OBJECTIVE: To quantify right ventriculo-arterial coupling in pulmonary hypertension by combining standard right heart catheterisation (RHC) and cardiac magnetic resonance (CMR) and to estimate it non-invasively with CMR alone. DESIGN: Cross-sectional analysis in a retrospective cohort of consecutive patients. SETTING: Tertiary care centre. PATIENTS: 139 adults referred for pulmonary hypertension evaluation. INTERVENTIONS: CMR and RHC within 2 days (n=151 test pairs). MAIN OUTCOME MEASURES: Right ventriculo-arterial coupling was quantified as the ratio of pulmonary artery (PA) effective elastance (E(a), index of arterial load) to right ventricular maximal end-systolic elastance (E(max), index of contractility). Right ventricular end-systolic volume (ESV) and stroke volume (SV) were obtained from CMR and adjusted to body surface area. RHC provided mean PA pressure (mPAP) as a surrogate of right ventricular end-systolic pressure, pulmonary capillary wedge pressure (PCWP) and pulmonary vascular resistance index (PVRI). E(a) was calculated as (mPAP - PCWP)/SV and E(max) as mPAP/ESV. RESULTS: E(a) increased linearly with advancing severity as defined by PVRI quartiles (0.19, 0.50, 0.93 and 1.63 mm Hg/ml/m(2), respectively; p<0.001 for trend) whereas E(max) increased initially and subsequently tended to decrease (0.52, 0.67, 0.54 and 0.56 mm Hg/ml/m(2); p=0.7). E(a)/E(max) was maintained early but increased markedly with severe hypertension (0.35, 0.72, 1.76 and 2.85; p<0.001), indicating uncoupling. E(a)/E(max) approximated non-invasively with CMR as ESV/SV was 0.75, 1.17, 2.28 and 3.51, respectively (p<0.001). CONCLUSIONS: Right ventriculo-arterial coupling in pulmonary hypertension can be studied with standard RHC and CMR. Arterial load increases with disease severity whereas contractility cannot progress in parallel, leading to severe uncoupling.
OBJECTIVE: To quantify right ventriculo-arterial coupling in pulmonary hypertension by combining standard right heart catheterisation (RHC) and cardiac magnetic resonance (CMR) and to estimate it non-invasively with CMR alone. DESIGN: Cross-sectional analysis in a retrospective cohort of consecutive patients. SETTING: Tertiary care centre. PATIENTS: 139 adults referred for pulmonary hypertension evaluation. INTERVENTIONS: CMR and RHC within 2 days (n=151 test pairs). MAIN OUTCOME MEASURES: Right ventriculo-arterial coupling was quantified as the ratio of pulmonary artery (PA) effective elastance (E(a), index of arterial load) to right ventricular maximal end-systolic elastance (E(max), index of contractility). Right ventricular end-systolic volume (ESV) and stroke volume (SV) were obtained from CMR and adjusted to body surface area. RHC provided mean PA pressure (mPAP) as a surrogate of right ventricular end-systolic pressure, pulmonary capillary wedge pressure (PCWP) and pulmonary vascular resistance index (PVRI). E(a) was calculated as (mPAP - PCWP)/SV and E(max) as mPAP/ESV. RESULTS: E(a) increased linearly with advancing severity as defined by PVRI quartiles (0.19, 0.50, 0.93 and 1.63 mm Hg/ml/m(2), respectively; p<0.001 for trend) whereas E(max) increased initially and subsequently tended to decrease (0.52, 0.67, 0.54 and 0.56 mm Hg/ml/m(2); p=0.7). E(a)/E(max) was maintained early but increased markedly with severe hypertension (0.35, 0.72, 1.76 and 2.85; p<0.001), indicating uncoupling. E(a)/E(max) approximated non-invasively with CMR as ESV/SV was 0.75, 1.17, 2.28 and 3.51, respectively (p<0.001). CONCLUSIONS: Right ventriculo-arterial coupling in pulmonary hypertension can be studied with standard RHC and CMR. Arterial load increases with disease severity whereas contractility cannot progress in parallel, leading to severe uncoupling.
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