Article Text
Abstract
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 (Ea, index of arterial load) to right ventricular maximal end-systolic elastance (Emax, 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). Ea was calculated as (mPAP − PCWP)/SV and Emax as mPAP/ESV.
Results Ea increased linearly with advancing severity as defined by PVRI quartiles (0.19, 0.50, 0.93 and 1.63 mm Hg/ml/m2, respectively; p<0.001 for trend) whereas Emax increased initially and subsequently tended to decrease (0.52, 0.67, 0.54 and 0.56 mm Hg/ml/m2; p=0.7). Ea/Emax was maintained early but increased markedly with severe hypertension (0.35, 0.72, 1.76 and 2.85; p<0.001), indicating uncoupling. Ea/Emax 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.
- Primary pulmonary hypertension
- imaging/CT MRI
- CT scanning
- MRI
- pulmonary vascular disease
- EBM
- STEMI
- stable angina
- NSTEMI
- coronary artery disease (CAD)
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Footnotes
Funding This work was partially supported by the Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain (CARDIOJOVEN Program to AG-A and CARDIOIMAGEN to JGM); Instituto de Formación e Investigación “Marqués de Valdecilla”, Santander, Spain (PostMIR Wenceslao López Albo grant to LF-F) and the SPANISH Society of Cardiology (Post-Residency Grant to LF-F and AG-A).
Competing interests None.
Ethics approval This study was conducted with the approval of the Institutional Review Board.
Provenance and peer review Not commissioned; externally peer reviewed.