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 (nϭ617), with hypertension but no heart failure (nϭ719), or with HFnlEF (nϭ244) 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 eЈ 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 (␣) and stiffness (␤) constants (EDPϭ␣EDV ␤ ). 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.

Clinical Phenotypes in Heart Failure With Preserved Ejection Fraction

“…The major effect of age on the vasculature is systolic hypertension with widening of the pulse pressure that results from age‐related increase in arterial stiffness and early wave reflections 43, 44. Arterial stiffening and early wave reflections are steady vascular features in HFpEF 45, 46, 47, 48, 49, 50, 51, 52. In the proximal arterial tree, vascular smooth cell loss of elastin increases systolic arterial pressure by lessening the “windkessel” effect 44, 45, 53.…”

Geographic variation in left ventricular mass and mass index: a systematic review

“…Therefore of the 13 cohorts (12 studies) of normal healthy men that would be classified as including people with mild LVH, five would also contain men with moderate LVH. [13][14][15][16][17] The LVM from eight cohorts matched the upper ASE reference limit ( ± 10 g) 12,[18][19][20][21][22][23][24] (two studies included subjects from the cohorts used to create the reference range, 12,22 and one appears to be the study on which the twodimensional reference ranges were based 23 ), and LVM from seven cohorts was less than the upper ASE reference limit. 12,[25][26][27][28][29][30] Of those that were less than the upper ASE reference limit, three studies from Asia 25,26,30 had upper values on average 38 g less than the ASE reference limits for m-mode or two-dimensional measurements.…”

“…Indexation of mass by BSA did not remove the disparity between studies and the reference ranges (Figure 3a). Of the 24 cohorts that report both indexed and unindexed mass, nine still exceeded the upper ASE reference limit for LVMI ( ± 5 g m À2 ) [13][14][15]17,21,[30][31][32][33] and five had ranges up to 29 g m À2 below the upper ASE reference limit. 12,19,25,27,29 Women In women, the range of measured LVM was compatible with the ASE reference range in a greater number of studies than in men; however, LVM from eight cohorts (seven studies) still exceeded the upper ASE reference value by 11-92 g (mean 40 g) (Figure 2b).…”

Effect of Mineralocorticoid Receptor Antagonists on Cardiac Structure and Function in Patients With Diastolic Dysfunction and Heart Failure With Preserved Ejection Fraction: A Meta‐Analysis and Systematic Review

“…Progression of LVDD has been shown to play an important role in development of symptomatic HF in patients with hypertensive heart disease 11, 12. As a result, there has been a significant interest in therapies that could ameliorate LVDD and adverse LV remodeling in order to potentially prevent or treat HFPEF.…”