Early ventricular fibrillation is not related to infarct size. After 24 h ischemic myocytes have either undergone necrosis or recovered, and the risk of ventricular fibrillation diminishes. The majority of the other complications occur in transmural infarcts. Cardiogenic shock is directly related to the proportion of the left ventricular muscle mass which has been lost. Large infarcts are more likely to be anterior because the left anterior descending coronary aretery supplies more than 60 per cent of the myocardial mass.
Cardiogenic shock may lead to an extension of the area of necrosis ( Fig, 2). Myocardial perfusion is dependent on the relation between aortic diastolic pressure and left ventricular cavity pressure. If aortic pressure falls and left ventricular diastolic pressure rises, subendocardial perfusion throughout the whole left ventricle falls; a circumferential zone of subendocardial necrosis occurs and the centers of the papillary muscles also undergo necrosis ( Fig,... . . 2). Patients enter a downward spiral in which falling myocardial perfusion causes new necrosis which in turn further depresses ventricular function.
Cardiac rupture, which is responsible for up to 10 per cent of infarct mortality, complicates transmural infarction alone. Rupture within the first 36 h is due to a tear developing at the margin of viable and non-viable myocardium. The tears are often slit-like and occur at a stage when the infarct is not readily apparent at autopsy. Later rupture is due to expansion of the infarct itself (We.!§m.§.D §0d...Me.a]y l9.8.Z). In infarct expansion (Fig. S), the necrotic tissue expands outward and the wall thins at the site. No increase in the volume of infarcted tissue occurs; it is purely a shape change and the ventricular cavity becomes asymmetric with one transverse axis greater than in a plane at right angles (Fig, 3). Expanding infarcts may rupture from day 3 onward and are associated with overlying pericarditis. Expansion is more common with large infarcts. The process of expansion begins within 24 h and continues for some days. As repair is initiated the expanded infarct is converted into a fibrous structure, permanently altering ventricular shape (remodeling) ( Pfeffei... §.D.d B.rauD.w.a.!d 1.9.90). The residual myocardium undergoes hypertrophy.
Ventricular aneurysms arise from severe degrees of acute infarct expansion and have a wide neck. A rarer form of aneurysm has a narrow entry into the left ventricle leading to a large external sac. These lesions follow a partial myocardial tear with a hematoma that develops beneath the visceral pericardium. These lesions are often referred to as 'pseudoaneurysms' because the outer wall is formed by pericardium rather than by the myocardium itself. Aneurysms which develop mural thrombus have a risk of systemic embolism. The factors which lead to thrombus with an aneurysm are not clear; apparently identical aneurysms may or may not be associated with thrombus in different individuals. Ventricular tachycardia is associated with the survival of subendocardial nests and strands of myocytes embedded in fibrous tissue at the margins of the aneurysm. These surviving myocytes form loops which may extend over several centimeters and act as a focus for re-entry.
Ventricular septal defects have the same characteristics as rupture of the left ventricular free wall. Papillary muscle rupture is not necessarily related to either transmural or large infarcts. Occlusion of the left marginal branch of the circumflex artery leads to very localized infarction of the anterolateral papillary muscle. Papillary muscle rupture also occurs in the setting of larger infarcts, and a combination of an expanding posteroseptal infarct, a ventricular septal rupture, and avulsion of the posteromedial papillary muscle occurs with proximal occlusions of dominant right coronary arteries. The magnitude of mitral regurgitation varies widely depending on whether avulsion occurs across the base of the papillary muscle or just in one subhead. Papillary muscle infarction without rupture occurs in up to 40 per cent of all acute infarcts, and subsequent fibrosis leading to either shortening or elongation is a factor in persistent mild mitral regurgitation.
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