Physicians' Academy for Cardiovascular Education

Obesity may be considered a distinct phenotype in heart failure with preserved EF

Evidence Supporting the Existence of a Distinct Obese Phenotype of Heart Failure With Preserved Ejection Fraction

Obokata M, Reddy YNV, Pislaru SV, et al. - Circulation. 2017;136:6-19

Background

To date, there is no evidence of treatment that improves the prognosis of heart failure with preserved ejection fraction (HFpEF), although it seems that the phenotyping of patients and consequent classification into pathophysiological homogenous groups, leads to a better targeting of treatments [1,2]. Obesity is common among HFpEF patients, and its negative impact on the cardiovascular system implies that obesity-related HFpEF may represent a clinical relevant phenotype within the broader spectrum of HFpEF [3-5].

In this study, a detailed characterization of cardiovascular structure, function and reserve capacity in subjects with HFpEF and class II or greater obesity was performed and compared with this of non-obese HFpEF and non-HF controls. For this purpose, participants were categorized according to BMI into non-obese HFpEF patients, defined as BMI <30kg/m2 or obese HFpEF patients, defined as class II obesity or greater (BMI ≥ 35 kg/m2). Patients with class I obesity (BMI 30-34.9 kg/m2) were excluded to maximize phenotypic differences associated with greater body mass. Obese and non-obese HFpEF subjects were also compared to non-obese controls (BMI <30kg/m2), without heart failure.

Main results

Conclusion

Obese patients with HFpEF had greater biventricular remodeling, volume overload, more RV dysfunction, greater ventricular interaction and pericardial restraint, worse exercise capacity, more profound hemodynamic derangements and impaired pulmonary vasodilation. These findings suggest that obesity may be considered as a specific HFpEF phenotype.

Editorial comment

In their editorial article [6], Kitzman and Lam comment on the lack of data regarding obese patients with HFpEF, and welcome the study of Obokata et al, since they ‘….add dramatically to evidence supporting obese HFpEF as a valid HFpEF phenotype, and effectively usher obese HFpEF from pariah to its rightful place as a central player in the HFpEF syndrome.’

The authors adopt the opinion that dyspnea in obese patients with HFpEF is not due to the mechanical burden of their excess weight, but the excess adipose tissue has a negative impact on several mechanisms that lead to real heart failure. And they conclude: ‘As we work to differentiate and better understand specific mechanisms of the various HFpEF phenotypes, including obese HFpEF, even greater rewards may result from efforts to identify the fundamental factors that underlie the HFpEF syndrome and unite its phenotypes.’

References

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Find this article online at Circulation