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Original Research: PULMONARY ARTERIAL HYPERTENSION |

Progressive Dilatation of the Main Pulmonary Artery Is a Characteristic of Pulmonary Arterial Hypertension and Is Not Related to Changes in Pressure

Bart Boerrigter, MD; Gert-Jan Mauritz, MSc; J. Tim Marcus, PhD; Frank Helderman, MSc; Pieter E. Postmus, MD, PhD, FCCP; Nico Westerhof, PhD; Anton Vonk-Noordegraaf, MD, PhD
Author and Funding Information

From the Departments of Pulmonary Diseases (Drs Boerrigter, Postmus, Westerhof, and Vonk-Noordegraaf and Mr Mauritz), Physics and Medical Technology (Dr Marcus and Mr Helderman), and Physiology (Dr Westerhof), Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands.

Correspondence to: Anton Vonk-Noordegraaf, MD, PhD, VU University Medical Center, PO Box 7057, 1007 MB Amsterdam, The Netherlands; e-mail: a.vonk@vumc.nl


Dr Boerrigter and Mr Mauritz contributed equally to this article.

Funding/Support: Dr Vonk-Noordegraaf was supported by the Netherlands Organisation for Scientific Research (NWO)-VIDI (project number 917.96.306).

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;138(6):1395-1401. doi:10.1378/chest.10-0363
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Background:  Pulmonary artery (PA) dilatation is one of the consequences of pulmonary arterial hypertension (PAH) and is used for noninvasive detection. However, it is unclear how the size of the PA behaves over time and whether it is related to pressure changes. The aim of this study was to evaluate PA size during follow-up in treated patients with PAH and whether it reflects pulmonary vascular hemodynamics.

Methods:  Fifty-one patients with PAH who underwent at least two right-sided heart catheterizations (RHCs) together with cardiac MRI (CMR) were included in this study. Another 18 patients who had normal pressure at RHC were included for comparison at baseline. From RHC, we derived PA pressures and cardiac output. From the CMR images we derived PA diameter (PAD) and the ratio of the PAD and ascending aorta diameter.

Results:  The PAD was significantly larger in patients with PAH than in patients without PAH (P < .001). A ratio of the PAD and ascending aorta diameter > 1 had a positive predictive value of 92% for PAH. Mean follow-up time was 942 days, and there was a significant dilatation during this period (P < .001). The change of the PAD did not correlate with the changes in pressure or cardiac output. A moderate correlation with follow-up time was found (r = 0.56; P < .001).

Conclusions:  A dilatated PA is useful for identifying patients with PAH. However, during patient follow-up, progressive dilatation of the PA is independent of the change in PA pressure and cardiac output and might become independent from hemodynamics.

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