Cardiac involvement in the antiphospholipid syndrome

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.