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Rheumatology 2008 47(Supplement 5):v42-v43; doi:10.1093/rheumatology/ken284
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

This article appears in the following Rheumatology issue: Update in systemic sclerosis [View the issue table of contents]

Right ventricular function in scleroderma-related pulmonary hypertension

A. Vonk Noordegraaf1 and R. Naeije2

1Department of Pulmonary Diseases, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands and 2Department of Pathophysiology, Faculty of Medicine, Free University of Brussels, Brussels, Belgium.

Correspondence to: A. Vonk Noordegraaf, Department of Pulmonary Diseases, VU University Medical Center, De Boelelaan 1117, PO Box 7057, 1007 MB Amsterdam, The Netherlands. E-mail: A.Vonk{at}VUmc.nl


  Abstract

SSc-associated pulmonary arterial hypertension (PAH) has a poorer prognosis than that of other types of pulmonary hypertension. Recent echocardiographic and haemodynamic studies suggest that right ventriculer (RV) pump function and filling characteristics are altered in SSc-PAH as compared with idiopathic PAH. This could be explained by intrinsic myocardial involvement of the disease, related to abnormal collagen deposition, also observed in the left ventricle, or an increased vulnerability to ischaemia due to coronary vasculopathy, abnormal collagen cross-linking and altered myocyte function. It is also possible that a relatively more important decrease in pulmonary arterial compliance as evidenced by recently reported increased characteristic impedance measurements, would contribute to RV-arterial decoupling. More pathological, imaging and haemodynamic studies are needed for a better understanding for relatively more important vulnerability of the RV in SSc-PAH.

KEY WORDS: Right ventricle, Scleroderma, Pulmonary hypertension, Pulmonary artery pressure

Submitted 1 May 2008; Accepted 19 June 2008


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