Fig. 11.14 Complicationsofmyocardialinfarction.(AtoC)Cardiacrupture.(A)Anteriorfreewallmyocardialrupture(arrow).(B)Ventricularseptalrupture(arrow).(C)Papillarymusclerupture.(D)Fibrinouspericarditis,withahemorrhagic,roughenedepicardialsurfaceoverlyinganacuteinfarct.(E)Recentexpan-sionofananteroapicalinfarctwithwallstretchingandthinning(arrow) andmuralthrombus.(F)Largeapicalleftventricularaneurysm(arrow).(A to E, Reproduced by permission from Schoen FJ: Interventionalandsurgicalcardiovascularpathology:clinicalcorrelationsandbasicprinciples,Philadelphia, 1989, Saunders; F, Courtesy of William D. Edwards, MD, Mayo Clinic, Rochester, Minnesota.) friction rub, pericarditis typically appears 2 to 3 days after infarction and then gradually resolves over the next few days. Extensive infarcts or severe pericardial inflammation occasionally can lead to large effusions or can organize to form dense adhesions that eventually manifest as a constrictive lesion.
Chamber dilation. Because of the weakening of necrotic muscle, there may be disproportionate stretching, thinning, and dilation of the infarcted region (especially with anteroseptal infarcts).
Mural thrombus. With any infarct, the combination of attenuated myocardial contractility (causing stasis), chamber dilation, and endocardial damage (causing a thrombogenic surface) can foster mural thrombosis (
Fig.
11.14E ), eventually leading to left-sided thromboembolism.
Ventricular aneurysm. A late complication, aneurysms of the ventricle most commonly result from a large trans-mural anteroseptal infarct that heals with the formation of a thinned wall of scar tissue (
Fig. 11.14F ). Although ventricular aneurysms frequently give rise to formation of mural thrombi, arrhythmias, and heart failure, they do not rupture.
Progressive heart failure. This is discussed under “ ” next.
The risk for complications and the overall prognosis depends on infarct size, site, and type (subendocardial versus transmural infarct). Thus, large transmural infarcts are associated with a higher probability of cardiogenic shock, arrhythmias, and late CHF, and patients with anterior transmural MIs are at greatest risk for free wall rupture, expansion, aneurysm formation, and formation of mural thrombi. By contrast, posterior transmural infarcts are more likely to be complicated by conduction blocks, right ventricular involvement, or both; when ventricular septal ruptures occur in this area, they are more difficult to manage. Overall, patients with anterior infarcts have a much more guarded prognosis than those with posterior infarcts. With subendocardial infarcts, thrombi may form on the endocardial surface, but pericarditis, rupture, and aneurysms rarely occur.
In addition to the aforementioned scarring, the remaining viable myocardium attempts to compensate for the loss of contractile mass. Noninfarcted regions undergo hypertrophy and dilation; in combination with the scarring and thinning of the infarcted zones, the changes are collectively termed ventricular remodeling. The initial compensatory hypertrophy of noninfarcted myocardium is hemodynamically beneficial. The adaptive effect of remodeling can be overwhelmed, however, and ventricular function may decline in the setting of ventricular aneurysm formation.
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