Late effects of acute infarct dilation on heart size: a two dimensional echocardiographic study

Dilation of the infarct zone (infarct expansion) has been shown to be a cause of regional left ventricular dilation within days of transmural anterior myocardial infarction. Whether this process stabilizes, continues or regresses thereafter, and whether uninfarcted myocardium is affected is unknown. To explore this, two to six (mean four) serial two dimensional echocardiographic studies were obtained over a 3 to 30 month period (mean 13) in 13 patients beginning 10 to 21 days after anterior transmural myocardial infarction. With use of the papillary muscles as internal left ventricular landmarks, anterior and posterior segmental dilation in each patient was assessed from the slope of the regression line of segment length versus time. Study patients were classified into those with (seven patients) and those without (six patients) infarct expansion. Infarct expansion was defined as an anterior segment length 10 to 21 days after infarction that exceeded the upper limit of normal determined from 13 age-and sex-matched normal control subjects. Ten to 21 days after infarction, the average anterior segment length in the seven patients with expansion was 65 percent greater than that in normal control subjects. The seven patients with infarct expansion showed significant and continuing dilation during long-term observation of both the infarcted anterior (p < 0.01) and the uninfarcted posterior (p < 0.05) segments. The average increase in anterior segment length was 1.1 cm (8 percent) and in posterior segment length 0.9 cm (19 percent). This represents an average increase in overall left ventricular circumference of 11 percent during the observation period. The six patients without infarct expansion showed no significant change in anterior or posterior segment length (mean ± standard error of the mean [SEM] -0.7 ± 0.3 and 0.2 ± 0.3 mm/mo, respectively). Six of the seven patients with infarct expansion were functionally limited by dyspnea or angina, or both; no patient without infarct expansion had functional cardiac limitation. Thus, infarct expansion occurring within 3 weeks of transmural myocardial infarction appears to be the main contributor to left ventricular dilation, and is associated with impaired functional status. Moreover, a significant increase in ventricular size due to infarct expansion appears to predict chronic progressive ventricular enlargement due to lengthening of both the infarcted zone and the uninfarcted segment.