Hypertensive patients with normal ejection fraction had significantly reduced global longitudinal left ventricular peak systolic strain compared to controls, demonstrating that normal ejection fraction is maintained by preserved absolute radial wall thickening.
Observational (n=112)
No
Does preserved absolute radial wall thickening explain normal ejection fraction despite reduced longitudinal systolic function in hypertensive patients?
In hypertensive patients with normal ejection fraction, preserved absolute radial wall thickening maintains normal ejection fraction despite reduced longitudinal left ventricular systolic function, supporting its role as a potential HFpEF precursor condition.
p-value: p=<0.05
BACKGROUND: MacIver and Townsend's hypothesis predicts, based on a mathematical model of left ventricular contraction, that preserved absolute radial wall thickening (radWT) due to left ventricular hypertrophy is responsible for the normal ejection fraction 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 at least 60-year-old 18 controls and 94 hypertensive patients with normal ejection fraction. RESULTS: Echocardiography revealed no left ventricular diastolic dysfunction in 38 out of 94 (40%) patients with hypertension (HTDD-negative group), and 56 out of 94 (60%) patients had diastolic dysfunction (HTDD-positive groups). The absolute values of global longitudinal left ventricular peak systolic S were significantly reduced in both patient groups (P < 0.05 for HTDD-negative, P < 0.01 for HTDD-positive groups) vs. the controls. There were no significant between-groups differences in circumferential and radial peak left ventricular systolic Ss, radWT and ejection fraction. Left ventricular mass (LVM) (P < 0.001), LVM/BMI (P < 0.01) increased in the HTDD-positive group and ejection fraction/LVM/BMI decreased in both patient groups (P < 0.01 for HTDD-negative, P < 0.001 for HTDD-positive groups) vs. the controls. LVM increased, ejection fraction/LVM/BMI decreased in the HTDD-positive group vs. the HTDD-negative group (P < 0.05 and P < 0.01, respectively). CONCLUSION: We demonstrated decreased longitudinal left ventricular systolic function and showed that preserved ejection fraction was due to preserved absolute radWT and not due to increased radial or circumferential systolic function in patients with hypertension and normal ejection fraction, a potential HFPEF precursor condition. Instead of ejection fraction, rather ejection fraction/LVM/BMI might be used to detect subtle left ventricular systolic dysfunction in hypertension and HFPEF.
Szelényi et al. (Wed,) conducted a observational in Hypertension with normal ejection fraction (n=112). Hypertension with normal ejection fraction vs. Normotensive healthy controls was evaluated on Global longitudinal left ventricular peak systolic strain (p=<0.05). Hypertensive patients with normal ejection fraction had significantly reduced global longitudinal left ventricular peak systolic strain compared to controls, demonstrating that normal ejection fraction is maintained by preserved absolute radial wall thickening.