Theoretical considerations in the use of dynamic cardiomyoplasty to treat dilated cardiomyopathy

Abstract

Clinical data describing the hemodynamic benefits of cardiomyoplasty are inconclusive, and there has not been any study detailing the mechanisms by which dynamic cardiomyoplasty may improve the functional and mechanical impairments of the failing heart. The left ventricle in dilated cardiomyopathy is characterized by increased end-diastolic volume, inadequate systolic myocardial wall thickening, increased wall stress, and decreased stroke volume. Based on experimental and preliminary clinical data, we propose that cardiac assistance by dynamic cardiomyoplasty is the consequence of enhanced volume translocation rather than increased potential for pressure generation. A small augmentation of dimensional shortening results in a large increment of stroke volume because of the enlarged resting chamber volume. Key geometric effects are enhanced systolic chamber shortening and increased wall thickening, resulting in a net decrease of myocardial wall stress. The contractile skeletal muscle may improve myocardial mechanics, and normalization of the afterload mismatch may be an important mechanism by which dynamic cardiomyoplasty augments cardiac output.