Ischemia (from the Greek “ischo” – to hold + “haema” – blood) of the myocardium is a condition in which the blood flow in the heart muscle becomes insufficient to maintain the rate of oxidative processes in the cardiomyocytes and there is a transition of intracellular respiration from the aerobic form to anaerobic. The paradox of the issue under discussion is that, despite the obvious simplicity for comprehending the literal meaning of the term “ischemia” and the apparent lack of reason for speculation, among cardiologists there is no uniform understanding of this condition. It suffices to point out that in an attempt to explain the concept of “ischemia” in response to a request addressed to the leading cardiologists of the world, there have come a lot of different variants containing from 3 to 403 words. The explanation for this, apparently, lies in the fact that for all the simplicity of the pathogenetic positions laid down in the definition, the consequences of ischemia are surprisingly diverse and have great differences underlying their pathophysiology. It is no accident that L. H. Opie figuratively called the spectrum of ischemic heart dysfunction “eternally extensible”.
The most reliable and early indication of myocardial ischemia is considered to be the development of regional dysfunction of the ventricular myocardium. But the effect of ischemia on the contractile function of the myocardium is so different in different patients that it is practically impossible to meet two identical cases (according to L. H. Opie, also as identical fingerprints). This depends on the variant of the lesion of the coronary arteries (severity and duration of ischemia), reperfusion (time and completeness of the restoration of blood flow), and myocardial response, which seems to have considerable flexibility in this response [145]. The simple statement that the heart muscle contracts less effectively in the case of blood flow limitation gives an incorrect idea of the complex com- plex of cardiovascular and biochemical reactions occurring in ischemic dysfunction. The results of intensively conducted scientific research over the past few years have greatly expanded our knowledge of this highly heterogeneous state.
Ischemic heart dysfunction can be acute and chronic. The most famous example of acute ischemic dysfunction is a local LV breach in patients with various angina variants (both painful and painless), as well as in patients with developing myocardial infarction and subsequent early reperfusion. In this case, dysfunction is transient, lasting only a few minutes or hours. If segmental violations of LV contractility in this case lead to its expressed global diastolic or systolic dysfunction, then clinical manifestations of heart failure arise (as is well known, the latter is often the equivalent of an anginal condition). Speaking at a meeting of the round table “Myocardial Ischemia: From the Understanding of Mechanisms to Adequate Treatment” of the Moscow City Scientific Cardiology Society, V. I. Kapelko noted that the process of myocardial contraction is closely related to energy metabolism. Four main metabolic consequences of ischemia, leading to contractile myocardial dysfunction, were identified: accumulation of hydrogen ions, excess phosphate, and an increased yield of adenosine and potassium ions from the cells. The problems of diagnosis, treatment and prevention of acute ischemic LV dysfunction, or more precisely – the conditions under which it is observed, are well studied and presented in the relevant sections of modern guidelines on cardiology.
With more pronounced and prolonged myocardial ischemia, there are irreversible processes of lysis of cellular structures in contracture cardiomyocytes, resulting in infarction followed by scarring. In this case, chronic LV dysfunction develops, usually associated with CHF syndrome, which is a progressive condition, which is accompanied by further damage to the heart muscle due to increased afterload, fluid retention and remodeling.
To date, severe persistent left ventricular dysfunction in patients with ischemic heart disease has been considered synonymous with MI and irreversible damage. This concept was based on the general belief that normal, viable cardiomyocytes can not be reduced. However, impressive advances in the study of the pathophysiology of myocardial ischemia made significant changes to the dominant concept and led to the realization that chronic ventricular dysfunction manifested by asynergy of myocardial contractility is not necessarily associated with permanent or irreversible damage to myocardial cells. It was found that various variants of occlusion of the coronary artery, in principle, can lead to five possible states: the absence of pronounced changes in the structure and function of the myocardium, myocardial ischemia (acute ischemic dysfunction), myocardial deafness, myocardial hibernation, and myocardial infarction. There are four more terms used to refer to conditions directly related to the problem of ischemic heart dysfunction, extending the usual thesaurus of cardiologists – preconditioning (a new phenomenon of adaptation to ischemia), ischemic cardiomyopathy, maimed myocardium and the phenomenon of “non-renewal blood flow. ”
The result of fruitful experimental studies carried out by G. R. Heyndrickx et al. Was the description of a delayed (more than 3 hours) recovery of the mechanical properties of the myocardium after acute (5 minutes) local ischemia. Then E. B. Braunwald and R. A. Kloner introduced the term “stunned myocardium,” to denote a delay in restorative contractility of the myocardium, which underwent a short (up to 10-15 minutes) ischemia followed by reperfusion (the functional activity of myocardiocytes was restored only after several hours or even days). The key elements of the stunned myocardium is a complete or pronounced decrease in coronary blood flow, the recoverability of coronary blood flow and a limited period (reversibility) of subsequent dysfunction (systolic and diastolic) of the LV. Also an important criterion of this condition is the discrepancy between coronary blood flow and myocardial function: normal or almost normal blood flow, but an abnormal function. This fundamentally distinguishes stunning from other forms of myocardial dysfunction, such as ischemia and hibernation, in which myocardial dysfunction, as a rule, corresponds to the degree of decrease in coronary blood flow.
The “scenario” of myocardial deafness is well reproduced under experimental conditions and can serve as a model of a viable myocardium. Many protocols for studying the myocardial response to ischemia and reperfusion allow one to observe stunning of the myocardium: 1) stunning after a single, completely reversible episode of regional ischemia in vivo; 2) stunning after repeated, completely reversible episodes of regional ischemia in vivo; 3) stunning after partially reversible episodes of regional ischemia in vivo (subendocardial infarction); 4) stunning after global ischemia in vitro; 5) stunning after global ischemia in vivo; 6) stunning after a load-induced ischemia (“hig-flow” ischemia). In this case, the changes occurring in the stunned myocardium can be summarized as follows: normal appearance with electronic microscopy, normal Ca2 + flow, reduced contractile response to Ca2 +, hyperproduction of calcium-binding proteins, displacement of enzymatic systems.
LV dysfunction caused by stunted myocardium occurs clinically after paroxysm of ventricular tachycardia, angiopathic angina attack, in patients with unstable angina, with thrombolytic agents in the acute period of myocardial infarction with early reperfusion, occlusion of the coronary artery with balloon during coronary angioplasty, with ischemia, caused by physical exertion, and also after open heart surgery with cardiac arrest and heart transplantation.