Background: Studies in anesthetized dogs have shown that myocardial fibers shorten approximately 8%. However, in the endocardium, shortening occurs to a much greater extent at 90 degrees to the fiber orientation ("cross-fiber shortening") than it does along the fiber direction. The purpose of this study was to estimate the extent of fiber and cross-fiber shortening in the normal human left ventricle and in patients with idiopathic dilated cardiomyopathy (IDC).
Methods and results: Ten normal subjects and nine patients with IDC were imaged with magnetic resonance tissue tagging. Finite strain analysis was used to calculate endocardial and epicardial shortening in the fiber and cross-fiber directions using anatomic fiber angles from representative autopsy specimens as references. Anatomic fiber angles were not different between normal subjects and IDC patients. Epicardial fiber strain was -0.14+/-0.01 in normal subjects and -0.08+/-0.01 in IDC patients (P<.0001 versus normal subjects). Epicardial cross-fiber strain was -0.08+/-0.01 in normal subjects and -0.06+/-0.01 in IDC patients (P=NS). Endocardial fiber strain was -0.16+/-0.01 in normal subjects and -0.09+/-0.01 in IDC patients (P<.0001), and endocardial cross-fiber strain was -0.26+/-0.01 in normal subjects and -0.15+/-0.01 in IDC patients (P<.0001). Cross-fiber shortening was greater than fiber shortening at the endocardium in both normal subjects (P<.0001) and IDC patients (P<.05).
Conclusions: In normal humans, the direction of maximal deformation aligns with the fiber direction in the epicardium but is perpendicular to the fiber direction in the endocardium. When strain in a coordinate system aligned to the fibers is estimated, cross-fiber shortening is found to be the dominant shortening strain at the endocardium. Normal fiber shortening is 15%, and this is markedly reduced in IDC. The normal transition in fiber orientation through the wall is not altered in IDC, and cross-fiber shortening is still the dominant strain at the endocardium, suggesting that interactions between myocardial layers persist in these patients.