Session Title: Echocardiography: Evaluation of Systolic and Diastolic Function III
Abstract 17785: Impaired Subendocardial Contractility and Longitudinal Shortening With Aging, Reduce Midwall Fiber Stress, Increasing Circumferential Shortening and Preserving Ejection Fraction
Introduction: Left ventricular (LV) longitudinal function declines with age, potentially due to subclinical pathological development of fibrosis and reduced perfusion in the subendocardial region. On the other hand, radial function is increased, thus preserving ejection fraction (EF). The mechanism of compensatory increased radial function is not fully understood.
Hypothesis: Impaired contractility in the subendocardium with predominantly longitudinal fibers, reduces longitudinal shortening but also reduces systolic midwall fiber stress. This reduced “afterload” of the predominantly circumferentially oriented midwall fibers, increases circumferential shortening which preserves EF.
Methods: We applied a finite element model of the LV which included nonlinear, transversely isotropic passive elastic myocardial properties, active fiber tension prescribed as a function of time and fiber length, and the anatomical transmural change in fiber orientation from endocardium to epicardium. Simulations of the cardiac cycle were performed; first with homogenous contractility and then with reduced contractility in the subendocardial region. We assessed changes in EF, peak systolic pressure, global longitudinal strain (GLS), global circumferential strain (GCS), and fiber stress.
Results: Reduced subendocardial contractility decreased longitudinal shortening (Figure), while circumferential shortening increased. There was practically no change in EF. Peak systolic pressure was moderately reduced. In the midwall, systolic fiber stress was reduced.
Conclusions: Reduced contractility in the subendocardium, reduces longitudinal shortening, but also reduces midwall circumferential fiber stress which seems to promote compensatory increased circumferential shortening that maintains EF. This mechanism may be one explanation for the observed changes in myocardial strains during aging.