Myocardial infarction: causes

Acute coronary syndromes (ACS) usually develop in cases when there is an acute thrombosis of an atherosclerotic coronary artery. Atherosclerotic plaque sometimes becomes unstable or inflames, which leads to its rupture. In this case, the contents of the plaque activate platelets and a cascade of coagulation, resulting in acute thrombosis. Activation of platelets leads to conformational changes in the IIb / IIIa glycoprotein receptors of the membrane, which leads to gluing (and, thus, accumulation) of platelets. Even an atherosclerotic plaque, which blocks the blood flow to a minimum, can tear and lead to thrombosis; more than 50% of cases the vessel is narrowed by less than 40%. As a result, the thrombus sharply limits the flow of blood to the sites of the myocardium. Spontaneous thrombosis occurs in about two-thirds of patients; after 24 h, obstruction by a thrombus is detected only in approximately 30% of cases. However, in fact, always a violation of the blood supply lasts long enough to cause tissue necrosis.

Sometimes these syndromes are caused by arterial embolism (for example, in mitral or aortic stenosis, infective endocarditis). The use of cocaine and other factors that lead to coronary artery spasm may sometimes result in myocardial infarction. To a myocardial infarction may result in a spasm of a normal or atherosclerotically altered coronary artery.

[1], [2]

Pathophysiology of myocardial infarction

Initial manifestations depend on the size, location and duration of obstruction, they range from transient ischemia to infarction. The study of new, more sensitive markers indicates that small areas of necrosis probably appear even with moderate ACS variants. Thus, ischemic events occur continuously, and their classification by subgroups, although useful, is however somewhat arbitrary. The consequences of an acute event depend primarily on the mass and type of heart tissue that has undergone a heart attack.

Myocardial dysfunction

Ischemic (but not necrotic) tissue reduces contractility, leading to hypokinesia or akinesia; these segments can expand or bulge during systole (the so-called paradoxical movement). The size of the affected area determines the effects that can range from minimal or moderate heart failure to cardiogenic shock. Heart failure of varying degrees is noted in two thirds of patients hospitalized with acute myocardial infarction. In the case of low cardiac output on the background of heart failure, ischemic cardiomyopathy is put. Ischemia involving the papillary muscles can lead to regurgitation on the mitral valve.

Myocardial infarction

Myocardial infarction - myocardial necrosis due to a sharp reduction in coronary blood flow to the affected area. Necrotized tissue irreversibly loses its functionality, but there is a zone of potentially reversible changes adjacent to the infarction zone.

In most cases, myocardial infarction affects the left ventricle, but damage can extend to the right ventricle (RV) or the atrium. Myocardial infarction of the right ventricle often develops when the right coronary or dominant left envelope of the artery is affected. It is characterized by a high filling pressure of the right ventricle, often with severe tricuspid regurgitation and a reduced cardiac output. Low-back myocardial infarction causes some degree of right ventricular dysfunction in about half of patients and in 10-15% of cases leads to the appearance of hemodynamic disorders. Right ventricular dysfunction should be assumed in any patient with low-back myocardial infarction and increased pressure in the jugular veins on the background of arterial hypotension and shock. Myocardial infarction of the right ventricle, which complicates myocardial infarction of the left ventricle, can significantly increase the risk of mortality.

Anterior myocardial infarction is often more extensive and has a worse prognosis than a low-back myocardial infarction. It is usually the result of occlusion of the left coronary artery, especially the left descending branch. Low-back infarction reflects the defeat of the right coronary or dominant left envelope of the artery.

Transmural myocardial infarction involves all the thickness of the myocardium (from the epicardium to the endocardium) into the necrosis zone and is usually characterized by the appearance of a pathological wave on the electrocardiogram. Nontransmural, or subendocardial, myocardial infarction does not extend to the entire thickness of the ventricle and leads only to segment or tooth changes (ST-T). Subendocardial infarction usually involves the involvement of the inner third of the myocardium in the place where there is the greatest stress of the ventricular wall and myocardial blood flow is most sensitive to changes in circulation. Such a myocardial infarction may be followed by a prolonged period of arterial hypotension. Since the transmural depth of necrosis can not be precisely determined clinically, infarction is usually classified by the presence or absence of an increase in segment or tooth on an electrocardiogram. The volume of necrotic myocardium can be estimated approximately by the degree and duration of the increase in the activity of CK.

Electrophysiological dysfunction of the myocardium

Ischemic and necrotic cells are incapable of normal electrical activity, which is expressed by various changes in ECG data (most often ST-T changes ), arrhythmias and conduction disorders. ST-T changes include segment reduction (often obliquely downward from point J), tooth inversion, segment elevation (often estimated as a measure of damage), and pointed high tines in the acute phase of myocardial infarction. Conduction abnormalities may reflect damage to the sinus node, atrioventricular (AV) node, or the conductive myocardium system. Most of the changes are transient; some remain forever.

[3], [4], [5], [6], [7], [8]