Evolution of reperfusion post-infarction ventricular remodeling: new MRI insights

Our current understanding is that left ventricular (LV) remodeling after acute myocardial infarction (AMI) is caused by expansion of the infarcted myocardium with thinning of the wall and eccentric hypertrophy of the remote myocardium. To study the geometric changes in the remodeling process after reperfused AMI we used cardiac magnetic resonance imaging (CMR).

Nine juvenile swine underwent a 120-min occlusion of the left circumflex coronary artery followed by reperfusion. CMR was performed at 3 and 36 days post-infarction. Global and regional LV remodeling was assessed including geometric changes of infarcted and remote myocardium; infarct longitudinal length (mm), mean circumferential length (mm), total infarct surface (mm(2)), end-diastolic wall thickness (EDWT) (mm) and transmural extent of infarction (TEI).

From 3 days to 36 days post-infarction end-diastolic volume increased by 43% (p<0.01). Infarct mass decreased by 36% (p<0.01), mainly by reduction of EDWT with 26%, while mean infarct circumferential length and longitudinal infarct length did not change. Remote myocardial mass increased by 23%, which was the result of an increase in its circumferential length from 95 ± 10 mm to 113 ± 11 mm (p<0.01), with no change in its EDWT. In contrast, EDWT in the infarct, peri-infarct and border zone decreased.

Contrary to the widely held view the present, using CMR measurements, shows that post-infarction remodeling was not associated with expansion of the infarcted myocardium. These findings suggest that eccentric hypertrophy of the remote myocardium, but not expansion of the infarct region, is responsible for left ventricular dilatation after AMI.