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Eur Heart J Cardiovasc Imaging · Dec 2013
Comparative StudyNon-invasive indices of right ventricular function are markers of ventricular-arterial coupling rather than ventricular contractility: insights from a porcine model of chronic pressure overload.
- Julien Guihaire, Francois Haddad, David Boulate, Benoît Decante, Andre Y Denault, Joseph Wu, Philippe Hervé, Marc Humbert, Philippe Dartevelle, Jean-Philippe Verhoye, Olaf Mercier, and Elie Fadel.
- Laboratory of Surgical Research and Inserm U999, University of Paris Sud, University of Paris XI, Marie Lannelongue Hospital, 133 avenue de la Résistance, Le Plessis Robinson, France.
- Eur Heart J Cardiovasc Imaging. 2013 Dec 1; 14 (12): 1140-9.
AimsTo investigate the physiological correlates of indices of RV function in a model of chronic pressure overload.Methods And ResultsChronic pulmonary hypertension (PH) was induced in piglets by ligation of the left pulmonary artery (PA) followed by weekly embolization of right lower lobe arteries for 5 weeks (the PH group, n = 11). These animals were compared with sham-operated animals (controls, n = 6). At 6 weeks, a subgroup of five PH pigs underwent surgical reperfusion of the left lung and four others were followed until 12 weeks without treatment. Right ventricular function was assessed using echocardiography and conductance catheter measurements. At 6 weeks, mean PA pressure was higher in PH group compared with controls (35 ± 9 vs. 14 ± 2 mmHg, P < 0.01). Although RV elastance (Ees) increased at 6 weeks in the PH group (0.55 ± 0.09 vs. 0.38 ± 0.05 mmHg/mL, P < 0.001), ventricular-arterial coupling measured by the ratio of Ees on PA elastance (Ea) was decreased (0.68 ± 0.17 vs. 1.18 ± 0.18, P < 0.001). There was a strong direct relationship between Ees/Ea and indices of RV function, while relationship between Ees and indices of RV function was moderate. Changes in indices of RV function with time and after left lung reperfusion were associated with changes in Ees/Ea.ConclusionUsual indices of RV function are associated with ventricular-arterial coupling rather than with ventricular contractility in a model of chronic pressure overload.
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