Detection of right ventricular dysfunction through right ventricular free wall strain in obese heart failure with preserved ejection fraction

Abstract Background Heart Failure with Preserved Ejection Fraction (HFpEF) is increasingly prevalent, yet effective diagnostic tools and a comprehensive understanding of disease phenotypes are lacking (1,2). In HFpEF, obesity is a distinct subgroup (3). Right ventricular (RV) function measured invasively is more impaired in obese HFpEF than in non-obese HFpEF (4). Also, RV dysfunction (RVD) is associated with worse outcomes in HFpEF patients (4,5). Several non-invasive RVD measurements are available, with RV free wall strain (RVFWS) being a sensitive tool to detect early disease (6). Given the limitations for invasive RV function testing in widespread clinical use, RVFWS may aid in early identification of RVD in obese HFpEF. Purpose We investigated the potential of RVFWS to identify RVD in obese HFpEF patients. Methods HFpEF was defined by an HFA-PEFF Score of ≥5 in patients from 2 cohort studies at a Heart Failure Center. The HFA-PEFF score was calculated as described previously (7). Clinical, laboratory and echocardiographic data were recorded and compared between obese (BMI ≥30) and non-obese HFpEF patients. RV imaging was obtained in a RV-focused apical four-chamber view. RVFWS was acquired via speckle-tracking echocardiography, using TomTec software automatically tracing six segments (basal, mid, and apical of free wall and septum), which were manually adjusted to fit the free wall. Results 153 HFpEF patients were identified, of which 42 (27.5%) were obese. In comparison, obese HFpEF patients were younger, more often smokers, had a higher prevalence of prior myocardial infarction and diabetes as well as displayed a higher estimated plasma volume (p 0.001, table 1). In non-obese HFpEF atrial fibrillation was more prevalent and NT-pro-BNP levels were higher (table 1). Left ventricular (LV) hypertrophy and left atrial diameter was greater in obese HFpEF (table 2). RVFWS was more negative (i.e. better) in non-obese HFpEF (-22.6% vs -21.5%, P = 0.010, table 2). RVD was more prevalent in obese HFpEF when using a RVFWS threshold of -20% (P = 0.045, table 2). Conventional parameters for RVD (TAPSE, S’, FAC) showed no differences between groups. After correcting for age and gender, BMI moderately influenced RVFWS (β = 0.23, P = 0.003, figure 1). Lastly, RVFWS was negatively associated with peak VO2 and Six Minute Walking Distance and was positively correlated with right atrial area (figure 2-4). Conclusion In this study RVFWS was a sensitive, non-invasive tool to detect RVD in obese HFpEF patients. Nonetheless, further studies are needed to determine optimal RVFWS cut-off thresholds for RVD in obese HFpEF. We also showed that, despite similar LV function, obesity in HFpEF is associated with subtle alterations in RV mechanics, which are further associated with exercise capacity. Further research into RVFWS in obese HFpEF might lead to a better understanding of the pathophysiology and inform phenotype-specific therapeutic strategies.Table 1 and Table 2 Linear Regression of RVFWS (Figure 1-4)