Characterization of dysfunctional remote myocardium in left ventricular anterior aneurysms and improvements following surgical ventricular restoration using cardiac magnetic resonance imaging: preliminary results.

Abstract

In patients with previous myocardial infarction, the remote uninfarcted regions, although contractile, demonstrate dysfunctional wall kinetics because of increased afterload, which improves after surgical ventricular restoration (SVR). We characterized left ventricular (LV) mean myocardial velocity (MMV) through an analysis of endocardial motion and wall thickening (WT) over the cardiac cycle using standard cardiac magnetic resonance (cMR). LV endocardial motion and WT from cMR data in 7 heart failure (HF) patients with postinfarction antero apical aneurysm were compared against normal controls to establish a baseline for the mean myocardial velocity during phases of the cardiac cycle. The HF patients' MMV and WT curves were compared with post-SVR data. Global MMV showed significant postoperative improvements in the ejection phase of systole and the early filling phase of diastole. The aneurysmal wall was dyskinetic in both systole and diastole. The remote myocardium preoperatively had a delayed peak velocity during the ejection phase of systole and diminished velocity during early filling in diastole. After SVR, the remote myocardium had an increased MMV with an earlier peaking during the ejection phase and slightly improved early diastolic velocity. WT increased cumulatively during systole and decreased during diastole with improved end-systolic and end-diastolic wall thickness after SVR. The end-systolic wall thickness showed a significant correlation with left ventricular ejection fraction (r(2) = 0.89, P = 0.001) and stroke volume (r(2) = 0.80, P = 0.02). The MMV had a significant correlation with WT over the phases of the cardiac cycle (r(2) = 0.953, P ≤ 0.0001). In patients with chronic ischaemic heart disease with LV aneurysms/large areas of scar, improvements in the remote myocardial MMV and WT underline LV systolic function improvements after SVR. The persistence of myocardial WT in early diastole is the likely mechanism for incomplete or absence of relief of LV diastolic dysfunction by SVR.