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Updated: Mar 18, 2026

Evaluation of Right Ventricular Function in Experimental Models of Pulmonary Arterial Hypertension
Published on: June 27, 2025
Abnormal right ventricular-pulmonary artery coupling with exercise in heart failure with preserved ejection fraction
Barry A Borlaug1, Garvan C Kane2, Vojtech Melenovsky2
1The Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic Rochester, 200 First Street SW, Rochester, MN 55906, USA borlaug.barry@mayo.edu.
Background:
Exercise intolerance is common in people with heart failure and preserved ejection fraction (HFpEF). Right ventricular (RV) dysfunction has been shown at rest in HFpEF but little data are available regarding dynamic RV-pulmonary artery (PA) coupling during exercise.
Methods And Results:
Subjects with HFpEF (n = 50) and controls (n = 24) prospectively underwent invasive cardiopulmonary exercise testing using high-fidelity micromanometer catheters along with simultaneous assessment of RV and left ventricular (LV) mechanics by echocardiography. Compared with controls at rest, subjects with HFpEF displayed preserved RV systolic and diastolic mechanics (RV s' and e'), impaired LV s' and e', higher biventricular filling pressures, and higher pulmonary artery pressures. On exercise, subjects with HFpEF displayed less increase in stroke volume, heart rate, and cardiac output (CO), with blunted increase in CO relative to O2 consumption (VO2). Enhancement in RV systolic and diastolic function on exercise was impaired in HFpEF compared with controls. Exercise-induced PA vasodilation was reduced in HFpEF in correlation with greater venous hypoxia. Elevations in biventricular filling pressures and limitations in CO reserve were strongly correlated with abnormal enhancement in ventricular mechanics in the RV and LV during stress.
Conclusions:
In addition to limited LV reserve, patients with HFpEF display impaired RV reserve during exercise that is associated with high filling pressures and inadequate CO responses. These findings highlight the importance of biventricular dysfunction in HFpEF and suggest that novel therapies targeting myocardial reserve in both the left and right heart may be effective to improve clinical status.
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