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This article is part of the supplement: Abstracts of the 2011 SCMR/Euro CMR Joint Scientific Sessions

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Evaluation of right ventriculoarterial coupling in pulmonary hypertension: a magnetic resonance study

Javier Sanz*, Ana Garcia-Alvarez, Leticia Fernandez-Friera, Ajith Nair, Jesus G Mirelis, Simonette Sawit, Sean Pinney and Valentin Fuster

  • * Corresponding author: Javier Sanz

Author Affiliations

Mount Sinai School of Medicine, New York, NY, USA

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Journal of Cardiovascular Magnetic Resonance 2011, 13(Suppl 1):O73  doi:10.1186/1532-429X-13-S1-O73

The electronic version of this article is the complete one and can be found online at:

Published:2 February 2011

© 2011 Sanz et al; licensee BioMed Central Ltd.

This is an open access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Inadequate right ventriculo-arterial coupling is an important determinant of heart failure in pulmonary hypertension, in turn the main determinant of outcome in this disease. Coupling can be quantified as the ratio of pulmonary artery effective elastance (Ea, an index of arterial load) to right ventricular maximal end-systolic elastance (Emax, an index of contractility).


To quantify right ventriculo-arterial coupling in pulmonary hypertension combining standard right heart catheterization and cardiac magnetic resonance (CMR), and to noninvasively estimate it with CMR alone.


We included 139 patients undergoing CMR and right heart catheterization within 2 days (n=151 test pairs) for the evaluation of known or suspected pulmonary hypertension. Right ventricular end-systolic volume index (ESVI) and stroke volume index (SVI) were obtained, respectively, from cardiac cine images and phase-contrast of the pulmonary artery after adjusting for body surface area. Right heart catheterization provided mean pulmonary artery 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)/SVI; and Emax as PAP/ESVI.


Ea increased linearly with advancing severity (as determined by PVRI quartiles; Figure, 1A), whereas Emax increased initially but tended to decrease subsequently (Figure, 1B). Thus, the ratio Ea/Emax was maintained in earlier stages but increased markedly (indicating uncoupling) with more severe pulmonary hypertension (Figure, 1C). According to underlying etiologies and after adjustment for age, gender and PVRI, there were no significant differences amongst World Health Organization groups in terms of Ea/Emax. Emax was independently associated with right atrial pressure after adjustment for PVRI (β=-2.81, p<0.05). Ea/Emax approximated noninvasively with CMR as ESVI/SVI equaled 0.75, 1.17, 2.28, and 3.51, for PVRI quartile groups (Q1 to Q4) respectively, showing excellent correlation with Ea/Emax derived from invasive measurements (r=0.93, p<0.001) and progressing similarly with disease severity (p<0.001).

thumbnailFigure 1. Ea, Emax and Ea/Emax according to pulmonary hypertension severity


Right ventriculo-arterial coupling in pulmonary hypertension can be studied combining standard right heart catheterization and CMR indices. In addition, it can be approximated with CMR alone in a completely noninvasive fashion. Arterial load increases with disease severity whereas contractility cannot progress in parallel, leading to severe uncoupling.