Objective: The purpose of this study was to evaluate infarction-related changes in the infarcted and the non-infarcted myocardium using a baseline assessment of ventricular function obtained prior to the infarction.
Background: Experimental studies have shown that both infarcted and non-infarcted myocardium contribute to the process of left ventricular dilatation soon after the infarction, but no data exist on the effect that the infarct has on the pre-infarct ventricular morphology in humans.
Methods and results: 10 patients, out of 721 admitted to our coronary care unit with a first acute myocardial infarction over a 3-year period, had had an echocardiographic examination performed before (354 +/- 407 days) and after (10 +/- 9 days) the infarction which were adequate for quantitative evaluation. Ventricular volume (Simpson) and regional wall motion (Centerline method) were evaluated by biplane apical sections and the endocardial length of the infarct and the non-infarct segments, imaged in a cross-sectional view at the papillary muscle level, were measured. After the infarction end-diastolic and end-systolic ventricular volume increased (P = 0.0003 and P < 0.0001, respectively); diastolic and systolic infarct segment length increased (P = 0.011 and P = 0.0008, respectively), while non-infarct segment had only diastolic lengthening (P = 0.019), without systolic changes. The ejection fraction decreased after the infarction (P < 0.0001), in inverse relation to infarct size and in direct relation to diastolic non-infarct segment lengthening. In the five patients in whom there was a significant diastolic lengthening of non-infarct segment (larger than mean +/- 2 S.D. of the interobserver variability) the decrease in ejection fraction was less than in the patients without significant lengthening of this segment (P = 0.017), despite a similar echocardiographic infarct size index.
Conclusion: Ventricular enlargement early after myocardial infarction is due to both infarct expansion and lengthening of non-infarct segment. However, while systolic stretching of the infarct segment is a deleterious process that accounts for the increase in end-systolic volume, diastolic non-infarct segment lengthening is the expression of a functional compensatory mechanism that counteracts the reduction of the ventricular pump function secondary to the infarction.