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Myocardial infarction: causes
Last reviewed: 04.07.2025
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Acute coronary syndromes (ACS) typically occur when an atherosclerotic coronary artery becomes acutely thrombosed. The atherosclerotic plaque sometimes becomes unstable or inflamed, causing it to rupture. The plaque contents then activate platelets and the coagulation cascade, resulting in acute thrombosis. Platelet activation results in conformational changes in the IIb/IIIa glycoprotein receptors on the membrane, causing platelet aggregation (and thus clumping). Even an atherosclerotic plaque that only minimally obstructs blood flow can rupture and cause thrombosis; in more than 50% of cases, the vessel is narrowed by less than 40%. The resulting thrombus severely restricts blood flow to areas of the myocardium. Spontaneous thrombosis occurs in approximately two-thirds of patients; After 24 hours, thrombus obstruction is detected in only about 30% of cases. However, in virtually all cases, the disruption of blood supply lasts long enough to cause tissue necrosis.
Sometimes these syndromes are caused by arterial embolism (e.g., mitral or aortic stenosis, infective endocarditis). Cocaine use and other factors that lead to coronary artery spasm may sometimes result in myocardial infarction. Myocardial infarction may result from spasm of a normal or atherosclerotically altered coronary artery.
[ Pathophysiology of myocardial infarction
The initial manifestations depend on the size, location, and duration of the obstruction, and range from transient ischemia to infarction. Research with new, more sensitive markers suggests that small areas of necrosis are likely to occur even in mild forms of ACS. Thus, ischemic events occur continuously, and classification into subgroups, although useful, is somewhat arbitrary. The consequences of an acute event depend primarily on the mass and type of cardiac tissue that is infarcted.
Myocardial dysfunction
Ischemic (but not necrotic) tissue reduces contractility, resulting in areas of hypokinesia or akinesia; these segments may widen or bulge during systole (called paradoxical motion). The size of the affected area determines the effects, which may range from minimal or moderate heart failure to cardiogenic shock. Heart failure of varying degrees occurs in two-thirds of patients hospitalized with acute myocardial infarction. Low cardiac output in the setting of heart failure is called ischemic cardiomyopathy. Ischemia involving the papillary muscles may result in mitral valve regurgitation.
Myocardial infarction
Myocardial infarction is myocardial necrosis due to a sharp reduction in coronary blood flow to the affected area. Necrotic tissue irreversibly loses functionality, but there is a zone of potentially reversible changes adjacent to the infarction zone.
Most myocardial infarctions involve the left ventricle, but damage may extend to the right ventricle (RV) or atria. Right ventricular myocardial infarction most often involves the right coronary artery or the dominant left circumflex artery. It is characterized by high right ventricular filling pressures, often with marked tricuspid regurgitation and reduced cardiac output. Inferoposterior myocardial infarction causes some degree of right ventricular dysfunction in approximately half of patients and causes hemodynamic compromise in 10% to 15%. Right ventricular dysfunction should be considered in any patient with inferoposterior myocardial infarction and elevated jugular venous pressure in the presence of hypotension and shock. Right ventricular myocardial infarction complicating left ventricular myocardial infarction may significantly increase the risk of mortality.
Anterior myocardial infarction is often more extensive and has a worse prognosis than inferoposterior myocardial infarction. It usually results from occlusion of the left coronary artery, especially the left descending branch. Inferoposterior infarction reflects involvement of the right coronary or dominant left circumflex artery.
Transmural myocardial infarction involves the entire thickness of the myocardium (from the epicardium to the endocardium) and is usually characterized by the appearance of an abnormal wave on the electrocardiogram. Nontransmural, or subendocardial, myocardial infarction does not extend through the entire thickness of the ventricle and results only in segment or wave (ST-T) changes. Subendocardial infarction usually involves the inner third of the myocardium at the site of greatest ventricular wall stress and myocardial blood flow most sensitive to changes in circulation. Such myocardial infarction may be followed by a prolonged period of arterial hypotension. Because the transmural depth of necrosis cannot be accurately determined clinically, infarction is usually classified by the presence or absence of segment or wave elevation on the electrocardiogram. The volume of necrotic myocardium can be roughly estimated from the degree and duration of CPK elevation.
Electrophysiological dysfunction of the myocardium
Ischemic and necrotic cells are unable to conduct normal electrical activity, resulting in a variety of ECG changes (most commonly ST-T changes), arrhythmias, and conduction abnormalities. Ischemic ST-T changes include downsloping (often sloping from the J point), inversion, upslope (often seen as an indicator of injury), and peaked, tall waves in the hyperacute phase of myocardial infarction. Conduction abnormalities may reflect injury to the sinus node, atrioventricular (AV) node, or myocardial conduction system. Most changes are transient; some are permanent.