Expansion of acute myocardial infarction: an experimental study.

Abstract

SUMMARY Expansion (regional dilatation and thinning) of acutely infarcted myocardium in man has been shown to correlate with overall cardiac dilatation and rupture. We studied gross and histopathologic features and the time course of expansion in rats. Infarcts were produced in 84 rats by ligation of the left coronary artery and studied at 1, 2, 3, 4, 5 and 7 days. All hearts were prepared by potassium diastolic arrest, gel distention and fixation. Expansion was graded 0 to 4+: 1+, mild thinning of infarcted wall; 2+, mild thinning and dilatation; 3+, moderate thinning and dilatation; and 4+, marked thinning and dilatation. There were 80 transmural infarcts, and 66% showed expansion; 36 of 80 (45%) were graded 1-2+ and 17 of 80 (21%) 3-4+. None of the four exclusively nontransmural infarcts showed expansion.Expansion was present in 61% of transmural infarcts at 1-2 days, in 65% at 3-4 days and in 80% at 5-7 days. The percentage of rats with severe (3-4+) expansion increased markedly over this period, from 0% at 1-2 days to 23% at 34 days to 65% at 5-7 days. Histopathologic infarct evolution was roughly twice as rapid as that of humans; 5-7-day-old infarcts showed well-developed granulation tissue.Thus, expansion can be produced in an animal model. A critical infarct size of 17% appeared necessary for significant (> 1+) expansion, and the degree of expansion correlated with infarct size. Although this phenomenon begins early after infarction, its extent progresses over days, making interventions to interrupt its development feasible.STUDIES of myocardial infarction have generally paid little attention to the gross topographic changes early after infarction or to the consequences of these changes." 2 Infarct expansion, defined as regional thinning and dilatation of the infarct zone, is a gross topographic change that occurs early after acute myocardial infarction in humanss and is associated with a poor clinical prognosis.' 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.5The 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. Materials and Methods Infarct ModelInfarcts were produced by left coronary artery ligation in female Sprague-Dawley rats weighing 220-300 g, as previously described.'"' The rats were anesthetized with sodium methohexital (Brevitol), 35 mg/kg, administered intraperitoneally. A left thoracotomy was performed in the fifth or sixth intercostal space. The rats were given intermittent positive-pres- sure ventilation with 95% 02 and 5% CO2. A pericardiotomy was performed and the left main coronary artery was occluded by snaring and tying a band of myocardium 2-3...

Quantitative analysis of myocardial infarct structure in patients with ventricular tachycardia.

“…The hearts of the ventricular tachycardia group were larger than those of the control group as measured by heart weight and were more dilated as indicated by the larger radii of the left ventricular cavity (table 4). Since infarction causes corresponding hypertrophy of surviving tissue21' 22 and left ventricular dilatation,23 24 the differences between the two groups could be caused by increased postinfarction hypertrophy and dilatation secondary to the larger myocardial infarcts in the ventricular tachycardia group. Alternatively, larger, more dilated hearts may get bigger infarcts.…”

Infarto do miocárdio experimental em ratos: análise do modelo

“…As a result, there is a narrowing of the region and dilation of the infarcted segment. This acute dilation, characterized by the thinning and distension of the infarcted region is called the infarction expansion [21][22][23] . Therefore, as a consequence of the expansion, the measurement of the infarction size by the internal perimeters can overestimate the size of the AMI 20 .…”

Cardiac remodelling: General aspects and mechanisms

“…Cardiac remodelling is defined as a group of molecular, cellular and interstitial changes that manifest clinically as alterations in the size, mass, geometry and function of the heart after a stressful stimulus (2). This process is triggered by ischemia (myocardial infarction) (3,4), inflammation (myocarditis) (2), hemodynamic overload (workload by volume or pressure) (5) and neurohormonal activation (6,7). Cardiac remodelling is considered to be not only an adaptive event but also a maladaptive phenomenon.…”