на сторінках ювілейного "Плейбою"
Кличко з підгузками сина увійшов до десятки
Федір Бондарчук з поламаною рукою рвався до Шуфрича і Ступки
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Те, що президент ніяким чином не хоче нести відповідальність за стан справ в країні, а скоріше, веде себе як сторонній спостерігач, критик та експерт з усіх внутрішньо- та зовнішньополітичних питань, зрештою стало причиною того, що Україна поступово де-факто перетворюється з президентської на парламентську державу.
Абсолютно закономірним також є ситуація, що склалася останнім часом, в якій президент фактично усунений від реального впливу на перебіг політичних та економічних подій. І знову ж таки не через дії явних чи уявних ворогів Ющенка, якими називаються Тимошенко, Янукович, Кремль тощо, а саме через бездіяльність або деструктивну діяльність президента та його секретаріату.
Ще недавно пропрезидентська фракція блоку "Наша Україна – Народна Самооборона", одним із варіантів назви якого перед останніми парламентськими виборами був "Блок Ющенка", наразі стала по суті антипрезидентською.
На наших очах здався останній плацдарм Ющенка – рідна партія "Народний союз Наша Україна", яка створювалась після феєричних революційних подій 2004 року під Ющенка і для Ющенка.
Явно послідовно закономірним є той факт, що розпад партії прискорився саме тоді, коли сам президент публічно її очолив.
Новини Життя
82,6% українців сидітимуть на Новий рік біля телевізора
Пластичний хірург заправляв своє авто жиром пацієнтів
Що європейці купують у порадунки на Різдво?
Останнє в блогах
Юрій Свірко:
Вчорашня "Сегодня" – ганьба України
Анатолій Луценко:
Час девальвації
Віктор Уколов:
''Нижче плінтуса''
Тимошенко поки набирає оберти, залучаючи на свою сторону все нові сили та нових союзників із різних таборів. Звичайно, то – ситуативні союзники, які хутко втечуть з корабля, якщо той почне тонути.
Янукович, після того, який в третій раз за своє політичне життя, практично тримаючи владу в руках, в черговий раз лоханувся і умудрився в останній момент втратити все (!!!), намагається просто зобразити "гарну міну за поганої гри" та втримати фракцію та партію від "серйозної внутрішньопартійної дискусії". Ще одна така ганебна поразка, і він – політичний труп. Показовою є нейтральність позиції Ахметова щодо ідеї створення коаліції ПР із БЮТ.
Ні Ющенко, ні Янукович вже не можуть стати центрами політичної консолідації в країні. Якщо економічна та фінансова криза змете теперішній уряд Тимошенко, нас чекає скоріше повна пертурбація теперішньої влади, ніж проста зміна "шила на мило", як ще надіються обидва Віктора.
І хай вони облишать свої "дівочі мрії".
Але такий хід подій – шанс для політиків нового покоління, які здатні нарешті зламати всевладдя злодійкуватих чиновників в країні.
Наразі бачиться найбільш ймовірними два варіанта розвитку подій в Україні найближчим часом: або уряд Тимошенко зуміє опанувати та зупинити економічну та фінансову кризу в Україні (що є дуже нелегким завданням!), або навесні нас чекає черговий неформальний Майдан.
І тоді дістанеться всім: і президенту, і уряду, і опозиції, і парламенту, і місцевій владі і т.д., і т.п.
Те, що про нинішнього президента згодом будуть складатися міфи, подібні до міфів про царя Мідаса – очевидно. Надто контраверсійним став час президентства Ющенка.
До речі: справжній, не міфологічний цар Мідас, в кінці свого царювання перебив своїх співвітчизників та став тираном. Закінчив життя самогубством, випивши бичачу кров.
Сергій Сорока
http://www.pravda.com.ua/news/2008/12/24/86711.htm
Все, до чого він доторкається, перетворюється в … попіл.
Жив у VII столітті до н.е. такий собі грецький цар Мідас, який, згідно міфології, мав унікальний дар: все, до чого він торкався, перетворювалось на золото. Спершу, коли в нього з'явився такий дар, жадібний цар дуже зрадів: він ходив своєю рідною країною, торкався до всього, що траплялося на очі, і підраховував прибутки.
Але пізніше виявився і інший бік медалі: цар Мідас мало не вмер з голоду, тому що їжа, до якої він торкався, теж перетворювалася в золото. Зрештою розум переміг жадобу: цар звернувся до бога Діоніса, щоб той позбавив його надприродного дару.
Час "царювання" Ющенка дуже нагадує події цього древньогрецького міфу: те, що спершу здавалося політичним золотом, виявилось м'яко кажучи попелом.
В хронічних поразках держави Україна та нинішнього українського істеблішменту можна звинувачувати кого завгодно і що завгодно.
Але головна відповідальність за всі політичні та економічні негаразди в країні повинна лежати на першій особі держави – президентові цієї держави. Інакше навіщо було брати на себе відповідальність за долю держави на цілих п'ять років?
Новини ТаблоID
Черновецький заспівав, як через нього не доспали. АУДІО
Мексиканську королеву краси затримали з партією наркотиків
Еротична фотосесія Астаф‘євої на сторінках ювілейного "Плейбою"
Кличко з підгузками сина увійшов до десятки
Федір Бондарчук з поламаною рукою рвався до Шуфрича і Ступки
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Те, що президент ніяким чином не хоче нести відповідальність за стан справ в країні, а скоріше, веде себе як сторонній спостерігач, критик та експерт з усіх внутрішньо- та зовнішньополітичних питань, зрештою стало причиною того, що Україна поступово де-факто перетворюється з президентської на парламентську державу.
Абсолютно закономірним також є ситуація, що склалася останнім часом, в якій президент фактично усунений від реального впливу на перебіг політичних та економічних подій. І знову ж таки не через дії явних чи уявних ворогів Ющенка, якими називаються Тимошенко, Янукович, Кремль тощо, а саме через бездіяльність або деструктивну діяльність президента та його секретаріату.
Ще недавно пропрезидентська фракція блоку "Наша Україна – Народна Самооборона", одним із варіантів назви якого перед останніми парламентськими виборами був "Блок Ющенка", наразі стала по суті антипрезидентською.
На наших очах здався останній плацдарм Ющенка – рідна партія "Народний союз Наша Україна", яка створювалась після феєричних революційних подій 2004 року під Ющенка і для Ющенка.
Явно послідовно закономірним є той факт, що розпад партії прискорився саме тоді, коли сам президент публічно її очолив.
Новини Життя
82,6% українців сидітимуть на Новий рік біля телевізора
Пластичний хірург заправляв своє авто жиром пацієнтів
Що європейці купують у порадунки на Різдво?
Останнє в блогах
Юрій Свірко:
Вчорашня "Сегодня" – ганьба України
Анатолій Луценко:
Час девальвації
Віктор Уколов:
''Нижче плінтуса''
Тимошенко поки набирає оберти, залучаючи на свою сторону все нові сили та нових союзників із різних таборів. Звичайно, то – ситуативні союзники, які хутко втечуть з корабля, якщо той почне тонути.
Янукович, після того, який в третій раз за своє політичне життя, практично тримаючи владу в руках, в черговий раз лоханувся і умудрився в останній момент втратити все (!!!), намагається просто зобразити "гарну міну за поганої гри" та втримати фракцію та партію від "серйозної внутрішньопартійної дискусії". Ще одна така ганебна поразка, і він – політичний труп. Показовою є нейтральність позиції Ахметова щодо ідеї створення коаліції ПР із БЮТ.
Ні Ющенко, ні Янукович вже не можуть стати центрами політичної консолідації в країні. Якщо економічна та фінансова криза змете теперішній уряд Тимошенко, нас чекає скоріше повна пертурбація теперішньої влади, ніж проста зміна "шила на мило", як ще надіються обидва Віктора.
І хай вони облишать свої "дівочі мрії".
Але такий хід подій – шанс для політиків нового покоління, які здатні нарешті зламати всевладдя злодійкуватих чиновників в країні.
Наразі бачиться найбільш ймовірними два варіанта розвитку подій в Україні найближчим часом: або уряд Тимошенко зуміє опанувати та зупинити економічну та фінансову кризу в Україні (що є дуже нелегким завданням!), або навесні нас чекає черговий неформальний Майдан.
І тоді дістанеться всім: і президенту, і уряду, і опозиції, і парламенту, і місцевій владі і т.д., і т.п.
Те, що про нинішнього президента згодом будуть складатися міфи, подібні до міфів про царя Мідаса – очевидно. Надто контраверсійним став час президентства Ющенка.
До речі: справжній, не міфологічний цар Мідас, в кінці свого царювання перебив своїх співвітчизників та став тираном. Закінчив життя самогубством, випивши бичачу кров.
Сергій Сорока
http://www.pravda.com.ua/news/2008/12/24/86711.htm
понедельник, 22 декабря 2008 г.
Если это "майбутнє" - всю президентскую рать на свалку, то тогда оно действительно совершается сегодня
Ющенко проведе підсумкову річну прес-конференцію
У вівторок, 23 грудня, о 18.00 в «Українському домі» розпочнеться підсумкова річна прес-конференція Президента України Віктора ЮЩЕНКА під назвою «Майбутнє твориться сьогодні».
Як повідомляв УНІАН, формат прес-конференції передбачає відповіді глави держави на запитання акредитованих медіа безпосередньо в «Українському домі», відповіді на запитання представників регіональних ЗМІ з усіх областей держави під час прямих телемостів з Одесою, Рівним та Дніпропетровськом, а також відповіді на запитання користувачів мережі Інтернет - переможців конкурсу «Спитай Президента України».
постiйна адреса статтi:
http://www.unian.net/ukr/news/news-291597.html
У вівторок, 23 грудня, о 18.00 в «Українському домі» розпочнеться підсумкова річна прес-конференція Президента України Віктора ЮЩЕНКА під назвою «Майбутнє твориться сьогодні».
Як повідомляв УНІАН, формат прес-конференції передбачає відповіді глави держави на запитання акредитованих медіа безпосередньо в «Українському домі», відповіді на запитання представників регіональних ЗМІ з усіх областей держави під час прямих телемостів з Одесою, Рівним та Дніпропетровськом, а також відповіді на запитання користувачів мережі Інтернет - переможців конкурсу «Спитай Президента України».
постiйна адреса статтi:
http://www.unian.net/ukr/news/news-291597.html
понедельник, 15 декабря 2008 г.
Бедная "эта страна", у которой такой Президент
В http://news.liga.net/news/N0868539.html Президент сказал: "В этой стране, кроме Президента, эту тему никто не поднимает, - отметил глава украинского государства. - И если вы хотите думать о рейтинге, лучше об этом не говорить. Но если вы хотите думать о поколении ваших детей, и если вы порядочный политик, у вас нет другого способа. Только вставать каждый день и говорить нации - мы должны быть самодостаточными, мы должны находиться под покровом тех моделей безопасности, которые говорят о вечной Украине".
воскресенье, 14 декабря 2008 г.
Хроническая болезнь почек или пример, достойный подражания
Зашел к студентам 6-го курса, а они рассматривают хроническую болезнь почек.
Я им о том, что есть большая река Днепр, которая с многих ручейков, потому что "с небольшого ручейка начинается река".
Но в большой воде Днепра какая вода с этого ручейка, это вопрос, потому что ответа на него просто нет. Все смешалось в водах Днепра.
Так же точно и у Давыдовского - в цепи причинно-следственных отношений первопричина с некоторого момента утрачивается и имеет исключительно историческое значение.
Поэтому и получается правильно, потому что работает "хроническая болезнь почек".
Если тему развить, распространить на другие системы, то МКБ следующего пересмотра "усушится" так, порядка на три.
Результат - и врачам будет легче, и пациентам лучше.
Действительно, пример, достойный подражания.
Я им о том, что есть большая река Днепр, которая с многих ручейков, потому что "с небольшого ручейка начинается река".
Но в большой воде Днепра какая вода с этого ручейка, это вопрос, потому что ответа на него просто нет. Все смешалось в водах Днепра.
Так же точно и у Давыдовского - в цепи причинно-следственных отношений первопричина с некоторого момента утрачивается и имеет исключительно историческое значение.
Поэтому и получается правильно, потому что работает "хроническая болезнь почек".
Если тему развить, распространить на другие системы, то МКБ следующего пересмотра "усушится" так, порядка на три.
Результат - и врачам будет легче, и пациентам лучше.
Действительно, пример, достойный подражания.
суббота, 13 декабря 2008 г.
От себя не убежишь
Понятно, спрятался от назначенной на эту дату интернет-конференции. И козе понятно, что давно нужны были действия, а не нарада точно на дату авансированной конференции. Но от себя не убежишь.
Ющенко проведе екстрену нараду
13.12.2008 21:32___ www.ПРАВДА.com.ua
У вівторок, 16 грудня, президент Віктор Ющенко проведе екстрену нараду з головами місцевих адміністрацій та мерами міст в зв'язку з проблемами теплопостачання в регіонах.
Українська правда
Ющенко проведе екстрену нараду
13.12.2008 21:32___ www.ПРАВДА.com.ua
У вівторок, 16 грудня, президент Віктор Ющенко проведе екстрену нараду з головами місцевих адміністрацій та мерами міст в зв'язку з проблемами теплопостачання в регіонах.
Українська правда
пятница, 12 декабря 2008 г.
Это не касается украинского политикума, в особенности, мнящего себя лидером нации
Гольбах писал: "в природе могут быть лишь естественные причины и следствия".
В нашем политикуме с ньюансами, что в названии,причины и следствия только искуственные. Возможно,потому, что он сам далеко не природная конструкция.
В нашем политикуме с ньюансами, что в названии,причины и следствия только искуственные. Возможно,потому, что он сам далеко не природная конструкция.
Ничто не рождается и не умирает в природе
Так писал Гольбах.
Но эта его мысль есть отражение хорошо известного латинского выражения - «разрушение одного — рождение другого»,или,в оригинале,«desiructio unius,generatio alterius».
Точно также и у человека - пока он жив,вернее,пока он выживает при болезнях,разрушение одного обязательно сменяется рождением другого.Не может быть поэтому у живого человека чисто разрушительных патологических процессов. Даже когда он умирает,то только потому, что созидательные процессы по моменту времени или интенсивности не отвечали разрушительным.
Но эта его мысль есть отражение хорошо известного латинского выражения - «разрушение одного — рождение другого»,или,в оригинале,«desiructio unius,generatio alterius».
Точно также и у человека - пока он жив,вернее,пока он выживает при болезнях,разрушение одного обязательно сменяется рождением другого.Не может быть поэтому у живого человека чисто разрушительных патологических процессов. Даже когда он умирает,то только потому, что созидательные процессы по моменту времени или интенсивности не отвечали разрушительным.
Поль Анри Гольбах
"человек должен искать в самой природе и в своих собственных силах средства удовлетворения своих потребностей, лекарства от своих страданий и пути к счастью" - сказано сильно.
Еще сильнее будет,когда прислушаемся к сказанному, и будем использовать его в своей повседневной деятельности.
Что касается здоровья человека,я бы первую часть выражения ограничил природой человека, а именно, "своей природой", а слово "природа", как и слово "человек", писал бы с заглавной.
Мысь тогда с ограничениями на здоровье приобрела бы такое очертание:
Человек должен искать в самой своей Природе и в своих собственных силах средства удовлетворения своих потребностей, лекарства от своих страданий и пути к счастью.
Еще сильнее будет,когда прислушаемся к сказанному, и будем использовать его в своей повседневной деятельности.
Что касается здоровья человека,я бы первую часть выражения ограничил природой человека, а именно, "своей природой", а слово "природа", как и слово "человек", писал бы с заглавной.
Мысь тогда с ограничениями на здоровье приобрела бы такое очертание:
Человек должен искать в самой своей Природе и в своих собственных силах средства удовлетворения своих потребностей, лекарства от своих страданий и пути к счастью.
понедельник, 8 декабря 2008 г.
Цена чашки сладкого чая или есть еще порох в пороховницах
Я не в буквальном, но переносном смысле.
Смысле, сколько стоит совет о чашке сладкого чая.
А суть такова.
Звонит старый давний друг, знаменитый профессор, знаменитее меня, думаю, которому так, около восьмидесяти, что с женой проблема, которая где-то того же возраста.
И проблема, что как позавтракает утром, так упадок сил. Ничего не может делать, и днями в постели. И консультантов крутится вокруг, хоть пруд пруди, и вроде ничего нет, ан проблема не решается.
Я как раз на поезд в командировку собирался, и с советом: "А Вы ей каждый раз перед завтраком минут за (30-40) хорошо подслащенного чая, а вернусь, посмотрим".
Прошло больше недели, вернулся, звоню.
Меня мой друг перебивает благодарностями: "Жена как на свет народилась, активная, дома все путем, супермаркеты чистит, ...". В общем я как бы спаситель.
Вот Вам и цена совета с чашкой сладкого чая.
Красивая клиническая задача принесла моральное удовлетворение: "Есть еще порох в пороховницах".
Смысле, сколько стоит совет о чашке сладкого чая.
А суть такова.
Звонит старый давний друг, знаменитый профессор, знаменитее меня, думаю, которому так, около восьмидесяти, что с женой проблема, которая где-то того же возраста.
И проблема, что как позавтракает утром, так упадок сил. Ничего не может делать, и днями в постели. И консультантов крутится вокруг, хоть пруд пруди, и вроде ничего нет, ан проблема не решается.
Я как раз на поезд в командировку собирался, и с советом: "А Вы ей каждый раз перед завтраком минут за (30-40) хорошо подслащенного чая, а вернусь, посмотрим".
Прошло больше недели, вернулся, звоню.
Меня мой друг перебивает благодарностями: "Жена как на свет народилась, активная, дома все путем, супермаркеты чистит, ...". В общем я как бы спаситель.
Вот Вам и цена совета с чашкой сладкого чая.
Красивая клиническая задача принесла моральное удовлетворение: "Есть еще порох в пороховницах".
воскресенье, 7 декабря 2008 г.
Грош цена ферритину
Гемоглобин в норме - в дециграммах на литр или еще как, а вот ферритина недостает. Недостает - сказано мягко,потому что ровно половина от нижнего уровня возрастной и половой нормы.
Так вот нужно железо такому пациенту или нет, вот в чем вопрос.
Потому что если критерии исключения для лечения препаратами железа в нормальном гемоглобине, так грош цена ферритину.
Ферритину, но не низкому уровню ферритина!
Так вот нужно железо такому пациенту или нет, вот в чем вопрос.
Потому что если критерии исключения для лечения препаратами железа в нормальном гемоглобине, так грош цена ферритину.
Ферритину, но не низкому уровню ферритина!
пятница, 5 декабря 2008 г.
Непостижимое в этом мире
Альберт Энштейн: "Самое непостижимое в этом мире - то, что он постижим".
Понимаю, правильно, не постижим, но постигаем, потому что постигать его и постигать.
Как и природу Человека, постижением которой занимается непостижимая по размерам плеяда медиков.
Непостижимая по размерам плеяда медиков постигает постигаемую, но не постижимую природу Человека.
Получается, непостижимое в этом мире - и постигаемая природа Человека тоже.
Понимаю, правильно, не постижим, но постигаем, потому что постигать его и постигать.
Как и природу Человека, постижением которой занимается непостижимая по размерам плеяда медиков.
Непостижимая по размерам плеяда медиков постигает постигаемую, но не постижимую природу Человека.
Получается, непостижимое в этом мире - и постигаемая природа Человека тоже.
среда, 3 декабря 2008 г.
Полагаться на закостенелые выражения не стоит
Природа "скупа" и не может под процесс - фермент. Под процесс фермент - это когда инвентаризация процессов не проводилась, и все посылаются на старые догмы, которые давно бы в архив ...
Увеличение активности фермента в крови - это не столько отражение процессов разрушительных, сколько процессов созидательных. И не имеет значения, какой фермент вы имеете ввиду.
Так что полагаться на закостенелые выражения не стоит.
Увеличение активности фермента в крови - это не столько отражение процессов разрушительных, сколько процессов созидательных. И не имеет значения, какой фермент вы имеете ввиду.
Так что полагаться на закостенелые выражения не стоит.
воскресенье, 30 ноября 2008 г.
Кто Вы, господин Ющенко, Президент Украины или президент политической силы?
Понял, шапка гаранта нации оказалась не по размеру, иначе бы как?:
Ющенко: крім НСНУ, нема кому подбати про Україну
Партія “Народний Союз Наша Україна” – єдина політична сила, яка послідовно відстоює стратегічні національні пріоритети України та працює над їхньою реалізацією, наголосив Президент України Віктор ЮЩЕНКО у своєму виступі на з`їзді НСНУ.
Як повідомляє прес-служба Президента, він заявив: «Я не бачу іншої політичної сили, яка б з такою чіткістю, ясністю і праведністю могла б формулювати і відстоювати національні пріоритети».
Глава держави підкреслив: «Наша Україна» працює не на короткострокові настрої і не женеться за рейтингами. «Ми – партія стратегічних інтересів. Наша політична сила підтримує все, що стосується української незалежності, українських цінностей», – сказав він.
«Фракція повинна бути більш дисциплінованою і консолідованою», – наголосив В.ЮЩЕНКО. «Ми багато втратили, бо послабили партійну дисципліну», – додав Президент.
В.ЮЩЕНКО закликав членів фракції НУ-НС до консолідованої роботи у непростий для країни час. «Головне, щоб ми формували національні пріоритети, навколо них об`єднували прихильників, які можуть конструктивно ставитися до спільної мети. У нас є цінності, які співпадають із цінностями нашої держави. Ми – та сила, яка основу своєї консолідації бачить саме у служінні цим цінностям», – наголосив глава держави.
постiйна адреса статтi:
http://www.unian.net/ukr/news/news-287310.html
Шальные мысли рождаются в шальных же головах!!!
Ющенко: крім НСНУ, нема кому подбати про Україну
Партія “Народний Союз Наша Україна” – єдина політична сила, яка послідовно відстоює стратегічні національні пріоритети України та працює над їхньою реалізацією, наголосив Президент України Віктор ЮЩЕНКО у своєму виступі на з`їзді НСНУ.
Як повідомляє прес-служба Президента, він заявив: «Я не бачу іншої політичної сили, яка б з такою чіткістю, ясністю і праведністю могла б формулювати і відстоювати національні пріоритети».
Глава держави підкреслив: «Наша Україна» працює не на короткострокові настрої і не женеться за рейтингами. «Ми – партія стратегічних інтересів. Наша політична сила підтримує все, що стосується української незалежності, українських цінностей», – сказав він.
«Фракція повинна бути більш дисциплінованою і консолідованою», – наголосив В.ЮЩЕНКО. «Ми багато втратили, бо послабили партійну дисципліну», – додав Президент.
В.ЮЩЕНКО закликав членів фракції НУ-НС до консолідованої роботи у непростий для країни час. «Головне, щоб ми формували національні пріоритети, навколо них об`єднували прихильників, які можуть конструктивно ставитися до спільної мети. У нас є цінності, які співпадають із цінностями нашої держави. Ми – та сила, яка основу своєї консолідації бачить саме у служінні цим цінностям», – наголосив глава держави.
постiйна адреса статтi:
http://www.unian.net/ukr/news/news-287310.html
Шальные мысли рождаются в шальных же головах!!!
пятница, 28 ноября 2008 г.
Найдите разницу
Разбитой можно считать лишь ту жизнь, которая остановилась в своем развитии, - говорил О.Уальд.
Коль в росте я остановлюсь, чей жертвой стану, все равно мне, - говорил В. Гете.
Жизнь, получается, - это когда каждый день победа над собой, чтобы не остановиться, не имеет значения, в росте или развитии, когда оба они здесь одно и то же.
Найдите разницу, ели найдете.
Коль в росте я остановлюсь, чей жертвой стану, все равно мне, - говорил В. Гете.
Жизнь, получается, - это когда каждый день победа над собой, чтобы не остановиться, не имеет значения, в росте или развитии, когда оба они здесь одно и то же.
Найдите разницу, ели найдете.
О природе соматических болезней у взрослых, или когда врачебные рекомендации не стоят ни гроша
У взрослых соматические болезни, в конечном итоге, являются фенотипической реализацией гетотипической вероятности. По генетическим обстоятельствам, другими словами, у человека имеется предрасположенность к развитию той или иной группы соматических заболеваний, которая реализуется в силу влияния совокупности неблагоприятных факторов среды (внешней и внутренней).
Образ жизни - это все или почти все, чтобы болезнь развилась или не развилась, а когда развилась, чтобы не протекала или протекала наиболее благоприятным из возможных образом.
Врачебные рекомендации, которые не строятся на платформе модифицированного должным путем образа жизни, не стоят ни гроша.
Образ жизни - это все или почти все, чтобы болезнь развилась или не развилась, а когда развилась, чтобы не протекала или протекала наиболее благоприятным из возможных образом.
Врачебные рекомендации, которые не строятся на платформе модифицированного должным путем образа жизни, не стоят ни гроша.
воскресенье, 23 ноября 2008 г.
Все равно подагра
Если приступ как приступ, но артрит во всех красках в ключично-грудинном сочленении,тщательнее поспрашивайте пациента. Вдруг окажется, что приступ провоцирован отжиманием, а сам пациент из отряда дровосеков. Для него ключно-грудинный, все равно, что первый межфаланговый правой стопы.
Ей, подагре, все равно, лишь бы сустав был "трудягой".
Тофусы здесь как документальное подтверждение, если найдете.
Ей, подагре, все равно, лишь бы сустав был "трудягой".
Тофусы здесь как документальное подтверждение, если найдете.
воскресенье, 16 ноября 2008 г.
Человечность, что мозг, шире небес
Emily Dickinson писал, что "the brain is wider than the sky."
Лучше не скажешь. Для меня давно тело - всего лишь слуга мозга, а мозг все равно, что Космос.
Каждый из нас индивидуальность, явление космического масштаба.
Ценим себя, свою индивидуальность,ценим человечество, человечность. Человечность прежде всего.
Человечность шире небес, как и мозг.
Лучше не скажешь. Для меня давно тело - всего лишь слуга мозга, а мозг все равно, что Космос.
Каждый из нас индивидуальность, явление космического масштаба.
Ценим себя, свою индивидуальность,ценим человечество, человечность. Человечность прежде всего.
Человечность шире небес, как и мозг.
суббота, 15 ноября 2008 г.
Хронические болезни: когда речь идет о социальном здоровье
Хронические, которые неизлечимые, с которыми до последнего вдоха. И только смерть ставит точку над такими болезнями.
В клинической практике мы оптимизируем течение хронических болезней, делаем так, чтобы их течение минимально сказывалось на ресурсах здоровья наших пациентов, чтобы, другими словами, плата ресурсами здоровья за них была минимальной.
Так мы не должны поступать, однако, когда речь идет о болезнях политикума, потому что плата за здоровье нации при, мягко выражаясь, паршивеньком или даже средней паршивости политикуме, оказывается слишком высокой.
И когда рейтинг кого-нибудь из них падает ниже уровня приличия, надо просить уступить место другим. Если не понимает, ну что же, надо сделать все, чтобы понял.
Речь идет то не об индивидуальном, но социальном здоровье. И здесь так здоровее и дешевле. А иногда, как сегодня, так критично важно, просто потому что в противном случае на месте страны образуется территория.
Не допустим, господин ...нт!
В клинической практике мы оптимизируем течение хронических болезней, делаем так, чтобы их течение минимально сказывалось на ресурсах здоровья наших пациентов, чтобы, другими словами, плата ресурсами здоровья за них была минимальной.
Так мы не должны поступать, однако, когда речь идет о болезнях политикума, потому что плата за здоровье нации при, мягко выражаясь, паршивеньком или даже средней паршивости политикуме, оказывается слишком высокой.
И когда рейтинг кого-нибудь из них падает ниже уровня приличия, надо просить уступить место другим. Если не понимает, ну что же, надо сделать все, чтобы понял.
Речь идет то не об индивидуальном, но социальном здоровье. И здесь так здоровее и дешевле. А иногда, как сегодня, так критично важно, просто потому что в противном случае на месте страны образуется территория.
Не допустим, господин ...нт!
пятница, 14 ноября 2008 г.
Лидер нации
Человек, который объединяет нацию.
Человек, для которого нет "белых" и "черных", "своих" и "врагов".
Но, боже упаси, не интриган и раскольник!
Человек, для которого нет "белых" и "черных", "своих" и "врагов".
Но, боже упаси, не интриган и раскольник!
вторник, 11 ноября 2008 г.
Кто он, человек с ограниченными возможностями здоровья
Человек с ограниченными возможностями здоровья в странах,образовавшихся на развалинах СССР, - инвалид.
На Западе тоже был инвалид, но сегодня именно, - человек с ограниченными возможностями здоровья.
Этим Запад решил проблему равноправия взаимоотношений между лицами без ограничений и с с ограниченными возможностями здоровья.
Так пришло время поступать и нам.
Термин естественно использовать и в клинической практике, когда пациент уже далеко и не больной, но именно человек с ограниченными возможностями здоровья.
Это не игра в термины, это другая философия и совершенно другие подходы.
Осилим?
На Западе тоже был инвалид, но сегодня именно, - человек с ограниченными возможностями здоровья.
Этим Запад решил проблему равноправия взаимоотношений между лицами без ограничений и с с ограниченными возможностями здоровья.
Так пришло время поступать и нам.
Термин естественно использовать и в клинической практике, когда пациент уже далеко и не больной, но именно человек с ограниченными возможностями здоровья.
Это не игра в термины, это другая философия и совершенно другие подходы.
Осилим?
понедельник, 3 ноября 2008 г.
Найти бы надо
Вы не найдете нижние уровни нормы холестерина как общего, так и его фракций. Но быть они должны по той простой причине, что холестерин так же необходим живому, как и вода, безразлично, живая или неживая.
Недостаточно хотестерина, и ждите проблем.
Но вот какие они, нижние уровни, пойдите и попробуйте найти.
Не найдете.
А я замечу, что у пациента с клинически манифестированным атеротромбозом не редко видим низкий холестерин.
Так как найти?
А найти бы надо.
Или открыть для всех.
Недостаточно хотестерина, и ждите проблем.
Но вот какие они, нижние уровни, пойдите и попробуйте найти.
Не найдете.
А я замечу, что у пациента с клинически манифестированным атеротромбозом не редко видим низкий холестерин.
Так как найти?
А найти бы надо.
Или открыть для всех.
воскресенье, 2 ноября 2008 г.
Что-то встречать таких не приходилось
Был в деревне - родственники по обоим линиям, которым, естественно,далеко за семдесят, в очередь со всякими болячками.
Я в ответ - радуйтесь, что болит, живете значит, и на каждое больное место движений в раза три больше, чем на здоровое.
Мое замечание, что встречать не приходилось, которые бы жили с обратным отсчетом времени, их обрадовало.
Радуемся каждому прожитому дню вместе.
Я в ответ - радуйтесь, что болит, живете значит, и на каждое больное место движений в раза три больше, чем на здоровое.
Мое замечание, что встречать не приходилось, которые бы жили с обратным отсчетом времени, их обрадовало.
Радуемся каждому прожитому дню вместе.
пятница, 31 октября 2008 г.
Ласточек нужно столько, сколько нужно
А сколько нужно, не ответит никто. Хотя я могу ответить:"Нужно столько, сколько людей будет вовлекаться в ласточкины орбиты". И причина проста - никто не учится на ошибках чужих.
Поэтому ошибки будут и будут повторяться, и каждый раз сначала.
Поэтому ошибки будут и будут повторяться, и каждый раз сначала.
вторник, 28 октября 2008 г.
Сколько еще нужно этих ласточек?
Очередная "ласточка" прилетела из J Am Geriatr Soc 2008; 56:1853-1859.
Оказывается, для пожилых лучше, когда систолическое артериальное давление больше 140 мм рт ст и хуже - когда меньше 120 мм рт ст. Во втором случае растут частоты деменции, сердечной недостаточности и смерти.
Оно и понятно, но не понятно, почему непонятно, что хотя "любви все возрасты покорны", в каждом возрасте она (любовь) своя, или по своему. Как больше нравится.
Медленно и пока еще неуверенно "наш паровоз" поворачивает в сторону возрастной нормы, которая, ой как отличается у лиц старшей возрастной группы.
Что еще надо сделать, сколько еще нуно ласточек, чтобы миром правил его величество случай?!
Оказывается, для пожилых лучше, когда систолическое артериальное давление больше 140 мм рт ст и хуже - когда меньше 120 мм рт ст. Во втором случае растут частоты деменции, сердечной недостаточности и смерти.
Оно и понятно, но не понятно, почему непонятно, что хотя "любви все возрасты покорны", в каждом возрасте она (любовь) своя, или по своему. Как больше нравится.
Медленно и пока еще неуверенно "наш паровоз" поворачивает в сторону возрастной нормы, которая, ой как отличается у лиц старшей возрастной группы.
Что еще надо сделать, сколько еще нуно ласточек, чтобы миром правил его величество случай?!
воскресенье, 26 октября 2008 г.
Unknown in English Media View on Mechanisms and Management of Acute Myocardial Infarction
Unknown in English Media View on Mechanisms and Management of Acute Myocardial Infarction
Yabluchansky Mykola (Nikolay)
Internal Diseases Dept. of School of Fundamental Medicine of Kharkiv Karazin National University (Ukraine)
The object of this publication is to present unknown in English media my understanding of acute myocardial infarction (AMI), that was developed at last two decades of previous century. This understanding is based on insight on AMI as one of types of acute inflammation.
Definition
AMI is a disease or a clinical syndrome accompanying other diseases, which is represented by acute coronarogenous aseptic inflammation of the part of a heart wall, and clinically correlates with stress reactions of body control systems and is determined by the extent, localization, nature, and stage of structural transformations in the infarction zone, as well as circulation changes, and their consequences.
'Myocardial infarction is coronarogenic myocardial necrosis', this inaccurate formulation travels with small variations from one book to another.
In terms of pathology, it may still be true. Though, even there, it is far from being accurate - infarction equals myocardial necrosis only if an inflammation reaction is absent and a necrotic tissue is never substituted with the granulation one. So, a patient dies early. But what we can say about the rest of patients? Is it not infarction any more? For example in case a patient dies during sub acute period AMI only granulations are found in the place of necrosis [1].
Everybody agrees that AMI goes clinically through the most acute, acute, sub acute, and post myocardial infarction periods. This is reflected in circulatory disturbances in the infarction zone, ischemia, first still reversible, then irreversible, necrosis, and the connective substitution of a necrotic myocardium with cicatrisation (of course, through inflammation, what can be the other way?) [3, 13, 15]. And it everything is tinted (and how) with stress-intermediary systemic reactions, secondary disturbances of biomechanics of heart functions, and intracardiac and central hemodynamics [9, 11, 12].
It is clear that this definition reflects the heart of the matter.
Etiology
As follows from the definition of AMI, it develops, when local coronary circulation disturbances as a triggering mechanism cross the time threshold and make the ischemia irreversible. Strictly speaking, acute ischemia that already crossed the threshold is just the formal cause of a further chain of events that results in pathology and the clinical picture of the disease.
All other causes are the sources not of AMI itself, but of the above mentioned 'local' triggering mechanism.
Mechanisms
The mechanisms of AMI should naturally be examined at systemic and local levels. They were selected by evolution. They are aimed at providing most favorable of possible courses of the disease [22]. Therefore, its complications can be understood only in terms of philosophy of failure of these mechanisms.
We should pray that, as often as possible, AMI followed mechanisms established genetically and selected by Nature. And the number of disturbances in them was as small as possible.
Systemic level
The response of organism systems to AMI is realized through stress and clinically manifests itself as brain mediated sympathetic activation and increased functional activity of a hypothalamic-pituitary an adrenal system with the change of functions of all target organs. For a favorable course and outcome of the disease, all other conditions being equal, an adequate organization of stress (eustress) becomes of primary importance.
Stress is switched on at the very beginning of ischemia. Its causes are different. These are changes in the interception of blood vessels and tissues in the infarction zone. It is also the entry of metabolic products from the infarction zone to the systemic circulation. Spasms of pain, sympathetic activation, hormones entering blood, blood leukocyte reactions, hyperdynamic circulation are the first manifestations of the stress [5, 19]. The pain signals an emergency. Besides, it makes the patient forget all other problems to devote attention to his health in real earnest.
Leukocyte reactions are important for the further development of the process, though they are usually considered to be of secondary importance. These reactions are triggered by the ejection of leukocytes from the depot to the systemic blood flow. Since the depot mainly contains neutrophils, leukocytosis appears as the shift in cell count, neutrophils are activated and migrate to the infarction zone by positive chemotaxis. Infarction zone products getting in the blood flow play the role of attractants for them. The activation of neutrophils appears as hyperenzymemia (transaminase, etc.), higher contents of eicosanoids, leukotrienes in particular, protein-carbohydrate complexes, and other biologically active agents.
Stress is changing as the process develops. Nervous and humoral regulations are regained. Leukocytosis declines, and the leukogram changes. Granulocyte counts decrease, and their functional activity is suppressed, while agranulocyte counts and their activity increase. The structural change of the leukogram is the result of controlling effects of infarction zone products getting in the blood flow. Thus, neutrophil decay products from the infarction zone are repellents for neutrophils and attractants for agranulocytes. An enzyme level in blood falls, while the proteins and protein-carbohydrate complexes content grows. These are the systemic manifestations of an inflammation process in the infarction zone. Thus, even such a special case as hyperfibrinogenemia is not a sign of the activation of blood coagulation system but is the evidence that the situation with AMI takes a satisfactory turn. Here, it is important to remember that great hopes, placed in anticoagulant therapy, were not justified. These lost hopes cost life to many patients. It was long ago…
With the termination of an AMI phase, regulation problems disappear and not a trace remains of the stress. I would ask to take notice of the fact that we speak of a natural uncomplicated pathologic process.
Local level
The local level is the heart. The components of a pathologic process at the local level are not only changes in the infarction zone and recovery of heart shape and sizes but also adaptive changes of biomechanics of heart functions.
Infarction zone
Here everything is clear. All that happens is inflammation. Special, aseptic, alterative but still inflammation.
Let us look at phase processes. The first one is ischemia, reversible myocardial changes. Strictly speaking, it is the precursor of AMI, the state of pre-infarction. It is fully reversible . But if…. AMI, of course.
The transfer to irreversible changes marks the onset of necrosis. Necrosis is a lesion. General pathology teaches that in the location of the lesion there is always inflammation [2, 3, 16]. The lesion is the cause of inflammation. Thus, with the transfer from ischemic changes in the infarction zone to the necrotic ones, the inflammation starts in accordance with its traditional scheme. The necrotized myocardium undergoes destruction, and decay products are removed through the peri-infarction zone. It is specifically destroyed by neutrophil getting by chemotaxis from blood into the infarction zone and producing cathepsins. Their migration rate is rather high, about 2-4 mm per hour. It is easy to calculate that even the largest possible infarction is infiltrated by neutrophils in 6 hours at the most. At the same time, fibroblast precursors enter the infarction zone and the recovery process begins. It is impossible to separate necrotic and recovery processes, to look at them as the individual ones. They are synchronized and interconnected not only at the level of the infarction zone itself but also at the systemic blood level.
An absolutely false view raised to the level of dogma exists: necrotic and recovery processes in AMI are separated, the recovery processes following the necrotic ones. If this were true, all patients would be dead. Most likely, because of heart rupture. If not because of heart rupture, then because of acute vast aneurysm, for sure.
Necrosis is destruction, tissue gangrene [16]. The tissue loses its functions, not only contractile characteristics but also strength properties [4]. If infarction were necrosis, the heart wall in the infarction zone would have raveled out as a rotten shirt. But it does not happen in the case of an uncomplicated process. The strength properties of the myocardium in the infarction zone do not decrease. Moreover, for various reasons they even increase during the acute period. The retained strength of the heart wall in the infarction zone demonstrates that infarction in survived patients is not necrosis but inflammation accompanied with synchronized necrotic and reparative processes.
The result of a natural inflammation course in the infarction zone is the formation of a full-fledged scar in the place of necrosis. Maturation of a granulation tissue results in its consolidation followed by a decrease in infarction zone sizes. Depending on conditions, they can decrease by 25% or more.\ We should remind those who want to strongly intervene in the infarction zone that the phenomena occurring there (inflammation, compensatory and adaptive responses) are protective reactions originated as the result of evolution. On the whole, it is clear. We may intervene but carefully.
Peri-infarction zone
Systemic mechanisms and the infarction zone are interconnected through the peri-infarction zone, first of all, through its microcirculatory bed. Wastes from the infarction zone are removed through it, and the products necessary for reparative processes enter there the same way.
The larger the infarction–peri-infarction zone interface, the better the mutual effect of the infarction zone and systemic control. The peri-infarction zone cannot be smaller than that required for uncomplicated healing of the infarction zone [1, 5]. Therefore all the efforts to restrict it were doomed to failure.
Heart shape and size
In the case of infarction, a part of a mycrocardium becomes disabled. Disabled forever. And the functions of this part should be compensated. Hypertrophy of an intact myocardium develops. Healing of the infarction zone accompanied with the consolidation of scar leads to a decrease in its size. At the same time, corresponding changes occur in the intact myocardium [4, 9]. The heart shape is remodelled in such a way that its anatomic proportions are restored to favour its pumping functions. In the best case, the traces of infarction are difficult to reveal, even after thorough investigations.
Heart biomechanics
As everything, it is governed by processes controlling the course of the disease. During early phases, poststress rigidity of an intact myocardium is developing as a response to stress. Diastolic filling of ventricles diminishes, and the heart force drops. Minute blood volume is maintained by an adequate heart rate growth. A drop in ventricular ejection, along with regulatory effects on vascular tension mediated by stress, result in a decrease in peripheral resistance. The heart load decreases. As a result, biomechanics is improved and a sufficient systemic blood flow is maintained. In the case of an uncomplicated process we cannot find defects in this system as well.
Complications
Frequency
AMI is a complex and vulnerable process. In the most optimistic estimations, its complications are observed somewhere in a quarter of cases [10, 14, 22]. Of course, if it is diagnosed and treated correctly.
Immediate cause
Lets start with predisposing factors. However many we can name, all of them hit one target. The immediate cause of complications is inadequate stress. In other words, distress. Have little patience, and we would see how distress is realized as complications.
Risk factors
AMI can happen in a practically healthy person. Then, there is a good chance that it would take a favorable course. If such serious factors as vast infarction zone size, involvement of a cardiac conduction system and serious cardiac rhythm disturbances do not appear.
Vast infarction determines hyperreactive distress with possible torpid phase of true cardiac shock, or it causes an initially hyporeactive course, most likely with a short and therefore missed hyporeactive phase. Small infarction induces systemic wave reactions, and there is danger of its spread.
But it is not all. Even under most favorable conditions, a natural cataclysm (e.g. magnetic storm at the Sun) may happen, and as a result, stress out steps the limits of adaptive changes.
Risk of complications is higher in young and elderly persons. The coronary system of young patients is not trained, thus, vigorous stress reactions are highly possible, and it is not so difficult for them to turn into hyperreactive distress. On the contrary, elderly patients have problems with regulatory processes and, thus, with sufficiency of stress.
The following previous diseases are of great importance: diabetes mellitus, arterial hypertension and hypotension, immunodeficiency, particularly in the form of chronic immunopathologic processes. The above and other predisposing factors are multiplied in their interaction in such a way that the effect of sum exceeds the sum of effects. Comments are needless.
Standard mechanism of complications
We would remind that the cause of complications is distress. It is hyperreactive, hyporeactive or intermittent. The mechanism of complications, irrespective of a distress type, is always the same, viz. desynchronization of necrotic and reparative processes.
Desynchronization of necrosis and reparation leads to the loss of heart wall strength in the infarction zone. It is but a step from here to the stretching with cardiac aneurysm or heart rupture outcomes. 'High arterial pressure is a threat of rupture', we are frightened. The threat, of course, if the heart wall strength in the infarction zone falls to a critical level.
The strength of a heart in the case of uncomplicated myocardial infarction as in healthy people is 'a hard nut to crack', even for the highest pressure. Since biomechanical properties of the infarction zone differ from those of the intact myocardium, healing of the infarction zone is complicated not only due to the loss of heart wall strength but also due to the concentration of stresses along its boundary. Their magnitude grows when other unfavorable factors are superimposed. Thus, the areas of marked curvature of inner heart ventricular surfaces (transition of an interventricular septum onto other ventricular walls, transition of ventricular walls onto papillary muscles, etc.) are anatomic stress concentrators. If the infarction zone boundary is close to such a concentrator, the loss of strength contributes to its easier rupture. Major factors of stress concentration along the infarction zone boundary that contribute to its rupture.
Hyperreactive distress is excessive activation of all its determining systems. The result is intensive and rapid migration of polynuclears to the infarction zone. Necrosis and destruction are accelerated. Reparative processes lag behind. There is the desynchronization. If the infiltration of polynuclears to the infarction zone is excessive, their decay products retard the entry of reparative agents. In such cases a pathologist finds classical myocardial infarction: nothing but coronarogenic necrosis. Fast destruction of myocardium in the infarction zone has one more consequence, viz. high concentration gradients of all products formed in it along the boundary with the peri-infarction zone. Why not a condition for the electric instability of a heart? As a result, arrhythmia.
In the case of hyporeactive distress, everything develops slowly. Systemic reactions are sluggish or are absent at all. Thus, there are problems with the infiltration of polynuclears to the infarction zone. As a result, the necrotic phase is slow, which leads to the delay of reparative processes and their slow development. So, the desynchronization.
Hyperreactive distress leads to more commonly seen arrhythmia, earlier cardiac aneurysm and heart rupture. Hyporeactive distress with a sluggish disease pattern determines large sizes of aneurysm. As a rule, heart rupture occurs in the thinnest area of aneurysm.
- 'Intermittent distress, what happens?'
- 'Superposition of the above mechanisms by the formula: 'out of the frying-pan into the fire'. Everything becomes much more dangerous.'
The result of healing complications accompanied with distress of any type, as it was already mentioned, is aneurysm (acute and chronic, naturally) and heart rupture. They happen earlier upon hyperreactive distress but cover much larger areas in other stress cases. Acute aneurysm is most often acute cardiac insufficiency, and chronic one is chronic cardiac insufficiency. It is difficult to imagine heart rupture without cardiac shock. Arrhythmia upon hyperreactive distress, especially in the hyperreactive phase of intermittent distress, is quite natural.
During subendocardial myocardial infarction, healing complications with retarded necrotic processes are ready to turn into thromboendocarditis. Just dare say that it is not a patch, protection from the loss of strength in the infarction zone? Thrombus formation disturbances give rise to thromboembolism [5].
We can continue this topic. But it is already clear that the share of healing complications is growing like a 'snow ball' in the complications of the disease in general.
Compensatory processes
AMI is a disease or a clinical syndrome accompanying other diseases. All that occurs simultaneously with infarction is highly pathologic but not physiologic. But it, in terms of Voino-Yasenetsky's philosophy [2], corresponds to current requirements and, therefore, is normal. Inflammation, the typical pathologic process underlying the disease, is just that by definition.
Let us remember transitional atrial flutter accompanying large acute myocardial infarction. Whatever they say, a decrease in heart preload is an extremely precise mechanism. Of course, if this arrhythmia is normosystolic, and what is more, at a rate within upper limits of the norm. Try to restore sinus rhythm in such a patient, and his heart would start to 'choke'. Have you ever met such a situation?
We have already discussed compensatory functions of naturally formed thromboendocarditis. But if this process is disturbed? Of course, when we actively intervene in blood coagulability with the purpose of treatment. Or let us remember coronaroactive drugs for improving the blood supply in the peri-infarction zone. It appeared that they robbed it. Simply, because Nature did it the way that in the case of infarction, the vessels of the infarction zone are dilated as much as possible. There is nowhere to dilate them any more. We administer coronaroactive drugs and dilate the vessels of an intact myocardium. Blood flows out of the peri-infarction zone. It is an old story.
The conclusion is simple. Before improving something, one should first think for a while. And no more than that.
Clinics
Uncomplicated and complicated AMI’s are entirely different phenomena. We have good reason to make such a conclusion. Uncomplicated infarction is an evolution-selected and practically realizable strategy of the best healing of the infarction zone with the most qualitative recovery of a patient. Complicated infarction is the result and manifestation of disturbances in the realization of this strategy [6, 7]. Its clinical picture is different. And the clinical picture of uncomplicated infarction is a standard for its complicated forms [5]. If so, lets start with the standard.
Uncomplicated acute myocardial infarction
Just because it is uncomplicated, it does not create problems either for a patient or for his doctor. Of course, there are clinical manifestations of stress and the local processes described above (at the level of the infarction zone and heart as a whole). There is no getting away from them, myocardial infarction nevertheless.
The clinical picture of uncomplicated healing: pain is rapidly reduced by rather moderate measures, and higher levels of hormones, leukocytes, enzymes, proteins, protein-carbohydrate complexes in blood accompanied with phase changes correspond to infarction zone size (not very low and not excessively high, just fit perfectly well). The spectral analysis of cardiac rhythm demonstrates its tendency to metronomization with the redistribution of regulatory effects in favour of humoral immunity and a sympathetic nervous system. However, heart rate variability increases very soon, and the contribution from parasympathetic regulation also grows. An enzyme level reaches its maximum by the 18th hour from the beginning of the AMI and then decreases regularly. A level of protein-carbohydrate complexes starts growing from the 2nd day and reaches its maximum no later than by the 5th day. Blood analysis: moderate leukocytosis with neutrophilia that in a day gives place to constantly growing agranulocytic reactions.
All this is the evidence of satisfactory control and synchronized necrotic and reparative processes in the infarction zone. As the saying goes, we are waiting for a good scar in the place of necrosis. The electrocardiogram exhibits AMI signs but with expected evolution: the ST segment rapidly returns to the isoline.
Ultrasound reveals segmental disturbances of myocardial contractility, but the thickness of the heart wall in the infarction zone is retained. A heart rate increases, a stroke volume falls, but a minute volume is adequate to current requirements. Even if there are rhythm disturbances, they are perceptible only on the first or the second day at the latest. These extrasystolae are not dangerous and will not require any measures.
Patients feel well and become more active very early. Such behaviour not half worsens the prognosis, it favours more rapid recovery. Let us be honest, we often fear not the early activation of patients but our responsibility. And that is the most irresponsible treatment of the problem.
Complicated acute myocardial infarction
Though its clinical picture is rather diverse, certain regularities are evident. It would be unjust to lose the chance. Distress is the precursor of a trouble, therefore, this is far and away that we should establish its possible causes in a patient, determine the contribution from each of them.
A threatening sign of serious complications is a recurring, difficult-to-stop pain. Levels of hormones, leukocytes, enzymes, proteins, and protein-carbohydrate complexes in blood are growing. But those growths are insufficient or exceed any reasonable bounds. Phase changes are always associated with certain problems. They are too late or are taking such features… Their most degenerated forms are clear evidence of intermittent distress. Cardiac rhythm is metronomized, its rate falls rapidly. The contribution from humoral regulation to the energy spectrum is incommensurably growing. A parasympathetic component is suppressed almost completely. In the most serious cases, the result of metronomization is an equally low level or almost complete absence of all parts of the energy spectrum [8].It is white noise instead of regulation.
These changes appear long before other clinical complications and retain enviable stability. A level of blood enzymes reaches its maximum very early, during the first 12-14 hours, or with a considerable delay, in a day or more. In contrast to this, in both cases a level of protein-carbohydrate complexes starts growing with a delay, in four or more days from the beginning of the catastrophe. Blood exhibits undeveloped or excessive leukocyte reactions, without neutrophilia or with almost total predominance of neutrophils over cellular forms. The change from granulocytic to agranulocytic reactions as well as a growth of protein-carbohydrate complex concentrations is also late.
All these are clinical manifestations of desynchronization of necrotic and reparative processes. Heart rupture, acute or chronic aneurysm are not far distant. This implies an emergence of different forms of acute cardiac insufficiency, from true cardiogenic shock to cardiac asthma attacks, the development of chronic cardiac insufficiency. The electrocardiogram does not display any evolution of the ST segment, and only a frozen monophase curve is seen (naturally, in the most dramatic cases).
Ultrasound can easily reveal aneurysm, rupture of papillary muscles with valvular insufficiency, defects of an interventricular septum, other signs of complications of the major (inflammatory!) process in the infarction zone. Even if a heart rate grows, it cannot compensate a drop of a stroke volume under all circumstances. Regulatory systems can 'get frustrated’, and then a small ejection is multiplied by bradycardia. Patients can give bradycardic reactions instead of tachycardic ones.
The dilatation of cardiac cavities with the slowing down of intracardiac flows, especially in the case of clumsy intervention in blood coagulation systems is a good precondition for the disturbance of thrombogenesis (with thromboembolism).
Rhythm disturbances are another matter. They are resistant to interventions; they appear when they are not waited for, especially, as regards the states threatening the life of a patient. The clinical picture answering hyperreactive distress includes early rhythm disturbances.
Pathologic remodeling of heart chamber shapes during the formation of postmyocardial infarction aneurysm increases diastolic rigidity of a myocardium. Cardiac insufficiency becomes systole-diastolic.
The growth of stresses in a heart wall as the result of pathologic remodeling is the source of tardy persistent arrhythmia. It arises in the development of complications by any of possible mechanisms, but it should be treated carefully. Sometimes this is compensatory extrasystole, e.g. atrial flutter observed in critical patients.
Defects in the immune system controlling an inflammatory process in the infarction zone result in immunopathologic reactions by a Dressler's syndrome type.
It is easy to come to the conclusion that the specific feature of any clinical picture of complicated infarction in a patient is the deviation of the inflammatory process in the infarction zone from its natural course. The cause of this deviation is problems with regulation and interaction of regulatory systems with the infarction zone.
Differential diagnosis and prognostication
It is important to differentiate not only uncomplicated infarction from its complications but also among its complicated forms. It is even more important not to simply differentiate but to foresee them. Only in this case, we get the real opportunity to control the process, from simple observation to intervention with bringing to uncomplicated conditions. Criteria of differentiation and prognostication are summarized in Table 1. AMI with intermittent distress can start from any form cited in Table 1. These criteria are tentative and correspond to infarction zone sizes of about 10-20% of the corresponding camera.
Management of patients
The approach to a patient with AMI has its specific features. But how can it be otherwise? We are dealing with the catastrophe. Any catastrophe first of all implies the introduction of urgent measures, adequate in letter and in spirit. Naturally, everything is important, including regimen. And everything [5, 15, 18] should happen in good time.
Urgent measures
The very first urgent measure is naturally resuscitation, especially if a patient is in the state of clinical death. The next question: does his state satisfy the criteria (indications and contraindications) of thrombolytic therapy? If yes, it should be started as soon as possible [12]. Both resuscitation and thrombolysis exert a direct influence on regulatory systems, and we should always expect the transformation of eustress into distress in such patients if it were not already there. Resuscitation measures include adrenergic drugs activating stress. Successful thrombolysis accelerates the entering of infarction zone products in the systemic blood flow. This is a natural mechanism of activation of regulatory systems, therefore, stress increases as a rule. A postreperfusion syndrome is not only the evidence of successful thrombolysis but also the danger of the transfer from eustress, if the disease started in such a way, to hyperreactive distress with known consequences. Likely life-threatening arrhythmia is only an episode. But successful thrombolysis can additionally regulate control systems if the disease started with hyporeactive distress. On the contrary, it would have disastrous consequences if we cannot solved the problem of hyperreactive distress following thrombolysis [5, 22]. Urgent measures also include the control of pain. Pain informed about the catastrophe. But here its constructive role comes to an end. Further, it is only the overstrain of regulatory systems, thus, hyperstress and hypostress that follows it. By alleviating pain, we can reduce stress reactivity, transform hyperreactive distress into eustress, eustress into hyporeactive distress, or aggravate hyporeactive distress even more.
Thus, urgent measures require one to control the state of regulatory systems and to intervene in case of necessity bringing them to eustress conditions. Therefore on hyperreactive distress, narcotic and nonnarcotic analgetics, alpha and beta adrenoblockaders, nonsteroid anti-inflammatory agents are usually used. Upon hyporeactive distress, they are alpha- and beta-adrenostimulants, corticosteroids, leukopoiesis stimulants. Doses and administration periods are determined by the transformation of distress into eustress, activity levels in its approach to eustress parameters.
Regimen
At the very beginning of the disease, physical activity should be restricted. It is the necessary condition for ensuring mechanisms and processes to be effected for a favourable outcome of the disease. The first two days are sufficient time in the uncomplicated case. After that, physical activity is extended. You need not be afraid, the safety margin of a heart is high enough even as regards the infarction zone, and in these cases, it never drops below the level for a healthy person.
If there are prognostic signs of complications or the complications are present, physical activation is delayed. In the case of complicated acute myocardial infarction, the strength of the heart wall in the infarction zone decreases. Here early physical activation enhances the formation or extension of aneurysm, or possible heart rupture. But even in the worst cases, the time sufficient for the substitution of a granulation tissue for the necrotized one is no more than 12-16 days, thus, it is beyond reason to postpone activation till later. Everything should be done in proper time.
As regards the diet, its quantity and caloric value should be limited during the first days, divided into frequent small meals. It is important to follow digestion, avoiding constipation and meteorism. All this exerts a negative influence on the state of a heart, blood circulation, and regulatory systems.
Regimen is one of the most important components of patient management. We cannot diminish the importance of psychotherapeutic assistance. In this connection, we should emphasize the necessity of simple personal contacts that are always insufficient for a patient and that favour common success to a very great extent [7, 17, 20, 21].
Drug Therapy
The uncomplicated course of the disease does not require any measures. Only observation. In complicated cases, we cannot do without pharmaceuticals. Regulatory systems and processes, occurring in the infarction zone, should be brought to the state when the development of complications becomes impossible. A sudden decrease in the energy spectrum of heart rate variability and its parasympathetic component can be controlled by small doses of belladonna preparations. Upon a simultaneous decrease of a sympathoparasympathetic component, small doses of blockaders of an angiotensin-converting enzyme (ACE) are prescribed for long periods.
Upon hyperreactive distress and accelerated necrotic processes, our aim is to decrease the former and to retard the latter, using beta blockaders and anti-inflammatory drugs administered enterally and/or parenterally.
Hyporeactive distress and retarded necrotic processes require the prescription of alpha -and beta-adrenostimulants, bacterial and leukocytic pyrogens, leukopoiesis stimulants, using several ways of administration.
Upon intermittent distress, the attitude should be even more careful to prevent wave recurrence of necrotic processes.
As the optimization of distress of any type is approached, pharmaceuticals, promoting reparation in the infarction zone, should be added. These are leucopoiesis stimulants, steroid and nonsteroid anabolics.
If the therapy is optimized, clinical complications do not develop or are not so serious. It refers to possible heart rupture, acute and chronic aneurysms, giving rise to acute and chronic cardiac insufficiency, arrhythmia, and other complications.
When necrotic and reparative processes are seriously desynchronized and we cannot expect the complete restoration of synchronization, additional measures are necessary. We can try and prevent the development of aneurysm or the formation of a scar of large sizes, reducing terminal diastolic filling and postload on heart cameras. Here the choice is the combination of ACE blockaders with depot-nitrates and nitrites.
Special attention should be paid to patients with immunopathologic reactions and states to avoid the development of a postmyocardial infarction syndrome. Here immunomodulators would be useful.
If a heart rate does not exceed its upper level by more than 10%, with a decrease in peripheral resistance and cardiac output, sinus tachycardia is certainly of compensatory nature, and it should not be intervened. Our attitude to it should also be the same in the case of aneurysm development. Any intervention would be more detrimental. If it is necessary to intervene in tachycardiac reactions, this intervention should be administered in such a way that a decreasing heart rate would still be retained at the upper level of a physiological norm.
Rate disturbances, even if they are associated with the involvement of conduction system elements in the infarction zone, require careful treatment all the same. Diuretics prescribed for a short period would probably shorten the exudative phase of inflammation, and as a result, conduction would be improved. An external pacemaker would also be useful for a short time. It would solve the problem precisely, and this is inaccessible for any pharmaceuticals.
Extrasystole and paroxysmal tachycardia during the most acute and acute periods of the disease are the evidence of possible hyperreactive distress and accelerated necrosis. Their correction reduces risk and frequency of arrhythmia. In this case, beta-blockers are anti-arrhythmic drugs with a pronounced antistress effect.
Sinus tachycardia as well as other forms of arrhythmia can be not only pathologic but also compensatory. Extrasystole accompanied with pronounced bradycardia requires pharmaceuticals increasing a heart rate, such as atropine, belladonna preparations, etc. Arrhythmia accompanying the development of acute and chronic aneurysms is caused by high pressure of left ventricle filling. Anti-arrhythmic measures decrease heart preload and effectively reduce diastolic ventricular filling. Ectopic substituting rhythms are the problem of a sinus node. Therefore, one should think first before their suppressing. Normosystolic atrial flutter, suddenly appearing on cardiac insufficiency, causes a local decrease of heart preload. And probably, with the improvement of hemodynamic status, it would disappear by itself.
Direct anticoagulants should be treated with care. Surgeons know well that these drugs retard the healing phase of a wound process, and thus, the reparative phase of acute myocardial infarction. Those who went through the enthusiasm for direct anticoagulants remember that the main cause of the death of patients was associated with thromboembolic complications. It is quite clear; Nature always takes vengeance for clumsy steps, e.g., the development of uncontrollable disseminated intravascular coagulation. Nowadays this enthusiasm has disappeared. And we can see that from the results, thank goodness. Even after thrombolysis, it is better to exclusively use heparins followed by small doses of anti-aggregants that also exhibit an anti-inflammatory effect.
There is one more danger in using direct anticoagulants. AMI with the involvement of an endocardium is accompanied with thromboendocarditis. A forming thrombus is the additional and effective way of penetration of agents ensuring and maintaining inflammation, thus, more effective reparation in the infarction zone. The thrombus formed is also a 'patch', protection from possible aneurysm and heart rupture. Direct coagulants disturb thrombogenesis. In this case, bulky, unconsolidated thrombi are formed. Why they should not tear and become the cause of thromboembolic complications? There are many things to think about, especially if you use your own experience of patient management. Maybe, a thrombus absent in transmural myocardial infarction is the cause of aneurysm or heart rupture.
The problem of coronaroactive drugs as basic therapeutic means does not require any discussions. The times have passed when it was considered that they improved circulation in the peri-infarction zone and favoured its healing. Thus, they are used only in accordance with strict indications.
It is desirable to recommend to hypodynamic patients with an atonic anterior abdominal wall to administer laxatives for a certain period of time. In the case of meteorism, enteral adsorbents are good.
Conclusion, or the most important principles
Everything is good in its season, therefore any measure should be well-timed. You cannot afford to be late. The human organism possesses such remarkable properties that any newly initiated process, including AMI and its complications, is subject to external therapeutic effects only for a certain period of time. As soon as the process is self-organized, it stops to be subject to those effects.
One of physician's percepts is festina lente. Not in the sense that you should not be in a hurry to respond. But in the sense that you should not be in a hurry to modify some or other functions and processes. You should be a good hand in 'transferring' a patient from hypertensive crisis to hypotensive one, from tachycardia to bradycardia, etc., what is more with AMI. This is 'out of the frying-pan into the fire'. Rapid actions are necessary only in the case of the catastrophe or for the period of the catastrophe.
After finding new syndromes and symptoms in a patient, the first thing you should do is to think. Why this syndrome all of a sudden? Of course, everything that happens in the case of AMI is pathologic. Here we refer to Voino-Yasenetsky again [2]. He was quite right that an appearing syndrome, maybe, met the requirement of the situation and, therefore, is normal. On the whole, you should measure thrice but, maybe, you will not have to cut.
Many physicians prefer the parenteral administration of drugs. And it is good. Still nobody can live without preferences. But for catastrophic health disorders, all the processes in a patient develop not so quickly. And problems with a digestive system is most likely an exceptional case, thus, there are no grounds to refuse it credence in the transport of drugs to the blood flow. Why not give preference to enteral forms of drugs?
The most important thing in AMI as in any other disease is that it is the mechanism of withdrawal from the catastrophe. In a specific way, losing a part of a contractile myocardium and substituting it with a connective tissue through inflammation, or through other irretrievable losses. We have already discussed them. Nevertheless we have nowhere to go. We have to go through the disease. And the most important thing: it should take the best of all possible courses, i.e. the optimum course. The task of a physician is to lead a patient through the disease, to lead a patient with AMI through his own AMI. Here the best strategy is the optimization of complicated forms of the disease bringing them to uncomplicated conditions.
This strategy is based on the disease optimum principle [6, 7], in accordance with the latter, the optimum is minimum health resources spent for recovery.
Principle components as applied to AMI:
• identification of its optimum for a patient;
• determination of an extent and nature of its deviations from the optimum;
• verification of a diagnosis in accordance with the above;
• determination of the global target of the disease optimum as the best possible outcome with maximum full-fledged substitution of a connective tissue for the necrotic one in the infarction zone;
• treatment of a patient by bringing the disease to its optimum depending on a mechanism and extent of deviations as well as time of therapy initiation;
• solution of local problems by methods that do not contradict the global aim.
The optimum management of a patient with AMI is within power of a real physician.
References
1. G. G. Avtandilov, N. I. Yabluchansky, K. D. Salbiev, and L. M. Nepomnyashchikh. Quantitative Morphology and Mathematical Simulation of Myocardial Infarction (in Russian), Nauka, Moscow, 1984.
2. M. I. Voino-Yasenetsky. Biology and Pathology of Infectious Processes (in Russian), Nauka, Moscow, 1981.
3. I. V. Davydovsky. General Human Pathology (in Russian), Meditsina, Moscow, 1969.
4. B. Ya. Kantor, N. I. Yabluchansky, and V. E. Shlyakhover. Nonlinear Cardiobiomechanics of a Left Ventricle (in Russian), Naukova Dumka, Kiev, 1991.
5. L. T. Malaya, N. I. Yabluchansky, and M. A. Vlasenko. Uncomplicated and Complicated Forms of Myocardial Infarction Healing (in Russian), Zdorovie, Kiev, 1992.
6. N. I. Yabluchansky, L. G. Vasilieva, and Yu. L. Volyansky. Disease Optimum Principle (in Russian), Osnova, Kharkov, 1992.
7. N. I. Yabluchansky. Optimum Management of Somatic Patients (General Approach) (in Russian), Osnova, Kharkov, 1995.
8. N. I. Yabluchansky, A. V. Martynenko, and A. S. Isaeva. Basics of Practical Application of Blood Circulation Variability Technology (in Russian), Osnova, Kharkov, 2000.
9. E. Braunwald. Approach to the Patient With Heart Disease. In: Harrison's Principles of Internal Medicine, 11th Ed., McGraw-Hill, New York, 1987.
10. P. F. Cohn. Silent Myocardial Ischemia and Infarction, 4th Ed., Dekker, New York, 2000.
11. T. E. David. Mechanical Complications of Myocardial Infarction, Chapman & Hall, New York, 1996.
12. G. S. Francis and J. S. Alpert. Coronary Care, 2nd Ed., Little Brown, Boston, 1995.
13. B. J. Gersh and S. H. Rahimtoola. Acute Myocardial Infarction, 2nd Ed., Chapman & Hall, New York, 1996.
14. K. Jennings. Acute Cardiac Care: Community and Hospital Management of Myocardial Infarction, Oxford University Press, New York, 1994.
15. D. Julian and E. Braunwald. Management of Acute Myocardial Infarction, W. B. Saunders, Philadelphia, 1994.
16. M. Kissane. Anderson's Pathology, 9th Ed., Mosby, St. Louise, 1990.
17. W. L. Morgan and G. L. Engel. The Clinical Approach to the Patient, W. B. Saunders, Philadelphia, 1969.
18. S. Nash and V. Fuster. Efficacy of Myocardial Infarction Therapy: An Evaluation of Clinical Trials, Dekker, New York, 1999.
19. H. Selye. The Stress of Life, McGraw-Hill, New York, Toronto, London, 1956.
20. P. A. Tumulty. The Effective Clinician: His Methods and Approach to Diagnosis and Care, W. B. Saunders, Philadelphia, 1973.
21. H. R. Wulff. Rational Diagnosis and Treatment: An Introduction to Clinical Decision Making, Mosby, St. Louise, 1981.
22. N. I. Yabluchansky. Acute Myocardial Infarction Strategy, Osnova, Kharkov, 2000.
Yabluchansky Mykola (Nikolay)
Internal Diseases Dept. of School of Fundamental Medicine of Kharkiv Karazin National University (Ukraine)
The object of this publication is to present unknown in English media my understanding of acute myocardial infarction (AMI), that was developed at last two decades of previous century. This understanding is based on insight on AMI as one of types of acute inflammation.
Definition
AMI is a disease or a clinical syndrome accompanying other diseases, which is represented by acute coronarogenous aseptic inflammation of the part of a heart wall, and clinically correlates with stress reactions of body control systems and is determined by the extent, localization, nature, and stage of structural transformations in the infarction zone, as well as circulation changes, and their consequences.
'Myocardial infarction is coronarogenic myocardial necrosis', this inaccurate formulation travels with small variations from one book to another.
In terms of pathology, it may still be true. Though, even there, it is far from being accurate - infarction equals myocardial necrosis only if an inflammation reaction is absent and a necrotic tissue is never substituted with the granulation one. So, a patient dies early. But what we can say about the rest of patients? Is it not infarction any more? For example in case a patient dies during sub acute period AMI only granulations are found in the place of necrosis [1].
Everybody agrees that AMI goes clinically through the most acute, acute, sub acute, and post myocardial infarction periods. This is reflected in circulatory disturbances in the infarction zone, ischemia, first still reversible, then irreversible, necrosis, and the connective substitution of a necrotic myocardium with cicatrisation (of course, through inflammation, what can be the other way?) [3, 13, 15]. And it everything is tinted (and how) with stress-intermediary systemic reactions, secondary disturbances of biomechanics of heart functions, and intracardiac and central hemodynamics [9, 11, 12].
It is clear that this definition reflects the heart of the matter.
Etiology
As follows from the definition of AMI, it develops, when local coronary circulation disturbances as a triggering mechanism cross the time threshold and make the ischemia irreversible. Strictly speaking, acute ischemia that already crossed the threshold is just the formal cause of a further chain of events that results in pathology and the clinical picture of the disease.
All other causes are the sources not of AMI itself, but of the above mentioned 'local' triggering mechanism.
Mechanisms
The mechanisms of AMI should naturally be examined at systemic and local levels. They were selected by evolution. They are aimed at providing most favorable of possible courses of the disease [22]. Therefore, its complications can be understood only in terms of philosophy of failure of these mechanisms.
We should pray that, as often as possible, AMI followed mechanisms established genetically and selected by Nature. And the number of disturbances in them was as small as possible.
Systemic level
The response of organism systems to AMI is realized through stress and clinically manifests itself as brain mediated sympathetic activation and increased functional activity of a hypothalamic-pituitary an adrenal system with the change of functions of all target organs. For a favorable course and outcome of the disease, all other conditions being equal, an adequate organization of stress (eustress) becomes of primary importance.
Stress is switched on at the very beginning of ischemia. Its causes are different. These are changes in the interception of blood vessels and tissues in the infarction zone. It is also the entry of metabolic products from the infarction zone to the systemic circulation. Spasms of pain, sympathetic activation, hormones entering blood, blood leukocyte reactions, hyperdynamic circulation are the first manifestations of the stress [5, 19]. The pain signals an emergency. Besides, it makes the patient forget all other problems to devote attention to his health in real earnest.
Leukocyte reactions are important for the further development of the process, though they are usually considered to be of secondary importance. These reactions are triggered by the ejection of leukocytes from the depot to the systemic blood flow. Since the depot mainly contains neutrophils, leukocytosis appears as the shift in cell count, neutrophils are activated and migrate to the infarction zone by positive chemotaxis. Infarction zone products getting in the blood flow play the role of attractants for them. The activation of neutrophils appears as hyperenzymemia (transaminase, etc.), higher contents of eicosanoids, leukotrienes in particular, protein-carbohydrate complexes, and other biologically active agents.
Stress is changing as the process develops. Nervous and humoral regulations are regained. Leukocytosis declines, and the leukogram changes. Granulocyte counts decrease, and their functional activity is suppressed, while agranulocyte counts and their activity increase. The structural change of the leukogram is the result of controlling effects of infarction zone products getting in the blood flow. Thus, neutrophil decay products from the infarction zone are repellents for neutrophils and attractants for agranulocytes. An enzyme level in blood falls, while the proteins and protein-carbohydrate complexes content grows. These are the systemic manifestations of an inflammation process in the infarction zone. Thus, even such a special case as hyperfibrinogenemia is not a sign of the activation of blood coagulation system but is the evidence that the situation with AMI takes a satisfactory turn. Here, it is important to remember that great hopes, placed in anticoagulant therapy, were not justified. These lost hopes cost life to many patients. It was long ago…
With the termination of an AMI phase, regulation problems disappear and not a trace remains of the stress. I would ask to take notice of the fact that we speak of a natural uncomplicated pathologic process.
Local level
The local level is the heart. The components of a pathologic process at the local level are not only changes in the infarction zone and recovery of heart shape and sizes but also adaptive changes of biomechanics of heart functions.
Infarction zone
Here everything is clear. All that happens is inflammation. Special, aseptic, alterative but still inflammation.
Let us look at phase processes. The first one is ischemia, reversible myocardial changes. Strictly speaking, it is the precursor of AMI, the state of pre-infarction. It is fully reversible . But if…. AMI, of course.
The transfer to irreversible changes marks the onset of necrosis. Necrosis is a lesion. General pathology teaches that in the location of the lesion there is always inflammation [2, 3, 16]. The lesion is the cause of inflammation. Thus, with the transfer from ischemic changes in the infarction zone to the necrotic ones, the inflammation starts in accordance with its traditional scheme. The necrotized myocardium undergoes destruction, and decay products are removed through the peri-infarction zone. It is specifically destroyed by neutrophil getting by chemotaxis from blood into the infarction zone and producing cathepsins. Their migration rate is rather high, about 2-4 mm per hour. It is easy to calculate that even the largest possible infarction is infiltrated by neutrophils in 6 hours at the most. At the same time, fibroblast precursors enter the infarction zone and the recovery process begins. It is impossible to separate necrotic and recovery processes, to look at them as the individual ones. They are synchronized and interconnected not only at the level of the infarction zone itself but also at the systemic blood level.
An absolutely false view raised to the level of dogma exists: necrotic and recovery processes in AMI are separated, the recovery processes following the necrotic ones. If this were true, all patients would be dead. Most likely, because of heart rupture. If not because of heart rupture, then because of acute vast aneurysm, for sure.
Necrosis is destruction, tissue gangrene [16]. The tissue loses its functions, not only contractile characteristics but also strength properties [4]. If infarction were necrosis, the heart wall in the infarction zone would have raveled out as a rotten shirt. But it does not happen in the case of an uncomplicated process. The strength properties of the myocardium in the infarction zone do not decrease. Moreover, for various reasons they even increase during the acute period. The retained strength of the heart wall in the infarction zone demonstrates that infarction in survived patients is not necrosis but inflammation accompanied with synchronized necrotic and reparative processes.
The result of a natural inflammation course in the infarction zone is the formation of a full-fledged scar in the place of necrosis. Maturation of a granulation tissue results in its consolidation followed by a decrease in infarction zone sizes. Depending on conditions, they can decrease by 25% or more.\ We should remind those who want to strongly intervene in the infarction zone that the phenomena occurring there (inflammation, compensatory and adaptive responses) are protective reactions originated as the result of evolution. On the whole, it is clear. We may intervene but carefully.
Peri-infarction zone
Systemic mechanisms and the infarction zone are interconnected through the peri-infarction zone, first of all, through its microcirculatory bed. Wastes from the infarction zone are removed through it, and the products necessary for reparative processes enter there the same way.
The larger the infarction–peri-infarction zone interface, the better the mutual effect of the infarction zone and systemic control. The peri-infarction zone cannot be smaller than that required for uncomplicated healing of the infarction zone [1, 5]. Therefore all the efforts to restrict it were doomed to failure.
Heart shape and size
In the case of infarction, a part of a mycrocardium becomes disabled. Disabled forever. And the functions of this part should be compensated. Hypertrophy of an intact myocardium develops. Healing of the infarction zone accompanied with the consolidation of scar leads to a decrease in its size. At the same time, corresponding changes occur in the intact myocardium [4, 9]. The heart shape is remodelled in such a way that its anatomic proportions are restored to favour its pumping functions. In the best case, the traces of infarction are difficult to reveal, even after thorough investigations.
Heart biomechanics
As everything, it is governed by processes controlling the course of the disease. During early phases, poststress rigidity of an intact myocardium is developing as a response to stress. Diastolic filling of ventricles diminishes, and the heart force drops. Minute blood volume is maintained by an adequate heart rate growth. A drop in ventricular ejection, along with regulatory effects on vascular tension mediated by stress, result in a decrease in peripheral resistance. The heart load decreases. As a result, biomechanics is improved and a sufficient systemic blood flow is maintained. In the case of an uncomplicated process we cannot find defects in this system as well.
Complications
Frequency
AMI is a complex and vulnerable process. In the most optimistic estimations, its complications are observed somewhere in a quarter of cases [10, 14, 22]. Of course, if it is diagnosed and treated correctly.
Immediate cause
Lets start with predisposing factors. However many we can name, all of them hit one target. The immediate cause of complications is inadequate stress. In other words, distress. Have little patience, and we would see how distress is realized as complications.
Risk factors
AMI can happen in a practically healthy person. Then, there is a good chance that it would take a favorable course. If such serious factors as vast infarction zone size, involvement of a cardiac conduction system and serious cardiac rhythm disturbances do not appear.
Vast infarction determines hyperreactive distress with possible torpid phase of true cardiac shock, or it causes an initially hyporeactive course, most likely with a short and therefore missed hyporeactive phase. Small infarction induces systemic wave reactions, and there is danger of its spread.
But it is not all. Even under most favorable conditions, a natural cataclysm (e.g. magnetic storm at the Sun) may happen, and as a result, stress out steps the limits of adaptive changes.
Risk of complications is higher in young and elderly persons. The coronary system of young patients is not trained, thus, vigorous stress reactions are highly possible, and it is not so difficult for them to turn into hyperreactive distress. On the contrary, elderly patients have problems with regulatory processes and, thus, with sufficiency of stress.
The following previous diseases are of great importance: diabetes mellitus, arterial hypertension and hypotension, immunodeficiency, particularly in the form of chronic immunopathologic processes. The above and other predisposing factors are multiplied in their interaction in such a way that the effect of sum exceeds the sum of effects. Comments are needless.
Standard mechanism of complications
We would remind that the cause of complications is distress. It is hyperreactive, hyporeactive or intermittent. The mechanism of complications, irrespective of a distress type, is always the same, viz. desynchronization of necrotic and reparative processes.
Desynchronization of necrosis and reparation leads to the loss of heart wall strength in the infarction zone. It is but a step from here to the stretching with cardiac aneurysm or heart rupture outcomes. 'High arterial pressure is a threat of rupture', we are frightened. The threat, of course, if the heart wall strength in the infarction zone falls to a critical level.
The strength of a heart in the case of uncomplicated myocardial infarction as in healthy people is 'a hard nut to crack', even for the highest pressure. Since biomechanical properties of the infarction zone differ from those of the intact myocardium, healing of the infarction zone is complicated not only due to the loss of heart wall strength but also due to the concentration of stresses along its boundary. Their magnitude grows when other unfavorable factors are superimposed. Thus, the areas of marked curvature of inner heart ventricular surfaces (transition of an interventricular septum onto other ventricular walls, transition of ventricular walls onto papillary muscles, etc.) are anatomic stress concentrators. If the infarction zone boundary is close to such a concentrator, the loss of strength contributes to its easier rupture. Major factors of stress concentration along the infarction zone boundary that contribute to its rupture.
Hyperreactive distress is excessive activation of all its determining systems. The result is intensive and rapid migration of polynuclears to the infarction zone. Necrosis and destruction are accelerated. Reparative processes lag behind. There is the desynchronization. If the infiltration of polynuclears to the infarction zone is excessive, their decay products retard the entry of reparative agents. In such cases a pathologist finds classical myocardial infarction: nothing but coronarogenic necrosis. Fast destruction of myocardium in the infarction zone has one more consequence, viz. high concentration gradients of all products formed in it along the boundary with the peri-infarction zone. Why not a condition for the electric instability of a heart? As a result, arrhythmia.
In the case of hyporeactive distress, everything develops slowly. Systemic reactions are sluggish or are absent at all. Thus, there are problems with the infiltration of polynuclears to the infarction zone. As a result, the necrotic phase is slow, which leads to the delay of reparative processes and their slow development. So, the desynchronization.
Hyperreactive distress leads to more commonly seen arrhythmia, earlier cardiac aneurysm and heart rupture. Hyporeactive distress with a sluggish disease pattern determines large sizes of aneurysm. As a rule, heart rupture occurs in the thinnest area of aneurysm.
- 'Intermittent distress, what happens?'
- 'Superposition of the above mechanisms by the formula: 'out of the frying-pan into the fire'. Everything becomes much more dangerous.'
The result of healing complications accompanied with distress of any type, as it was already mentioned, is aneurysm (acute and chronic, naturally) and heart rupture. They happen earlier upon hyperreactive distress but cover much larger areas in other stress cases. Acute aneurysm is most often acute cardiac insufficiency, and chronic one is chronic cardiac insufficiency. It is difficult to imagine heart rupture without cardiac shock. Arrhythmia upon hyperreactive distress, especially in the hyperreactive phase of intermittent distress, is quite natural.
During subendocardial myocardial infarction, healing complications with retarded necrotic processes are ready to turn into thromboendocarditis. Just dare say that it is not a patch, protection from the loss of strength in the infarction zone? Thrombus formation disturbances give rise to thromboembolism [5].
We can continue this topic. But it is already clear that the share of healing complications is growing like a 'snow ball' in the complications of the disease in general.
Compensatory processes
AMI is a disease or a clinical syndrome accompanying other diseases. All that occurs simultaneously with infarction is highly pathologic but not physiologic. But it, in terms of Voino-Yasenetsky's philosophy [2], corresponds to current requirements and, therefore, is normal. Inflammation, the typical pathologic process underlying the disease, is just that by definition.
Let us remember transitional atrial flutter accompanying large acute myocardial infarction. Whatever they say, a decrease in heart preload is an extremely precise mechanism. Of course, if this arrhythmia is normosystolic, and what is more, at a rate within upper limits of the norm. Try to restore sinus rhythm in such a patient, and his heart would start to 'choke'. Have you ever met such a situation?
We have already discussed compensatory functions of naturally formed thromboendocarditis. But if this process is disturbed? Of course, when we actively intervene in blood coagulability with the purpose of treatment. Or let us remember coronaroactive drugs for improving the blood supply in the peri-infarction zone. It appeared that they robbed it. Simply, because Nature did it the way that in the case of infarction, the vessels of the infarction zone are dilated as much as possible. There is nowhere to dilate them any more. We administer coronaroactive drugs and dilate the vessels of an intact myocardium. Blood flows out of the peri-infarction zone. It is an old story.
The conclusion is simple. Before improving something, one should first think for a while. And no more than that.
Clinics
Uncomplicated and complicated AMI’s are entirely different phenomena. We have good reason to make such a conclusion. Uncomplicated infarction is an evolution-selected and practically realizable strategy of the best healing of the infarction zone with the most qualitative recovery of a patient. Complicated infarction is the result and manifestation of disturbances in the realization of this strategy [6, 7]. Its clinical picture is different. And the clinical picture of uncomplicated infarction is a standard for its complicated forms [5]. If so, lets start with the standard.
Uncomplicated acute myocardial infarction
Just because it is uncomplicated, it does not create problems either for a patient or for his doctor. Of course, there are clinical manifestations of stress and the local processes described above (at the level of the infarction zone and heart as a whole). There is no getting away from them, myocardial infarction nevertheless.
The clinical picture of uncomplicated healing: pain is rapidly reduced by rather moderate measures, and higher levels of hormones, leukocytes, enzymes, proteins, protein-carbohydrate complexes in blood accompanied with phase changes correspond to infarction zone size (not very low and not excessively high, just fit perfectly well). The spectral analysis of cardiac rhythm demonstrates its tendency to metronomization with the redistribution of regulatory effects in favour of humoral immunity and a sympathetic nervous system. However, heart rate variability increases very soon, and the contribution from parasympathetic regulation also grows. An enzyme level reaches its maximum by the 18th hour from the beginning of the AMI and then decreases regularly. A level of protein-carbohydrate complexes starts growing from the 2nd day and reaches its maximum no later than by the 5th day. Blood analysis: moderate leukocytosis with neutrophilia that in a day gives place to constantly growing agranulocytic reactions.
All this is the evidence of satisfactory control and synchronized necrotic and reparative processes in the infarction zone. As the saying goes, we are waiting for a good scar in the place of necrosis. The electrocardiogram exhibits AMI signs but with expected evolution: the ST segment rapidly returns to the isoline.
Ultrasound reveals segmental disturbances of myocardial contractility, but the thickness of the heart wall in the infarction zone is retained. A heart rate increases, a stroke volume falls, but a minute volume is adequate to current requirements. Even if there are rhythm disturbances, they are perceptible only on the first or the second day at the latest. These extrasystolae are not dangerous and will not require any measures.
Patients feel well and become more active very early. Such behaviour not half worsens the prognosis, it favours more rapid recovery. Let us be honest, we often fear not the early activation of patients but our responsibility. And that is the most irresponsible treatment of the problem.
Complicated acute myocardial infarction
Though its clinical picture is rather diverse, certain regularities are evident. It would be unjust to lose the chance. Distress is the precursor of a trouble, therefore, this is far and away that we should establish its possible causes in a patient, determine the contribution from each of them.
A threatening sign of serious complications is a recurring, difficult-to-stop pain. Levels of hormones, leukocytes, enzymes, proteins, and protein-carbohydrate complexes in blood are growing. But those growths are insufficient or exceed any reasonable bounds. Phase changes are always associated with certain problems. They are too late or are taking such features… Their most degenerated forms are clear evidence of intermittent distress. Cardiac rhythm is metronomized, its rate falls rapidly. The contribution from humoral regulation to the energy spectrum is incommensurably growing. A parasympathetic component is suppressed almost completely. In the most serious cases, the result of metronomization is an equally low level or almost complete absence of all parts of the energy spectrum [8].It is white noise instead of regulation.
These changes appear long before other clinical complications and retain enviable stability. A level of blood enzymes reaches its maximum very early, during the first 12-14 hours, or with a considerable delay, in a day or more. In contrast to this, in both cases a level of protein-carbohydrate complexes starts growing with a delay, in four or more days from the beginning of the catastrophe. Blood exhibits undeveloped or excessive leukocyte reactions, without neutrophilia or with almost total predominance of neutrophils over cellular forms. The change from granulocytic to agranulocytic reactions as well as a growth of protein-carbohydrate complex concentrations is also late.
All these are clinical manifestations of desynchronization of necrotic and reparative processes. Heart rupture, acute or chronic aneurysm are not far distant. This implies an emergence of different forms of acute cardiac insufficiency, from true cardiogenic shock to cardiac asthma attacks, the development of chronic cardiac insufficiency. The electrocardiogram does not display any evolution of the ST segment, and only a frozen monophase curve is seen (naturally, in the most dramatic cases).
Ultrasound can easily reveal aneurysm, rupture of papillary muscles with valvular insufficiency, defects of an interventricular septum, other signs of complications of the major (inflammatory!) process in the infarction zone. Even if a heart rate grows, it cannot compensate a drop of a stroke volume under all circumstances. Regulatory systems can 'get frustrated’, and then a small ejection is multiplied by bradycardia. Patients can give bradycardic reactions instead of tachycardic ones.
The dilatation of cardiac cavities with the slowing down of intracardiac flows, especially in the case of clumsy intervention in blood coagulation systems is a good precondition for the disturbance of thrombogenesis (with thromboembolism).
Rhythm disturbances are another matter. They are resistant to interventions; they appear when they are not waited for, especially, as regards the states threatening the life of a patient. The clinical picture answering hyperreactive distress includes early rhythm disturbances.
Pathologic remodeling of heart chamber shapes during the formation of postmyocardial infarction aneurysm increases diastolic rigidity of a myocardium. Cardiac insufficiency becomes systole-diastolic.
The growth of stresses in a heart wall as the result of pathologic remodeling is the source of tardy persistent arrhythmia. It arises in the development of complications by any of possible mechanisms, but it should be treated carefully. Sometimes this is compensatory extrasystole, e.g. atrial flutter observed in critical patients.
Defects in the immune system controlling an inflammatory process in the infarction zone result in immunopathologic reactions by a Dressler's syndrome type.
It is easy to come to the conclusion that the specific feature of any clinical picture of complicated infarction in a patient is the deviation of the inflammatory process in the infarction zone from its natural course. The cause of this deviation is problems with regulation and interaction of regulatory systems with the infarction zone.
Differential diagnosis and prognostication
It is important to differentiate not only uncomplicated infarction from its complications but also among its complicated forms. It is even more important not to simply differentiate but to foresee them. Only in this case, we get the real opportunity to control the process, from simple observation to intervention with bringing to uncomplicated conditions. Criteria of differentiation and prognostication are summarized in Table 1. AMI with intermittent distress can start from any form cited in Table 1. These criteria are tentative and correspond to infarction zone sizes of about 10-20% of the corresponding camera.
Management of patients
The approach to a patient with AMI has its specific features. But how can it be otherwise? We are dealing with the catastrophe. Any catastrophe first of all implies the introduction of urgent measures, adequate in letter and in spirit. Naturally, everything is important, including regimen. And everything [5, 15, 18] should happen in good time.
Urgent measures
The very first urgent measure is naturally resuscitation, especially if a patient is in the state of clinical death. The next question: does his state satisfy the criteria (indications and contraindications) of thrombolytic therapy? If yes, it should be started as soon as possible [12]. Both resuscitation and thrombolysis exert a direct influence on regulatory systems, and we should always expect the transformation of eustress into distress in such patients if it were not already there. Resuscitation measures include adrenergic drugs activating stress. Successful thrombolysis accelerates the entering of infarction zone products in the systemic blood flow. This is a natural mechanism of activation of regulatory systems, therefore, stress increases as a rule. A postreperfusion syndrome is not only the evidence of successful thrombolysis but also the danger of the transfer from eustress, if the disease started in such a way, to hyperreactive distress with known consequences. Likely life-threatening arrhythmia is only an episode. But successful thrombolysis can additionally regulate control systems if the disease started with hyporeactive distress. On the contrary, it would have disastrous consequences if we cannot solved the problem of hyperreactive distress following thrombolysis [5, 22]. Urgent measures also include the control of pain. Pain informed about the catastrophe. But here its constructive role comes to an end. Further, it is only the overstrain of regulatory systems, thus, hyperstress and hypostress that follows it. By alleviating pain, we can reduce stress reactivity, transform hyperreactive distress into eustress, eustress into hyporeactive distress, or aggravate hyporeactive distress even more.
Thus, urgent measures require one to control the state of regulatory systems and to intervene in case of necessity bringing them to eustress conditions. Therefore on hyperreactive distress, narcotic and nonnarcotic analgetics, alpha and beta adrenoblockaders, nonsteroid anti-inflammatory agents are usually used. Upon hyporeactive distress, they are alpha- and beta-adrenostimulants, corticosteroids, leukopoiesis stimulants. Doses and administration periods are determined by the transformation of distress into eustress, activity levels in its approach to eustress parameters.
Regimen
At the very beginning of the disease, physical activity should be restricted. It is the necessary condition for ensuring mechanisms and processes to be effected for a favourable outcome of the disease. The first two days are sufficient time in the uncomplicated case. After that, physical activity is extended. You need not be afraid, the safety margin of a heart is high enough even as regards the infarction zone, and in these cases, it never drops below the level for a healthy person.
If there are prognostic signs of complications or the complications are present, physical activation is delayed. In the case of complicated acute myocardial infarction, the strength of the heart wall in the infarction zone decreases. Here early physical activation enhances the formation or extension of aneurysm, or possible heart rupture. But even in the worst cases, the time sufficient for the substitution of a granulation tissue for the necrotized one is no more than 12-16 days, thus, it is beyond reason to postpone activation till later. Everything should be done in proper time.
As regards the diet, its quantity and caloric value should be limited during the first days, divided into frequent small meals. It is important to follow digestion, avoiding constipation and meteorism. All this exerts a negative influence on the state of a heart, blood circulation, and regulatory systems.
Regimen is one of the most important components of patient management. We cannot diminish the importance of psychotherapeutic assistance. In this connection, we should emphasize the necessity of simple personal contacts that are always insufficient for a patient and that favour common success to a very great extent [7, 17, 20, 21].
Drug Therapy
The uncomplicated course of the disease does not require any measures. Only observation. In complicated cases, we cannot do without pharmaceuticals. Regulatory systems and processes, occurring in the infarction zone, should be brought to the state when the development of complications becomes impossible. A sudden decrease in the energy spectrum of heart rate variability and its parasympathetic component can be controlled by small doses of belladonna preparations. Upon a simultaneous decrease of a sympathoparasympathetic component, small doses of blockaders of an angiotensin-converting enzyme (ACE) are prescribed for long periods.
Upon hyperreactive distress and accelerated necrotic processes, our aim is to decrease the former and to retard the latter, using beta blockaders and anti-inflammatory drugs administered enterally and/or parenterally.
Hyporeactive distress and retarded necrotic processes require the prescription of alpha -and beta-adrenostimulants, bacterial and leukocytic pyrogens, leukopoiesis stimulants, using several ways of administration.
Upon intermittent distress, the attitude should be even more careful to prevent wave recurrence of necrotic processes.
As the optimization of distress of any type is approached, pharmaceuticals, promoting reparation in the infarction zone, should be added. These are leucopoiesis stimulants, steroid and nonsteroid anabolics.
If the therapy is optimized, clinical complications do not develop or are not so serious. It refers to possible heart rupture, acute and chronic aneurysms, giving rise to acute and chronic cardiac insufficiency, arrhythmia, and other complications.
When necrotic and reparative processes are seriously desynchronized and we cannot expect the complete restoration of synchronization, additional measures are necessary. We can try and prevent the development of aneurysm or the formation of a scar of large sizes, reducing terminal diastolic filling and postload on heart cameras. Here the choice is the combination of ACE blockaders with depot-nitrates and nitrites.
Special attention should be paid to patients with immunopathologic reactions and states to avoid the development of a postmyocardial infarction syndrome. Here immunomodulators would be useful.
If a heart rate does not exceed its upper level by more than 10%, with a decrease in peripheral resistance and cardiac output, sinus tachycardia is certainly of compensatory nature, and it should not be intervened. Our attitude to it should also be the same in the case of aneurysm development. Any intervention would be more detrimental. If it is necessary to intervene in tachycardiac reactions, this intervention should be administered in such a way that a decreasing heart rate would still be retained at the upper level of a physiological norm.
Rate disturbances, even if they are associated with the involvement of conduction system elements in the infarction zone, require careful treatment all the same. Diuretics prescribed for a short period would probably shorten the exudative phase of inflammation, and as a result, conduction would be improved. An external pacemaker would also be useful for a short time. It would solve the problem precisely, and this is inaccessible for any pharmaceuticals.
Extrasystole and paroxysmal tachycardia during the most acute and acute periods of the disease are the evidence of possible hyperreactive distress and accelerated necrosis. Their correction reduces risk and frequency of arrhythmia. In this case, beta-blockers are anti-arrhythmic drugs with a pronounced antistress effect.
Sinus tachycardia as well as other forms of arrhythmia can be not only pathologic but also compensatory. Extrasystole accompanied with pronounced bradycardia requires pharmaceuticals increasing a heart rate, such as atropine, belladonna preparations, etc. Arrhythmia accompanying the development of acute and chronic aneurysms is caused by high pressure of left ventricle filling. Anti-arrhythmic measures decrease heart preload and effectively reduce diastolic ventricular filling. Ectopic substituting rhythms are the problem of a sinus node. Therefore, one should think first before their suppressing. Normosystolic atrial flutter, suddenly appearing on cardiac insufficiency, causes a local decrease of heart preload. And probably, with the improvement of hemodynamic status, it would disappear by itself.
Direct anticoagulants should be treated with care. Surgeons know well that these drugs retard the healing phase of a wound process, and thus, the reparative phase of acute myocardial infarction. Those who went through the enthusiasm for direct anticoagulants remember that the main cause of the death of patients was associated with thromboembolic complications. It is quite clear; Nature always takes vengeance for clumsy steps, e.g., the development of uncontrollable disseminated intravascular coagulation. Nowadays this enthusiasm has disappeared. And we can see that from the results, thank goodness. Even after thrombolysis, it is better to exclusively use heparins followed by small doses of anti-aggregants that also exhibit an anti-inflammatory effect.
There is one more danger in using direct anticoagulants. AMI with the involvement of an endocardium is accompanied with thromboendocarditis. A forming thrombus is the additional and effective way of penetration of agents ensuring and maintaining inflammation, thus, more effective reparation in the infarction zone. The thrombus formed is also a 'patch', protection from possible aneurysm and heart rupture. Direct coagulants disturb thrombogenesis. In this case, bulky, unconsolidated thrombi are formed. Why they should not tear and become the cause of thromboembolic complications? There are many things to think about, especially if you use your own experience of patient management. Maybe, a thrombus absent in transmural myocardial infarction is the cause of aneurysm or heart rupture.
The problem of coronaroactive drugs as basic therapeutic means does not require any discussions. The times have passed when it was considered that they improved circulation in the peri-infarction zone and favoured its healing. Thus, they are used only in accordance with strict indications.
It is desirable to recommend to hypodynamic patients with an atonic anterior abdominal wall to administer laxatives for a certain period of time. In the case of meteorism, enteral adsorbents are good.
Conclusion, or the most important principles
Everything is good in its season, therefore any measure should be well-timed. You cannot afford to be late. The human organism possesses such remarkable properties that any newly initiated process, including AMI and its complications, is subject to external therapeutic effects only for a certain period of time. As soon as the process is self-organized, it stops to be subject to those effects.
One of physician's percepts is festina lente. Not in the sense that you should not be in a hurry to respond. But in the sense that you should not be in a hurry to modify some or other functions and processes. You should be a good hand in 'transferring' a patient from hypertensive crisis to hypotensive one, from tachycardia to bradycardia, etc., what is more with AMI. This is 'out of the frying-pan into the fire'. Rapid actions are necessary only in the case of the catastrophe or for the period of the catastrophe.
After finding new syndromes and symptoms in a patient, the first thing you should do is to think. Why this syndrome all of a sudden? Of course, everything that happens in the case of AMI is pathologic. Here we refer to Voino-Yasenetsky again [2]. He was quite right that an appearing syndrome, maybe, met the requirement of the situation and, therefore, is normal. On the whole, you should measure thrice but, maybe, you will not have to cut.
Many physicians prefer the parenteral administration of drugs. And it is good. Still nobody can live without preferences. But for catastrophic health disorders, all the processes in a patient develop not so quickly. And problems with a digestive system is most likely an exceptional case, thus, there are no grounds to refuse it credence in the transport of drugs to the blood flow. Why not give preference to enteral forms of drugs?
The most important thing in AMI as in any other disease is that it is the mechanism of withdrawal from the catastrophe. In a specific way, losing a part of a contractile myocardium and substituting it with a connective tissue through inflammation, or through other irretrievable losses. We have already discussed them. Nevertheless we have nowhere to go. We have to go through the disease. And the most important thing: it should take the best of all possible courses, i.e. the optimum course. The task of a physician is to lead a patient through the disease, to lead a patient with AMI through his own AMI. Here the best strategy is the optimization of complicated forms of the disease bringing them to uncomplicated conditions.
This strategy is based on the disease optimum principle [6, 7], in accordance with the latter, the optimum is minimum health resources spent for recovery.
Principle components as applied to AMI:
• identification of its optimum for a patient;
• determination of an extent and nature of its deviations from the optimum;
• verification of a diagnosis in accordance with the above;
• determination of the global target of the disease optimum as the best possible outcome with maximum full-fledged substitution of a connective tissue for the necrotic one in the infarction zone;
• treatment of a patient by bringing the disease to its optimum depending on a mechanism and extent of deviations as well as time of therapy initiation;
• solution of local problems by methods that do not contradict the global aim.
The optimum management of a patient with AMI is within power of a real physician.
References
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2. M. I. Voino-Yasenetsky. Biology and Pathology of Infectious Processes (in Russian), Nauka, Moscow, 1981.
3. I. V. Davydovsky. General Human Pathology (in Russian), Meditsina, Moscow, 1969.
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11. T. E. David. Mechanical Complications of Myocardial Infarction, Chapman & Hall, New York, 1996.
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14. K. Jennings. Acute Cardiac Care: Community and Hospital Management of Myocardial Infarction, Oxford University Press, New York, 1994.
15. D. Julian and E. Braunwald. Management of Acute Myocardial Infarction, W. B. Saunders, Philadelphia, 1994.
16. M. Kissane. Anderson's Pathology, 9th Ed., Mosby, St. Louise, 1990.
17. W. L. Morgan and G. L. Engel. The Clinical Approach to the Patient, W. B. Saunders, Philadelphia, 1969.
18. S. Nash and V. Fuster. Efficacy of Myocardial Infarction Therapy: An Evaluation of Clinical Trials, Dekker, New York, 1999.
19. H. Selye. The Stress of Life, McGraw-Hill, New York, Toronto, London, 1956.
20. P. A. Tumulty. The Effective Clinician: His Methods and Approach to Diagnosis and Care, W. B. Saunders, Philadelphia, 1973.
21. H. R. Wulff. Rational Diagnosis and Treatment: An Introduction to Clinical Decision Making, Mosby, St. Louise, 1981.
22. N. I. Yabluchansky. Acute Myocardial Infarction Strategy, Osnova, Kharkov, 2000.
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