Pathogenesis of left ventricular aneurysms: An experimental study in the rat model

Abstract

Left ventricular aneurysms, convex protrusions at sites of transmural scar, are clinically recognized late after myocardial infarction because of their hemodynamic or arrhythmic complications. Whether aneurysms develop from dilation of freshly infarcted myocardium early after myocardial infarction or from late dilation of scar is not known. To investigate this question, the time course of changes in shape of the left ventricle early and late after myocardial infarction was studied. One hundred forty-one myocardial infarcts were produced in rats by coronary ligation, and the animals were killed at time periods of up to 6 weeks. True aneurysms developed as early as 2 weeks and only in rats with a transmural infarct. The percent of rats that manifested “aneurysmal shape changes” (defined as a protrusion of the full thickness of the left ventricular wall) increased from day 1 to day 5, but did not change significantly thereafter. The extent of left ventricular dilation in hearts with early aneurysmal shape changes did not progress significantly up to day 42. Accordingly, in the rat, regional aneurysmal shape alterations are due not to late dilation of scar tissue, but rather to “expansion” of freshly necrotic myocardium within the first 5 days of infarction. Thus, early changes in shape appear to determine late aneurysm formation.