Left ventricular enlargement after myocardial infarction is a poor prognostic sign, the mechanism of which has not been well defined. Early left ventricular dilation may be due to the Frank-Starling effect, which results in an increase in the length of uninfarcted segments in response to a reduction in contractile muscle mass. In contrast to this adaptive physiologic mechanism, left ventricular dilation may alternatively be caused by a pathologic process that stretches and thins the infarcted myocardial segment (that is, infarct expansion). To determine the relative contributions of these two mechanisms to left ventricular dilation after an initial transmural anterior myocardial infarction, two-dimensional echocardiograms were obtained from 27 patients within 72 hours of the onset of symptoms of myocardial infarction and from 13 healthy control subjects. In the minor-axis echocardiographic view at the level of the papillary muscles, anterior and posterior endocardial segment lengths at end-diastole were measured with a microprocessor-based graphic system. The papillary muscles were used as internal landmarks to demarcate the anterior and posterior segments. Anterior (infarcted) segment length in patients with myocardial infarction was 11.6 +/- 2.2 cm (mean +/- SD), whereas in control subjects, anterior segment length was 8.6 +/- 1.2 cm (p less than 0.001). Posterior (uninfarcted) segment length in the patients was not significantly different from posterior segment length in the control subjects (5.4 +/- 1.2 versus 5.3 +/- 1.0 cm, respectively). Measurable left ventricular dilation during the first 3 days after transmural anterior myocardial infarction is due to dilation of the infarcted segment and not of the normal uninfarcted segment.(ABSTRACT TRUNCATED AT 250 WORDS)