TY - JOUR
T1 - Early dilation of the infarcted segment in acute transmural myocardial infarction
T2 - Role of infarct expansion in acute left ventricular enlargement
AU - Erlebacher, Jay A.
AU - Weiss, James L.
AU - Weisfeldt, Myron L.
AU - Bulkley, Bernadine Healy
N1 - Funding Information:
From the Hopkins Hospital, Baltimore, Maryland. This study was supported in part by National Institutes of Health Grant 2RO1 HL-19232, Specialized Center of Research Grant P50-HL-17655, Bethesda, Maryland, and a Grant-inAid from the Maryland Heart Association, Maryland Chapter, Baltimore, Maryland. Manuscript received April 25, 1983; revised manuscript received January 30, 1984, accepted March 16, 1984. Dr. Erlebacher was a Fellow of the American Heart Association, Maryland Chapter during 1979-1980.
PY - 1984
Y1 - 1984
N2 - Left ventricular enlargement after myocardial infarction is a poor prognostic sign, the mechanism of which has not been well denned. 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 < 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. Thus, infarct expansion appears to be the major cause of early left ventricular enlargement in these patients. This mechanism of left ventricular enlargement may have significant implications for ventricular mechanics, infarct size estimation and early therapeutic intervention.
AB - Left ventricular enlargement after myocardial infarction is a poor prognostic sign, the mechanism of which has not been well denned. 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 < 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. Thus, infarct expansion appears to be the major cause of early left ventricular enlargement in these patients. This mechanism of left ventricular enlargement may have significant implications for ventricular mechanics, infarct size estimation and early therapeutic intervention.
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U2 - 10.1016/S0735-1097(84)80203-X
DO - 10.1016/S0735-1097(84)80203-X
M3 - Article
C2 - 6234343
AN - SCOPUS:0021224150
VL - 4
SP - 201
EP - 208
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
SN - 0735-1097
IS - 2
ER -