Is remodeling the dominant compensatory mechanism in both chronic heart failure with preserved and reduced left ventricular ejection fraction?

The mechanisms of heart failure are ill understood with multiple, heterogeneous hypotheses proposed to describe the condition. This study examines the individual effects of left ventricular hypertrophy, long-axis shortening and the effect of left ventricular remodeling on ejection fraction, end-diastolic volume and stroke volume using a mathematical model of left ventricular contraction. Reducing long-axis shortening caused a decline in stroke volume independently of hypertrophy. Increasing concentric left ventricular hypertrophy resulted in an increase in ejection fraction secondary to augmented wall thickening. A decline in stroke volume occurred despite a preserved ejection fraction when concentric hypertrophy was present. Normalization of stroke volume by remodeling resulted in a marked increase in end-diastolic volume in the absence of hypertrophy and an end-diastolic volume similar to normal in the presence of concentric hypertrophy. The model predicts that the dominant compensatory mechanism in chronic heart failure is remodeling with normalization of stroke volume. Observational data cited supports this conclusion.