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Recent Advances in Chest Medicine |

The Right Ventricle Under Pressure: Cellular and Molecular Mechanisms of Right-Heart Failure in Pulmonary Hypertension

Harm J. Bogaard, MD, PhD; Kohtaro Abe, MD, PhD; Anton Vonk Noordegraaf, MD, PhD, FCCP; Norbert F. Voelkel, MD
Author and Funding Information

*From the Department of Pulmonary Medicine (Drs. Bogaard and Vonk Noordegraaf), VU University Medical Center, Amsterdam, the Netherlands; Department of Pulmonary Medicine and Critical Care (Dr. Voelkel), Virginia Commonwealth University, Richmond, VA; and Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences (Dr. Abe), Fukuoka, Japan.

Correspondence to: Norbert Voelkel, MD, Department of Pulmonary Medicine and Critical Care, Virginia Commonwealth University, 1101 E Marshall St, Sanger Hall, Rm 7-024, Richmond, VA 23284; e-mail: nvoelkel@mcvh-vcu.edu


Dr. Bogaard received a Dekker Stipend from the Netherlands Heart Foundation, grant NHS #2006T22.

The authors have no conflicts of interest to disclose.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2009;135(3):794-804. doi:10.1378/chest.08-0492
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Pulmonary arterial hypertension (PAH) is a deadly disease in which vasoconstriction and vascular remodeling both lead to a progressive increase in pulmonary vascular resistance. The response of the right ventricle (RV) to the increased afterload is an important determinant of patient outcome. Little is known about the cellular and molecular mechanisms that underlie the transition from compensated hypertrophy to dilatation and failure that occurs during the course of the disease. Moreover, little is known about the direct effects of current PAH treatments on the heart. Although the increase in afterload is the first trigger for RV adaptation in PAH, neurohormonal signaling, oxidative stress, inflammation, ischemia, and cell death may contribute to the development of RV dilatation and failure. Here we review cellular signaling cascades and gene expression patterns in the heart that follow pressure overload. Most data are derived from research on the left ventricle, but where possible specific information on the RV response to pressure overload is provided. This overview identifies the gaps in our understanding of RV failure and attempts to fill them, when possible. Together with the online supplement, it provides a starting point for new research and aims to encourage the pulmonary hypertension research community to direct some of their attention to the RV, in parallel to their focus on the pulmonary vasculature.

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