My myocardial infarction phylosophy

В русском читайте стратегию острого инфаркта миокарда. На английский переведена давно, должна же выстрелить.

Overheard Conversation

–          Are you serious?

–          ‘bout what?

–          Hmmmm… that myocardial infarction is not the same as necrosis?

–          Why is that? It is necrosis… in the dead cases.  But in the end it is not necrosis… for those who’s alive.

–          Then what is it?

–          Inflammation.

–          Inflammation?

–          Yip. Just an inflammation.

–          ?

–          Unusual one, coronarogenous, alterative. But … it is the inflammation.

–          ?

–          Judge yourself. At first it is blood flow local disturbance. Then it is the ischemia, that is reversible in the beginning, and then it is not. Then go two interfaced processes – necrosis & granulation tissue development for the infarction zone heart wall durability being saved. And all of these are controlled by stress mechanisms.

–          It is very complicated. And in the end what do we need these for?

–          It is totally different strategy! Inflammation, as we know, is the protective compensatory-adaptive reaction to injury, that had formed under the organism evolution …

–          Do you want to say …  that acute myocardial infarction patient … doesn’t need any treatment at all?

–          It really won’t if there is no complication, or inflammation disturbances.  Another cases – it does.

–          How?

–          First of all through the inflammation optimization.

–          What are you talking ‘bout?

–          About the strategy. The acute myocardial infarction strategy, that is not against the Nature laws, but works according to them.

–          Then I have to get acquainted with your philosophy.

–          I’ll appreciate it.


 The object of this book is to present optimal management strategy of acute myocardial infarction. The new understanding of its healing mechanisms would ensure the most effective recovery.

This is impossible if we cannot create the conditions for uncomplicated healing of the infarction zone. We can restore the blood flow in a thrombosed artery, restrict infarction zone size, suppress arrhythmia, reduce cardiac pre- and afterload, improve microcirculation. We can reach any other local goal. But, what if God forbid, an  aneurysm is formed on the site of  the necrosis …

Therefore the uncomplicated healing is the only most important goal of the myocardial infarction management strategy. All other goals have to comply with it. We should not a fetish of local goals.

Is it possible to master this strategy? The answer is yes. Quite a little is needed. Jast multiply your knowledge and experience by the proper understanding of acute myocardial infarction. Then add in the philosophy of the disease optimum principle. You can do it.

Only one remark: the book is intended for a prepared reader. Those who are interested in more comprehensive presentation of the approach can look through the list of references.


Acute myocardial infarction 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 rue. 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 about the rest of them? Is it not infarction any more? For example, when a patient dies during subacute period only granulations are found in the place of necrosis [1].

Everybody agrees that acute myocardial infarction goes clinically through the most acute, acute, subacute, and postmyocardial 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 cicatrization (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 my definition reflects the heart of the matter.


Acute myocardial infarction is agreed to be one of the forms of myocardial ischemia. Thus, both share common predisposing factors [5, 12].

As follows from the definition of acute myocardial infarction, 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, if you like, in pathology and the clinical picture of the disease.

All other causes are the sources not of acute myocardial infarction itself,  but of the above mentioned ‘local’ triggering mechanism.


The mechanisms of acute myocardial infarction should naturally be examined at systemic and local levels. They were selected by evolution. They are aimed at providing most favourable 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, acute myocardial infarction 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 acute myocardial infarction is realized through stress and clinically manifests itself as brain mediated sympathetic activation and increased functional activity of a hypothalamo-pituitary an adrenal system with the change of functions of all target organs. For a favourable 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 interoception 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. Pain, sympatoadrenal system activation, hormones entering blood, blood leukocyte reactions, hyperdynamic circulation are the first manifestations of the stress syndrome [5, 19]. The pain sygnals 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 an evidence that the situation with myocardial infarction 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 acute myocardial infarction 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 sizs 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 acute myocardial infarction, the state of pre-infarction. It is fully reversible . But if…. Myocardial infarction, 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 produsing cathepsins. Their migration rate is rather high, about 2-4 mm per hour. It is easy to calculate that even the lugest 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. I described this phenomenon in the previous section, illustrating by the mechanisms of leukocytic blood reaction changes (Fig. 2).

An absolutely false view raised to the level of dogma exists: necrotic and recovery processes in acute myocardial infarction 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 mycrocardium 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.



Acute myocardial infarction 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

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