This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tenedios, F Articles by Lockshin, M D Search for Related Content PubMed PubMed Citation Articles by Tenedios, F Articles by Lockshin, M D Social Bookmarking                   What's this?

Cardiac involvement in the antiphospholipid syndrome

Department of Rheumatology, Hospital for Special Surgery, Weill Medical College of Cornell University, New York, USA, tenediosf{at}hss.edu

D Erkan

Department of Rheumatology, Hospital for Special Surgery, Weill Medical College of Cornell University, New York, USA

M D Lockshin

Department of Rheumatology, Hospital for Special Surgery, Weill Medical College of Cornell University, New York, USA

Antiphospholipid syndrome (APS) is a systemic autoimmune disease, associated with a hypercoagulable state and fetal loss and with other clinical manifestations including cardiac involvement. Cardiac manifestations of APS are valve abnormalities (valve thickening and vegetations), occlusive arterial disease (atherosclerosis and myocardial infarction), intracardiac emboli, ventricular dysfunction, and pulmonary hypertension. Antiphospholipid antibodies (aPLs) may have a role in the accelerated atherosclerotic arterial disease observed in APS, related to their ability to induce endothelial activation. aPLs have been incriminated in the pathogenesis of heart valve lesions in APS patients. Markers of endothelial cell activation are up-regulated with prominent deposition of aPL in heart valves, suggesting aPL deposition initiates an inflammatory process that recruits complement leading to the valve lesion. Autoantibody-mediated endothelial cell activation probably plays a role in sustaining a proadhesive, proinflammatory, and procoagulant phenotype. The heterogeneity of APS clinical manifestations is likely linked to the varied effects that aPL can induce on endothelial cells and to the different functions that endothelial cells display depending on the anatomic localization.

Key Words: antiphospholipid syndrome • atherosclerosis • coronary artery disease • valvular disease

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				S. Sangle and D. D'Cruz Syndrome X (angina pectoris with normal coronary arteries) and myocardial infarction in patients with anti-phospholipid (Hughes) syndrome Lupus, February 1, 2008; 17(2): 83 - 85. [PDF]

				H. Gorki, V. Malinovski, and R. D.L. Stanbridge The antiphospholipid syndrome and heart valve surgery Eur. J. Cardiothorac. Surg., February 1, 2008; 33(2): 168 - 181. [Abstract] [Full Text] [PDF]

				C. Christodoulou, S. Sangle, and D. P. D'Cruz Vasculopathy and arterial stenotic lesions in the antiphospholipid syndrome Rheumatology, June 1, 2007; 46(6): 907 - 910. [Abstract] [Full Text] [PDF]

				G R V Hughes and H Phillips Mycophenolate mofetil and cardiovascular disease Lupus, November 1, 2006; 15(11_suppl): 1 - 2. [Abstract] [PDF]

				R. Maksimovic, P. M. Seferovic, A. D. Ristic, B. Vujisic-Tesic, D. S. Simeunovic, G. Radovanovic, M. Matucci-Cerinic, and B. Maisch Cardiac imaging in rheumatic diseases Rheumatology, October 1, 2006; 45(suppl_4): iv26 - iv31. [Abstract] [Full Text] [PDF]

				W. Lim, M. A. Crowther, and J. W. Eikelboom Management of Antiphospholipid Antibody Syndrome: A Systematic Review JAMA, March 1, 2006; 295(9): 1050 - 1057. [Abstract] [Full Text] [PDF]

				A Doria and P Sarzi-Puttini Heart, rheumatism and autoimmunity: an old intriguing link Lupus, September 1, 2005; 14(9): 643 - 645. [PDF]