The mechanism of reduced longitudinal left ventricular systolic function in hypertensive patients with normal ejection fraction.

Background: MacIver and Townsend’s hypothesis predicts, based on a mathematical model of left ventricular (LV) contraction, that preserved absolute radial wall thickening (radWT) due to LV hypertrophy is responsible for the normal ejection fraction (EF) in patients with heart failure with preserved ejection fraction (HFPEF). Methods: We tested the validity of this hypothesis by detailed echocardiography including evaluation of ventricular myocardial strain (S) using speckle tracking imaging in >60-year-old 18 controls and 94 hypertensive patients with normal EF. Results: Echocardiography revealed no LV diastolic dysfunction in 38/94(40%) patients with HT (HTDD- group), and 56/94(60%) patients had diastolic dysfunction (HTDD+ group). The absolute values of global longitudinal LV peak systolic S were significantly reduced in both patient groups (p<0.05 for HTDD-, p<0.01 for HTDD+ groups) versus the controls. There were no significant between-groups differences in circumferential and radial peak LV systolic Ss, radWT and EF. LV mass (LVM) (p<0.001), LVM/body mass index (BMI) (p<0.01) increased in the HTDD+ group and EF/LVM/BMI decreased in both patient groups (p<0.01 for HTDD-, p<0.001 for HTDD+ groups) versus the controls. LVM increased, EF/LVM/BMI decreased in the HTDD+ group versus the HTDD- group (p<0.05 and p<0.01 respectively). Conclusions: We demonstrated decreased longitudinal LV systolic function, and showed that preserved EF was due to preserved absolute radWT and not to increased radial or circumferential systolic function in patients with HT and normal EF, a potential HFPEF precursor condition. Instead of EF, rather EF/LVM/BMI might be used to detect subtle LV systolic dysfunction in hypertension and HFPEF.