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Right ventriculo-arterial coupling in pulmonary hypertension: a magnetic resonance study
  1. Javier Sanz1,
  2. Ana García-Alvarez1,2,3,
  3. Leticia Fernández-Friera1,2,
  4. Ajith Nair1,
  5. Jesús G Mirelis1,2,
  6. Simonette T Sawit1,
  7. Sean Pinney1,
  8. Valentin Fuster1,2
  1. 1The Zena and Michael A Wiener Cardiovascular Institute and Marie-Josee and Henry R Kravis Center for Cardiovascular Health, Mount Sinai School of Medicine, New York, USA
  2. 2The Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain
  3. 3Thorax Institute, Cardiology Department, Hospital Clinic, Barcelona, Spain
  1. Correspondence to Dr Javier Sanz, Cardiovascular Institute, Mount Sinai Hospital, One Gustave L Levy Place, Box 1030, New York, NY 10029, USA; javier.sanz{at}


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
  • stable angina
  • coronary artery disease (CAD)

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  • 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.