Patients with hibernating myocardium show altered left ventricular volumes and shape, which revert after revascularization: evidence that dyssynergy might directly induce cardiac remodeling.

Abstract

The purpose of this study was to investigate whether post-ischemic left ventricular (LV) remodeling might be induced by regional contractile dysfunction per se (i.e., in the absence of transmural necrosis) and whether this phenomenon is potentially reversible after contractile recovery. Formation of extensive scar tissue is thought to be chiefly responsible for post-infarction LV remodeling; however, myocardial necrosis also causes loss of contractility. We investigated LV geometry and shape in a setting in which contractile dysfunction occurs in the presence of preserved myocyte viability, and thus it is potentially reversible. In 42 patients with chronically dysfunctional myocardium, we evaluated (by two-dimensional echocardiography) LV global and regional function, volumes, and sphericity index (SI), at baseline and 8 +/- 3 months after coronary revascularization. Myocardial viability before revascularization was evaluated by dobutamine echocardiography. At baseline, regional and global function were depressed and LV dilation was present. Revascularization was followed by recovery of ejection fraction (from 33 +/- 6% to 45 +/- 10%, p < 0.0001) and wall motion score index (from 2.29 +/- 0.31 to 1.74 +/- 0.42, p < 0.0001). After revascularization, significant improvement of end-systolic volume index (from 78 +/- 23 ml/m2 to 56 +/- 23 ml/m2, p < 0.0001), end-diastolic volume index (from 118 +/- 26 ml/m2 to 99 +/- 26 ml/m2, p < 0.0001), and SI (from 0.69 +/- 0.14 to 0.52 +/- 0.11, p < 0.0001) was also observed. Improvement in LV volumes and SI were significantly correlated to the number of segments recovering function after revascularization. Hibernating myocardium is associated with major alterations in LV volumes and shape, which significantly revert after revascularization. Thus, chronic dyssynergy per se is sufficient to induce ischemic LV remodeling in patients.