Cardiac structure and ventricular-vascular function in persons with heart failure and preserved ejection fraction from Olmsted County, Minnesota

Abstract

Background: Mechanisms purported to contribute to the pathophysiology of heart failure with normal ejection fraction (HFnlEF) include diastolic dysfunction, vascular and left ventricular systolic stiffening, and volume expansion. We characterized left ventricular volume, effective arterial elastance, left ventricular end-systolic elastance, and left ventricular diastolic elastance and relaxation noninvasively in consecutive HFnlEF patients and appropriate controls in the community.

Methods and results: Olmsted County (Minn) residents without cardiovascular disease (n=617), with hypertension but no heart failure (n=719), or with HFnlEF (n=244) were prospectively enrolled. End-diastolic volume index was determined by echo Doppler. End-systolic elastance was determined using blood pressure, stroke volume, ejection fraction, timing intervals, and estimated normalized ventricular elastance at end diastole. Tissue Doppler e' velocity was used to estimate the time constant of relaxation. End-diastolic volume (EDV) and Doppler-derived end-diastolic pressure (EDP) were used to derive the diastolic curve fitting (alpha) and stiffness (beta) constants (EDP=alphaEDVbeta). Comparisons were adjusted for age, sex, and body size. HFnlEF patients had more severe renal dysfunction, yet smaller end-diastolic volume index and cardiac output and increased EDP compared with both hypertensive and healthy controls. Arterial elastance and ventricular end-systolic elastance were similarly increased in hypertensive controls and HFnlEF patients compared with healthy controls. In contrast, HFnlEF patients had more impaired relaxation and increased diastolic stiffness compared with either control group.

Conclusions: From these cross-sectional observations, we speculate that the progression of diastolic dysfunction plays a key role in the development of heart failure symptoms in persons with hypertensive heart disease.

Conflict of interest statement

Conflict of interest disclosures

None.

Figures

Figure 1

Schematic of group-averaged end-systolic pressure-volume relationship (ESPVR), where ESP = Ees(ESV-V0) (Ees = end-systolic elastance; V0 = volume intercept). Solid lines represent the mean ESPVR and dotted lines the 95% confidence intervals for each group. For comparison of Ees (slope) between groups, *p<0.05 vs CON.

Figure 2

Bar graphs of indexed end-diastolic volume (EDVI), indexed left atrial volume (LAVI), end-diastolic pressure (EDP), plasma brain natriuretic peptide (BNP) and derived tau by subject group. Data are mean ± SD; *p

Figure 3

Schematic of group-averaged end-diastolic pressure-volume relationship (EDPVR), where EDP = αEDVβ (α = curve fitting constant; β = diastolic stiffness constant). Solid lines represent the mean EDPVR and dotted lines the 95% confidence intervals for each group. For comparison of indexed EDV at a common EDP of 20 mmHg (EDVI20) between groups, *p<0.05 vs CON; † p<0.05 vs HTN.