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Original Research |

Progressive Changes in Right Ventricular Geometric Shortening and Long-term Survival in Pulmonary Arterial HypertensionGeometric Shortening in Pulmonary Hypertension

Gert-Jan Mauritz, MSc; Taco Kind, MD; J. Tim Marcus, PhD; Harm-Jan Bogaard, MD, PhD; Mariëlle van de Veerdonk, MD; Pieter E. Postmus, MD, PhD, FCCP; Anco Boonstra, MD, PhD; Nico Westerhof, PhD; Anton Vonk-Noordegraaf, MD, PhD
Author and Funding Information

From the Department of Pulmonary Diseases (Mr Mauritz and Drs Kind, Bogaard, van de Veerdonk, Postmus, Boonstra, Westerhof, and Vonk-Noordegraaf), Department of Physics and Medical Technology (Dr Marcus), and Department of Physiology (Dr Westerhof), Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands; and the Department of Medicine (Dr Bogaard), Division of Pulmonary and Critical Care, Virginia Commonwealth University, Richmond, VA.

Correspondence to: Anton Vonk-Noordegraaf, MD, PhD, Department of Pulmonary Diseases, VU University Medical Center, Boelelaan 1117, 1007 MB, Amsterdam, The Netherlands; e-mail: a.vonk@vumc.nl


Mr Mauritz and Dr Kind contributed equally to this article.

Funding/Support: This studywas financially supported by The Netherlands Organisation for Scientific Research (NWO) Toptalent grant [021.001.120 to Dr Kind] and the NWO Vidi Grant [91.796.306 to Dr Vonk-Noordegraaf].

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


© 2012 American College of Chest Physicians


Chest. 2012;141(4):935-943. doi:10.1378/chest.10-3277
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Background:  Until now, many investigators have focused on describing right ventricular (RV) dysfunction in groups of patients with pulmonary arterial hypertension (PAH), but very few have addressed the deterioration of RV function over time. The aim of this study was to investigate time courses of RV geometric changes during the progression of RV failure.

Methods:  Forty-two patients with PAH were selected who underwent right-sided heart catheterization and cardiac MRI at baseline and after 1-year follow-up. Based on the survival after this 1-year run-in period, patients were classified into two groups: survivors (26 patients; subsequent survival of > 4 years) and nonsurvivors (16 patients; subsequent survival of < 4 years). Four-chamber cine imaging was used to quantify RV longitudinal shortening (apex-base distance change), RV transverse shortening (septum-free wall distance change), and RV fractional area change (RVFAC) between end diastole and end systole.

Results:  Longitudinal shortening, transverse shortening, and RVFAC measured at the beginning of the run-in period and 1 year later were significantly higher in subsequent survivors than in nonsurvivors (P < .05). Longitudinal shortening did not change during the run-in period in either patient group. Transverse shortening and RVFAC did not change during the run-in period in subsequent survivors but did decrease in subsequent nonsurvivors (P < .05). This decrease was caused by increased leftward septal bowing.

Conclusions:  Progressive RV failure in PAH is associated with a parallel decline in longitudinal and transverse shortening until a floor effect is reached for longitudinal shortening. A further reduction of RV function is due to progressive leftward septal displacement. Because transverse shortening incorporates both free wall and septum movements, this parameter can be used to monitor the decline in RV function in end-stage PAH.

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