Mathematical modeling of left ventricular hypertrophy with reduced long-axis shortening showed preserved ejection fraction but reduced stroke volume, suggesting a novel mechanism for heart failure.
This theoretical model suggests that preserved ejection fraction in heart failure may be explained by left ventricular hypertrophy amplifying radial thickening despite reduced long-axis shortening, leading to reduced stroke volume.
BACKGROUND: Patients with heart failure and a normal left ventricular ejection fraction have significantly reduced left ventricular long-axis function. This paper proposes an explanation for this apparent paradox and suggests a new mechanism of "diastolic" heart failure. METHOD: The effect of changes in left ventricular hypertrophy on stroke volume and ejection fraction in non-dilated left ventricles was calculated using the area-length method. Further, the effect of a reduction in long-axis shortening on these parameters was determined. RESULTS: Increasing left ventricular hypertrophy resulted in augmentation of systolic wall thickening and ejection fraction but not stroke volume when long-axis shortening was normal. In the presence of abnormal long-axis function, stroke volume was reduced but ejection fraction was preserved. CONCLUSION: The model predicts that the normal ejection fraction in patients with heart failure may be explained by the presence of left ventricular hypertrophy. The resulting amplified radial thickening in the setting of reduced long-axis shortening explains the preservation of ejection fraction. The reduced stroke volume in the precompensated state rather than diastolic dysfunction may be the cause of heart failure.
MacIver et al. (Sat,) conducted a other in Heart failure with normal ejection fraction. Left ventricular hypertrophy with reduced long-axis shortening vs. Normal long-axis shortening was evaluated on Stroke volume and ejection fraction. Mathematical modeling of left ventricular hypertrophy with reduced long-axis shortening showed preserved ejection fraction but reduced stroke volume, suggesting a novel mechanism for heart failure.