Expansion of transmural myocardial infarction: a pathophysiologic factor in cardiac rupture.

Abstract

SUMMARY The 10-20% incidence of cardiac rupture in acute fatal myocardial infarction has not changed in the past century, and little is known about its pathophysiology. To determine whether expansion acute dilatation and thinning of the area of infarction not explained by resorption of necrotic tissue -may be a variable predictive for rupture, we studied 110 consecutive autopsied patients who died of acute myocardial infarction. The presence and severity of expansion was determined qualitatively on a scale of 0-4+ from review of the postmortem radiographs, and quantitatively by a ratio of wall thickness adjacent to the rupture site to thickness of noninfarcted wall. By radiographs, 54 (49%) had expansion, of whom 23 (43%) had rupture in the zone of expansion; of the 56 cases without expansion only one (2%) had ruptured (p < 0.005). The severity of expansion related to rupture: 50% with 3-4+ expansion ruptured, compared with only 23% with 1-2 + expansion. Wall thickness ratios for patients without expansion were 0.93 ± 0.10; for those with expansion but no rupture, 0.62 ± 0.16; and 0.49 ± 0.13 for those with expansion and rupture (p < 0.01). Wall thinning in these three groups was noted at average postinfarction intervals of 8, 7 and 5.5 days, respectively too early to be caused by resorption.Thus, expansion of acute myocardial infarction is a previously unappreciated variable that appears to be predictive of rupture, suggesting that regional dilatation and thinning of newly infarcted myocardium may be of pathogenetic importance in the development of rupture. Since expansion can be identified with twodimensional echocardiography, and occurs over days, these findings suggest that patients at high risk for rupture might be recognized early and interventions to prevent further expansion and rupture evaluated.CARDIAC RUPTURE in acute fatal myocardial infarction has a 10-20% incidence that has not changed in the past century." 2 The effective use of antiarrhythmic drugs has reduced the mortality of myocardial infarction. Attempts are underway to limit myocardial infarct size, and to support patients with cardiogenic shock with the hope of improving mortality. Yet the percentage of patients with acute myocardial infarction who die from cardiac rupture still remains high. Cardiac rupture is estimated to account for 25,000 fatalities a year in the United States,2 and, after cardiogenic shock and arrhythmias, is the most common cause of death in patients with myocardial infarction. This mortality is especially troublesome in that most reports2-10 agree that patients who die from cardiac rupture tend to have only one relatively small transmural infarction. One would expect that if these patients had not ruptured, their prognosis would have been favorable.Little is known of the pathophysiology of rupture, a factor that limits any attempts to alter its occurrence. Postulated mechanisms for cardiac rupture include a decrease in tensile strength, a high intracavitary pressure, ruptured intramural venous channels and a paradoxi...

Relation of circulating interleukin‐6 to left ventricular remodeling in patients with reperfused anterior myocardial infarction

“…However, progressive remodeling of the myocardium leads to global LV enlargement, which results in congestive heart failure and subacute cardiac rupture. 3,4 There is a general consensus that large infarct size, wall stress, and overexpression of the renin-angiotensin-aldosteronesystem promote structural LV remodeling after MI, and thus, postinfarct remodeling is a complex process.…”

Therapeutic Potential of HDL in Cardioprotection and Tissue Repair

“…This leads to infarct expansion characterised by the disproportionate thinning and dilatation of the infarct segment (Erlebacher et al 1984). Infarct expansion predisposes to myocardial rupture and congestive heart failure (Eaton et al 1979;Erlebacher et al 1982;Jugdutt and Michorowski 1987;Schuster and Bulkley 1979). Increased wall stress as a result of infarct expansion leads to mechanical stretch-elicited local angiotensin II release and activation of a fetal gene programme (Sutton and Sharpe 2000).…”

Expansion of acute myocardial infarction: an experimental study.

“…Pathologic studies show that severe expansion occurs most commonly in transmural and first myocardial infarcts.5 The process occurs within days of myocardial infarction, before resorption of necrotic tissue has occurred,3 and appears to be a major factor in overall acute cardiac dilatation and cardiac rupture after infarction. 5 The present study was designed to develop an experimental model of infarct expansion, and to use this model to investigate the time course of expansion and its correlation with the size and histopathology of the infarct.…”