Obese ZSF1 rats exhibit significantly increased right ventricular stiffness mainly due to cardiomyocyte hypertrophy, not fibrosis, indicating biventricular diastolic dysfunction in HFpEF.
In the ZSF1 rat model of HFpEF, right ventricular diastolic dysfunction is present and driven primarily by cardiomyocyte hypertrophy rather than myocardial fibrosis.
Absolute Event Rate: 0% vs 0%
Abstract Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome defined by diastolic dysfunction and limited therapeutic options, with increasing recognition of right ventricular (RV) involvement. Using invasive pressure-volume loop analysis, we assessed biventricular hemodynamics in lean and obese ZSF1 rats, a well-established rodent model of HFpEF. Obese rats exhibited significantly increased RV and left ventricular (LV) chamber stiffness, with a positive correlation between RV and LV stiffness constants, indicating biventricular diastolic dysfunction. RV end-systolic elastance was preserved, whereas LV contractility was increased. Despite elevated RV stiffness, myocardial fibrosis was unchanged, while RV and septal cardiomyocyte hypertrophy was significantly increased. These findings demonstrate that RV diastolic dysfunction in this HFpEF model is driven primarily by myocytic stiffening rather than fibrotic remodeling. Our data provide invasive hemodynamic evidence of RV involvement in HFpEF and further support the translational relevance of the ZSF1 rat model for studying biventricular HFpEF pathophysiology.
Schlotter et al. (Wed,) reported a other. Obese ZSF1 rats exhibit significantly increased right ventricular stiffness mainly due to cardiomyocyte hypertrophy, not fibrosis, indicating biventricular diastolic dysfunction in HFpEF.