April 24, 2026Open Access
View Full PaperContractility and Ventricular Systolic Stiffening in Hypertensive Heart Disease
Key Result
Impaired myocardial contractility, but not left ventricular end-systolic stiffness, was associated with increased age-adjusted mortality in patients with heart failure and preserved ejection fraction.
Key Points
- To compare left ventricular systolic stiffness and contractility among normal subjects, hypertensive patients, and those with heart failure and preserved ejection fraction (HFpEF).
- Examined 617 healthy controls, 719 hypertensive patients without heart failure, and 244 patients with HFpEF using echo-Doppler techniques.
- Measured arterial and left ventricular end-systolic stiffness and contractility metrics.
- Adjusted data for cardiac geometry.
- Increased end-systolic stiffness observed in both hypertensive groups compared to controls, with similar ventricular-arterial coupling.
- In hypertensive patients, higher end-systolic stiffness linked to enhanced myocardial contractility; however, reduced contractility noted in HFpEF patients versus other groups.
- Impaired myocardial contractility in HFpEF associated with increased mortality risk after age adjustment.
Study Design
Type
Observational (n=1,580)
Structured PICO
P
Population
1,580 subjects including healthy controls (n=617), hypertensive patients without heart failure (n=719), and patients with heart failure and preserved ejection fraction (HFpEF) (n=244, 96% hypertensive).
O
Outcome
Left ventricular (LV) systolic stiffness, myocardial contractility, and their association with mortality in HFpEF patientssurrogate
Progression from hypertensive heart disease to HFpEF is associated with impaired myocardial contractility, which predicts increased mortality.
Abstract
1) Compare left ventricular (LV) systolic stiffness and contractility in normal subjects, hypertensives without heart failure, and patients with heart failure and preserved ejection fraction (HFpEF); and 2) Determine whether LV systolic stiffness or myocardial contractility are associated with mortality in HFpEF. Arterial load is increased in hypertension and is matched by increased end-systolic LV stiffness (ventricular-arterial coupling). Increased end-systolic LV stiffness may be mediated by enhanced myocardial contractility or processes which increase passive myocardial stiffness. Healthy controls (n=617), hypertensives (No HF, n=719) and patients with HFpEF (n=244, 96% hypertensive) underwent echo-Doppler characterization of arterial (Ea) and LV end-systolic (Ees) stiffness (elastance), ventricular-arterial coupling (Ea/Ees ratio), chamber-level and myocardial contractility (stress-corrected midwall shortening). Ea and Ees were similarly elevated in hypertensives with or without HFpEF compared with controls, but ventricular-arterial coupling was similar across groups. In hypertensives, elevated Ees was associated with enhanced chamber-level and myocardial contractility, while in HFpEF, chamber and myocardial contractility were depressed compared with both hypertensives and controls. Group differences persisted after adjusting for geometry. In HFpEF, impaired myocardial contractility (but not Ees) was associated with increased age-adjusted mortality. While arterial load is elevated and matched by increased LV systolic stiffness in hypertension with or without HFpEF, the mechanisms of systolic LV stiffening differ substantially. These data suggest that myocardial contractility increases to match arterial load in asymptomatic hypertensive heart disease, but that progression to HFpEF may be mediated by processes which simultaneously impair myocardial contractility and increase passive myocardial stiffness. Keywords: Contractility , Heart Failure , Hypertension , Pathophysiology