Accumulating clinical and experimental evidence has identified an increasing array
of humoral autoantibodies that disrupt cardiovascular autonomic function. Their diverse
clinical presentations encompass bradyarrhythmias, tachyarrhythmias, and hypotension.
For example, fetal exposure to maternal anti-Ro or anti-La antibodies in systemic
lupus erythematosis may produce complete heart block. In Chagas disease, anti-M2 receptor
antibodies are associated with dilated cardiomyopathy, QT dispersion, and atrial fibrillation.
Anti-β1 and anti-β2 adrenergic receptor antibodies are associated with inappropriate sinus tachycardia
and atrioventricular block. Anti-sinus node antibodies are associated with sick sinus
syndrome. Anti-N-methyl-D-aspartate (NMDA) receptor antibodies, which cause autoimmune encephalitis,
can also cause tachycardia or bradycardia with sinus arrest and asystole. Anti-myosin
heavy chain antibodies can cause atrial fibrillation. Antibodies to voltage-gated
potassium channel subfamily H (KCNH2) and, as we have described, to the ganglionic α3-acetylcholine (G-ACh) receptor have
been associated with QT dispersion and ventricular tachycardia. Functional autoantibodies
associated with neurogenic orthostatic hypotension include those to G-ACh receptors,
β2 adrenergic receptors, and M2 muscarinic receptors. Recognition of these syndromes
is revealing an autoimmune basis in a subset of a number of common cardiovascular
autonomic conditions that were previously idiopathic and highlights the multiple levels
of interaction between the immune system and autonomic neurons. Ongoing research in
this area holds promise for elucidating the cellular and synaptic pathophysiological
mechanisms underlying autoimmune cardiovascular autonomic disorders, which is an essential
step toward discovering more effective treatments and prevention strategies.
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© 2015 Published by Elsevier Inc.