Abstract

BACKGROUND: Obesity related heart failure with preserved ejection fraction (HFpEF) is an independent phenotype, notably common in China. Cardiovascular magnetic resonance imaging-feature tracking (CMR-FT) allows for recognizing subtle and early functional alterations of this phenotype. This study therefore aimed to investigate the clinical features and CMR-FT derived subtle clinical dysfunction in Obese HFpEF phenotype.

METHODS: We prospectively included 70 obese HFpEF, 40 normal-weight HFpEF patients and 28 clinically healthy controls underwent CMR examination from Aug 2019 to Jul 2021. Clinical features and CMR-FT derived strain parameters were recorded and analyzed.

RESULTS: Compared with normal-weight HFpEF, obese HFpEF patients were younger males (48±15 vs 64±10 years, P<0.001), used more calcium channel blocker (48.5% vs. 23.9%, P<0.05), and showed higher plasma volume (3104±651 vs. 2324±343 mL, P<0.001), hypersensitive C-reactive protein (Hs-CRP, median, 1.30 vs. 0.84 mg/L, P<0.05). Moreover, obese HFpEF patients showed greater left ventricular (LV) mass index, LV end-diastole volume index, LV end-systole volume index and worse CMR-FT derived strain parameters (all P≤0.001) compared to normal-weight HFpEF and clinically healthy controls. After adjusting for age, sex, diastolic blood pressure, calcium channel blocker use, estimated plasma volume, Hs-CRP, and N-terminal pro–brain natriuretic peptide levels, only early-diastolic global longitudinal strain rate (EGLSR, 0.60±0.03 vs. 0.74±0.05/s, P=0.031), early-diastolic global circumferential strain rate (EGCSR, 0.72±0.04/s vs. 0.91±0.07/s, P=0.033), early-diastolic global radial strain rate (-1.90±0.11/s vs. -2.47±0.19/s, P=0.023) and global circumferential strain (GCS, -18.5±4.0% vs -21.7±2.5%, P=0.048) were obviously impaired in obese HFpEF versus normal-weight HFpEF patients. In addition, increased plasma volume and body mass was modestly, inversely associated with GCS, EGLSR, and EGCSR (all P<0.01).

DISCUSSION: In this well-defined cohort of prospectively studied heart failure patients, we illustrated clinical features of obese HFpEF phenotype with more remarkable inflammation response, and CMR derived left ventricular remodeling and worse subtle dysfunction, compared to normal-weight HFpEF and clinically healthy controls. In addition, diastolic dysfunction (impaired EGLSR, EGCSR, and EGRSR) and subtle systolic dysfunction (impaired GCS) were more prominent characteristics of obese HFpEF patients, showed modest to moderate correlations with body mass and estimated plasma volume, and assisted in the diagnosis of obese HFpEF. Together, these findings provided a basis for an improved identification algorithm and targeted management in obese HFpEF patients using comprehensive clinical features and CMR approach including strain parameters, especially early-diastolic strain rate. To note, as emphasized by the present data, three-directional early-diastolic strain rate—direct marker of diastolic dysfunction, EGLSR, EGCSR, and EGRSR—were all significantly impaired in obese HFpEF patients compared to normal-weight HFpEF, not only in line with previous investigations demonstrating the independent phenotype of obese HFpEF, but also on the strength of comparison with normal-weight HFpEF. Several studies have showed excellent intra- and interobserver reliability of early-diastolic strain rate and shared conformity with echocardiography. Our study further expanded the use of early-diastolic strain rate in differentiation and confirmation of the severe diastolic dysfunction in obese HFpEF subgroup. In addition, patients with higher body mass and elevated PV levels were inversely associated worse GCS, EGLSR and EGCSR. This indicated the good representation of strain and strain rate for clinical features, and may become the accessible, additional, functional parameter of obese HFpEF. According to 2021 ESC guideline, weight loss therapies to prevent progression of HFpEF may be also particularly recommended for Chinese patients with BMI≥28kg/m2. The present results may pave the way for the development of new strain-guided treatment strategies and immediate monitoring. Nonetheless, now we are only at the beginning of the—maybe revolutionary—journey of CMR-FT in obese HFpEF phenotype, and more research is needed to establish CMR-FT in routine clinical decision-making processes.

CONCLUSIONS: In this well-defined obese HFpEF cohort, higher volume overload and inflammatory response, and more impaired EGLSR, EGCSR, and GCS are prominent characteristics, comparing with normal-weight HFpEF. Myocardial strain may potentially assist in identification of obese HFpEF phenotype.

Acknowledgements

None.