Cardiac involvement in the antiphospholipid syndrome

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F Tenedios1, D Erkan, M D Lockshin

  • 1Department of Rheumatology, Hospital for Special Surgery, Weill Medical College of Cornell University, New York, USA. tenediosf@hss.edu

Lupus
|October 13, 2005
PubMed

Insights

Antiphospholipid syndrome (APS) causes heart issues like valve problems and atherosclerosis. Antiphospholipid antibodies (aPLs) trigger inflammation and endothelial cell activation, leading to cardiac damage in APS patients.

Area of Science:

  • Cardiology
  • Immunology
  • Rheumatology

Background:

  • Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by a hypercoagulable state, fetal loss, and diverse clinical manifestations.
  • Cardiac involvement is a significant feature of APS, encompassing valve abnormalities, arterial occlusive disease, intracardiac emboli, ventricular dysfunction, and pulmonary hypertension.

Purpose of the Study:

  • To elucidate the role of antiphospholipid antibodies (aPLs) in the pathogenesis of cardiac manifestations in Antiphospholipid syndrome (APS).
  • To investigate the mechanisms by which aPLs contribute to endothelial activation and subsequent cardiovascular damage in APS.

Main Methods:

  • Review of existing literature on cardiac manifestations of APS.
  • Analysis of the proposed mechanisms involving aPLs, endothelial activation, and inflammatory pathways.

Main Results:

  • Antiphospholipid antibodies (aPLs) are implicated in accelerated atherosclerosis and myocardial infarction in APS, potentially through endothelial activation.
  • aPLs contribute to heart valve lesions in APS, with evidence of aPL deposition initiating inflammatory processes involving complement activation.
  • Endothelial cell activation by autoantibodies promotes a proadhesive, proinflammatory, and procoagulant phenotype, sustaining cardiovascular damage.

Conclusions:

  • Antiphospholipid antibodies (aPLs) play a crucial role in the development of cardiac manifestations in Antiphospholipid syndrome (APS).
  • The varied effects of aPLs on endothelial cells contribute to the heterogeneity of APS clinical manifestations, including cardiac involvement.

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