Background: Heart failure with preserved ejection fraction (HFpEF) is a prevalent disorder for which no effective treatment yet exists. Pulmonary hypertension (PH) and right atrial (RA) and ventricular (RV) dysfunction are frequently observed. The question remains whether the PH with the associated RV/RA dysfunction in HFpEF are markers of disease severity. Methods: To obtain insight in the relative importance of pressure-overload and left-to-right interaction, we compared RA and RV function in 3 groups: 1. HFpEF (n=13); 2. HFpEF-PH (n=33), and; 3. pulmonary arterial hypertension (PAH) matched to pulmonary artery pressures of HFpEF-PH (PH limited to mPAP ≥30 and ≤50 mmHg) (n=47). Patients underwent right heart catheterization and cardiac magnetic resonance imaging. Results: The right ventricle in HFpEF-PH was less dilated and hypertrophied than in PAH. In addition, RV ejection fraction was more preserved (HFpEF-PH: 52±11 versus PAH: 36±12%). RV filling patterns differed: vena cava backflow during RA contraction was observed in PAH only. In HFpEF-PH, RA pressure was elevated throughout the cardiac cycle (HFpEF-PH: 10 [8–14] versus PAH: 7 [5–10] mm Hg), while RA volume was smaller, reflecting excessive RA stiffness (HFpEF-PH: 0.14 [0.10–0.17] versus PAH: 0.08 [0.06–0.11] mm Hg/mL). RA stiffness was associated with an increased eccentricity index (HFpEF-PH: 1.3±0.2 versus PAH: 1.2±0.1) and interatrial pressure gradient (9 [5 to 12] versus 2 [−2 to 5] mm Hg). Conclusions: RV/RA function was less compromised in HFpEF-PH than in PAH, despite similar pressure-overload. Increased RA pressure and stiffness in HFpEF-PH were explained by left atrial/RA-interaction. Therefore, our results indicate that increased RA pressure is not a sign of overt RV failure but rather a reflection of HFpEF-severity.

Introduction: Heart failure with preserved ejection fraction (HFpEF) is a prevalent condition for which no treatment exists. Pulmonary hypertension (PH) and right atrial (RA) and right ventricular (RV) dysfunction are frequently observed. The question remains whether PH and the associated RV/RA dysfunction in HFpEF are treatment targets or a mere reflection of disease severity. Methods: To study the relative contribution of pressure-overload and left-to-right interaction, we compared RA/RV function in three groups: 1. HFpEF (n=13); 2. HFpEF-PH (n=33), and; 3. pulmonary arterial hypertension (PAH) matched to pulmonary artery pressures of HFpEF-PH (n=47). Patients underwent right heart catheterization and cardiac magnetic resonance imaging. Groups were compared using one-way ANOVA, after which post-hoc analysis with unpaired t-test and Bonferroni correction was performed. Results: The right ventricle in HFpEF-PH was less dilated and hypertrophied than in PAH and RV ejection fraction was more preserved (HFpEF-PH: 52±11 vs. PAH: 36±12%). RV filling patterns were altered: vena cava backflow during RA contraction was observed in PAH only. In HFpEF-PH, RA pressure was elevated throughout the cardiac cycle (HFpEF-PH: 10[8-14] vs. PAH: 7[5-10] mmHg), while RA volume was smaller, reflecting excessive RA stiffness (HFpEF-PH: 0.14[0.10-0.17] vs. PAH: 0.08[0.06-0.11]mmHg/mL). RA stiffness was associated with an increased RA eccentricity index (HFpEF-PH: 1.3±0.2 vs PAH: 1.2±0.1) and transmural pressure gradient (9[5-12] vs 2[-2-5] mmHg). Conclusions: Despite similar pressure-overload, RV/RA function was less compromised in HFpEF-PH than in PAH. Increased RA pressure and stiffness in HFpEF-PH were explained by left atrial/RA-interaction. Our results indicate that increased RA pressure is not a sign of overt RV failure, but rather a reflection of HFpEF-severity.