Autoantibodies and cardiac arrhythmias

Abstract

Autoimmune diseases are associated with significant morbidity and mortality, afflicting about 5% of the US population. They encompass a wide range of disorders that affect all organs of the human body and have a predilection for women. In the past, autoimmune pathogenesis was not thought to be a major mechanism for cardiovascular disorders, and potential relationships remain understudied. However, accumulating evidence suggests that a number of vascular and cardiac conditions are autoimmune mediated. Recent studies indicate that autoantibodies play an important role in the development of cardiac arrhythmias, including atrial fibrillation, modulation of autonomic influences on heart rate and rhythm, conduction system abnormalities, and ventricular arrhythmias. This article will review the current evidence for the role of autoantibodies in the development of cardiac arrhythmias.

Figure 1

Immunologic tolerance and autoimmune diseases. An illustration showing the normal intrinsic and extrinsic mechanisms of immunologic tolerance. Loss of tolerance results in inappropriate production of autoantibodies and in autoimmune diseases.

Figure 2

Autoantibodies and cardiac arrhythmias. Autoantibodies known to contribute to the development of bradyarrhythmias (red) and tachyarrhythmias (green) are illustrated here.

Figure 3

Mechanisms of autoantibody-induced cellular events that lead to the development of cardiac arrhythmias. A Anti-Ro/SSA antibodies. B Anti-β1-adrenergic receptor antibodies. C Anit-M2 muscarinic cholinergic receptor antibodies. D Anti-Na/K-ATPase antibodies.