Obesity and Heart Failure With Preserved Ejection Fraction

Study Questions:

What are the clinical characteristics of patients with obesity-related heart failure with preserved ejection fraction (HFpEF)?

Methods:

Using echocardiography and invasive hemodynamic exercise testing, the study investigators characterized the cardiovascular structure, function, and reserve capacity in subjects with HFpEF and class II or greater obesity (body mass index [BMI], ≥35 kg/m2, n = 99), and compared these findings with nonobese HFpEF (BMI <30 kg/m2, n = 99) HF patients and non-HF (n = 71) controls. They abstracted clinical history, laboratory data, and current medications from the medical records. They calculated ideal body weight based on height (a + b x [height in cm – 150], where a = 48 for men and 45 for women, and b = 1.1 for men and 0.9 for women, respectively). And they estimated plasma volume by (1-hematocrit) x (a + [b x weight in kg], where a = 1530 for men and 864 for women, and b = 41 for men and 47.9 for women, respectively). They used both linear and nonlinear regressions to assess associations between two variables.

Results:

Subjects with nonobese HFpEF were older, but gender, height, and ideal body weight were similar across groups. The investigators found that subjects with obese HFpEF, when compared to both nonobese HFpEF and controls, displayed more concentric left ventricular remodeling, greater right ventricular (RV) dilatation (base 34 ± 7 vs. 31 ± 6 and 30 ± 6 mm, p = 0.0005; length 66 ± 7 vs. 61 ± 7 and 61 ± 7 mm, p < 0.0001), more RV dysfunction (RV fractional area change % 48 ± 9, vs. 49 ± 9 vs. 52 ± 7, p < 0.02), increased epicardial fat thickness (10 ± 2 vs. 7 ± 2 and 6 ± 2 mm, p < 0.0001), greater total epicardial heart volume (945 [831,1105] vs. 797 [643,979] and 632 [517,768] ml, p < 0.0001), and increased plasma volume (3907 [3563,4333] vs. 2772 [2555,3133] and 2680 [2380,3006] ml, p < 0.0001), despite lower N-terminal pro-B-type natriuretic peptide levels. Pulmonary capillary wedge pressure (PCWP) was correlated with body mass and plasma volume in obese HFpEF (r = 0.22 and 0.27, both p < 0.05), but not in nonobese HFpEF (p ≥ 0.3).

They also found that increase in heart volumes in obese HFpEF was associated with greater pericardial restraint and heightened ventricular interdependence, reflected by increased ratio of right-to-left heart filling pressures (0.64 ± 0.17 vs. 0.56 ± 0.19 and 0.53 ± 0.20, p = 0.0004) and greater left ventricular eccentricity index (1.10 ± 0.19 vs. 0.99 ± 0.06 and 0.97 ± 0.12, p < 0.0001). Interdependence was enhanced as pulmonary artery pressure load increased (interaction p < 0.05).

The investigators found that obese HFpEF subjects, as compared to nonobese HFpEF and controls, showed worse exercise capacity (peak oxygen consumption 7.7 ± 2.3 vs. 10.0 ± 3.4 and 12.9 ± 4.0 ml/min * kg, p < 0.0001), higher biventricular filling pressures (right atrium mm Hg 21 ± 7, vs. 17 ± 6 vs. 8 ± 4, p < 0.0001 and PCWP mm Hg 33 ± 7 vs. 30 ± 5, vs. 15 ± 5, p < 0.0001) with exercise.

Conclusions:

The authors concluded that obesity-related HFpEF is a genuine form of cardiac failure and a clinically relevant phenotype that may require specific treatments.

Perspective:

This is an important study because it demonstrates that there is substantial heterogeneity in HFpEF subjects and that clinical trials targeting such patients should keep this in mind during study design. Also, the findings of this study may allow better understanding of the ‘obesity paradox’ associated with HF.


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