BACKGROUND: Right ventricular (RV) maladaptation and failure determine outcome in pulmonary hypertension. The adaptation of RV function to loading (RV-pulmonary arterial coupling) is defined by a ratio of end-systolic to arterial elastances (Ees/Ea). How RV-pulmonary arterial coupling relates to pulmonary hypertension severity and onset of RV failure (defined by excessive volume increase and ejection fraction [EF] decrease) is not exactly known. METHODS AND RESULTS: We performed cardiac magnetic resonance (CMR) imaging within 24 hours of a diagnostic right heart catheterization and invasive measurement of RV pressure-volume loops in 42 patients with pulmonary hypertension. Median (interquartile range) Ees and Ea were 0.49 (0.35-0.74) and 0.74 (0.45-1.04) mm Hg/mL, respectively; Ees/Ea was 0.73 (0.47-1.07). End-diastolic elastance (Eed) was 0.14 (0.06-0.24) mm Hg/mL. RV EF was 39±13%. End-systolic volume and end-diastolic volume/body surface area (BSA) were 62 (45-101) and 104 (83-143) mL/m2, respectively. Ees/Ea decreased with increasing RV end-diastolic volume/BSA, mass/BSA, and pulmonary arterial stiffness, and with decreasing EF, from 0.89 to 1.09 in the least impaired tertiles to 0.55 to 0.61 in the most impaired tertiles. Eed increased with increasing RV mass/BSA, end-diastolic volume/BSA, and T1 mapping and with decreasing EF. Receiver operating characteristic analysis identified an Ees/Ea cutoff of 0.805 associated with onset of RV failure defined by increased RV volumes with EF <35%. CONCLUSIONS: RV-pulmonary arterial coupling (Ees/Ea) has considerable reserve, from normal values of 1.5-2 to <0.8, and has the ability to detect pending RV failure in patients with pulmonary hypertension. Clinical Trial Registration URL: https://www.clinicaltrials.gov . Unique identifier: NCT03403868.
BACKGROUND: Right ventricular (RV) maladaptation and failure determine outcome in pulmonary hypertension. The adaptation of RV function to loading (RV-pulmonary arterial coupling) is defined by a ratio of end-systolic to arterial elastances (Ees/Ea). How RV-pulmonary arterial coupling relates to pulmonary hypertension severity and onset of RV failure (defined by excessive volume increase and ejection fraction [EF] decrease) is not exactly known. METHODS AND RESULTS: We performed cardiac magnetic resonance (CMR) imaging within 24 hours of a diagnostic right heart catheterization and invasive measurement of RV pressure-volume loops in 42 patients with pulmonary hypertension. Median (interquartile range) Ees and Ea were 0.49 (0.35-0.74) and 0.74 (0.45-1.04) mm Hg/mL, respectively; Ees/Ea was 0.73 (0.47-1.07). End-diastolic elastance (Eed) was 0.14 (0.06-0.24) mm Hg/mL. RV EF was 39±13%. End-systolic volume and end-diastolic volume/body surface area (BSA) were 62 (45-101) and 104 (83-143) mL/m2, respectively. Ees/Ea decreased with increasing RV end-diastolic volume/BSA, mass/BSA, and pulmonary arterial stiffness, and with decreasing EF, from 0.89 to 1.09 in the least impaired tertiles to 0.55 to 0.61 in the most impaired tertiles. Eed increased with increasing RV mass/BSA, end-diastolic volume/BSA, and T1 mapping and with decreasing EF. Receiver operating characteristic analysis identified an Ees/Ea cutoff of 0.805 associated with onset of RV failure defined by increased RV volumes with EF <35%. CONCLUSIONS: RV-pulmonary arterial coupling (Ees/Ea) has considerable reserve, from normal values of 1.5-2 to <0.8, and has the ability to detect pending RV failure in patients with pulmonary hypertension. Clinical Trial Registration URL: https://www.clinicaltrials.gov . Unique identifier: NCT03403868.
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