Health & Medical Heart Diseases

Cardiovascular Features of Heart Failure With Preserved Ejection Fraction

Cardiovascular Features of Heart Failure With Preserved Ejection Fraction

Abstract and Introduction

Abstract


Objectives: The purpose of this study was to identify cardiovascular features of patients with heart failure with preserved ejection fraction (HFpEF) that differ from those in individuals with hypertensive left ventricular hypertrophy (HLVH) of similar age, gender, and racial background but without failure.
Background: Heart failure with preserved ejection fraction often develops in HLVH patients and involves multiple abnormalities. Clarification of changes most specific to HFpEF may help elucidate underlying pathophysiology.
Methods: A cross-sectional study comparing HFpEF patients (n = 37), HLVH subjects without HF (n = 40), and normotensive control subjects without LVH (n 56). All subjects had an EF of >50%, sinus rhythm, and insignificant valvular or active ischemic disease, and groups were matched for age, gender, and ethnicity. Comprehensive echo-Doppler and pressure analysis was performed.
Results: The HFpEF patients were predominantly African-American women with hypertension, LVH, and obesity. They had vascular and systolic-ventricular stiffening and abnormal diastolic function compared with the control subjects. However, most of these parameters either individually or combined were similarly abnormal in the HLVH group and poorly distinguished between these groups. The HFpEF group had quantitatively greater concentric LVH and estimated mean pulmonary artery wedge pressure (20 mm Hg vs. 16 mm Hg) and shorter isovolumic relaxation time than the HLVH group. They also had left atrial dilation/dysfunction unlike in HLVH and greater total epicardial volume. The product of LV mass index and maximal left atrial (LA) volume best identified HFpEF patients (84% sensitivity, 82% specificity).
Conclusions: In an urban, principally African American, cohort, HFpEF patients share many abnormalities of systolic, diastolic, and vascular function with nonfailing HLVH subjects but display accentuated LVH and LA dilation/failure. These latter factors may help clarify pathophysiology and define an important HFpEF population for clinical trials.

Introduction


Nearly one-half of patients with heart failure have an ejection fraction (EF) at or above 50%. Despite the high prevalence, morbidity, and economic burden of heart failure with preserved ejection fraction (HFpEF), its patho-physiology remains somewhat controversial and evidencebased guidelines for management are lacking. A majority of HFpEF patients are elderly women with a history of systolic hypertension, many with cardiac hypertrophy and obesity. These are common features in the general population, and frequent among African-American women, who have the highest prevalence of hypertension worldwide. Most are without heart failure (HF) symptoms, and although they may have preclinical disease only a subgroup develops clinical HFpEF.

Cardiovascular features that might best distinguish patients with HF symptoms from those with similar clinical features such as hypertensive left ventricular hypertrophy (HLVH) but without HF remain unknown, because most studies have contrasted HFpEF patients to healthy normotensive (non-LVH) control subjects. Abnormal diastolic function, vascular stiffening, and increased ventricular end-systolic stiffness (elastance) have all been implicated, but it is unclear which descriptors are most specific and independent. Accordingly, the goal of the present study was to comprehensively assess resting ventricular and vascular physiologic properties in an inner-city cohort of HFpEF patients, and compare the findings with those obtained in 2 control groups with similar mean age, race, and gender with or without chronic HLVH. We hypothesized that many ventricular and arterial abnormalities thought to underlie HFpEF would be shared by asymptomatic HLVH subjects, but that other changes would be observed more selectively in HFpEF that might highlight critical maladaptations and/or novel pathophysiology.

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