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Am J Physiol Heart Circ Physiol 290: H1528-H1533, 2006. First published November 11, 2005; doi:10.1152/ajpheart.01031.2005
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Impaired left ventricular filling due to right-to-left ventricular interaction in patients with pulmonary arterial hypertension

C. Tji-Joong Gan,1 Jan-Willem Lankhaar,1,2 J. Tim Marcus,2 Nico Westerhof,3 Koen M. Marques,4 Jean G. F. Bronzwaer,4 Anco Boonstra,1 Pieter E. Postmus,1 and Anton Vonk-Noordegraaf1

Departments of 1Pulmonary Diseases, 2Physics and Medical Technology, 3Physiology, and 4Cardiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands

Submitted 29 September 2005 ; accepted in final form 10 November 2005

The aim of this study was to investigate the contribution of direct right-to-left ventricular interaction to left ventricular filling and stroke volume in 46 patients with pulmonary arterial hypertension (PAH) and 18 control subjects. Stroke volume, right and left ventricular volumes, left ventricular filling rate, and interventricular septum curvature were measured by magnetic resonance imaging and left atrial filling by transesophageal echocardiography. Stroke volume, left ventricular end-diastolic volume, and left ventricular peak filling rate were decreased in PAH patients compared with control subjects: 28 ± 13 vs. 41 ± 10 ml/m2 (P < 0.001), 46 ± 14 vs. 61 ± 14 ml/m2 (P < 0.001), and 216 ± 90 vs. 541 ± 248 ml/s (P < 0.001), respectively. Among PAH patients, stroke volume did not correlate to right ventricular end-diastolic volume or mean pulmonary arterial pressure but did correlate to left ventricular end-diastolic volume (r = 0.62, P < 0.001). Leftward interventricular septum curvature was correlated to left ventricular filling rate (r = 0.64, P < 0.001) and left ventricular end-diastolic volume (r = 0.65, P < 0.001). In contrast, left atrial filling was normal and not correlated to left ventricular end-diastolic volume. In PAH patients, ventricular interaction mediated by the interventricular septum impairs left ventricular filling, contributing to decreased stroke volume.

ventricular interdependence; stroke volume



Address for reprint requests and other correspondence: A. Vonk-Noordegraaf, Dept. of Pulmonary Diseases, VU Univ. Medical Center, De Boelelaan 1117, PO Box 7057, 1007 MB Amsterdam, The Netherlands (e-mail: a.vonk{at}vumc.nl)




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