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. Author manuscript; available in PMC: 2013 Dec 7.
Published in final edited form as: Heart Rhythm. 2011 Jul 6;8(11):10.1016/j.hrthm.2011.06.032. doi: 10.1016/j.hrthm.2011.06.032

TABLE 1.

AUTOANTIBODIES AND BRADYARRHYTHMIAS

Arrhythmias Autoantibodies Associated Diseases Mechanisms
Sinus Bradycardia Anti-sinus node Sick sinus syndrome
Anti-Ro/SSA, Anti-La/SSB Neonatal lupus syndrome Cross-reaction with α1D and α1C subunits of T- and L-type Ca2+ channels
↓ ICa,L, ↓ICa,T
Anti-M2 receptor Dilated cardiomyopathy and Chagas” disease Agonist-liked activity on M2 receptor
↓cAMP, ↑ IKACh, ↓ ICa,L
Conduction Abnormalities Anti-β1 and anti-β2- adrenergic receptor Idiopathic conduction disturbances (AV block and intraventricular conduction block) Dilated cardiomyopathy Agonist-liked activity on β2-adrenergic receptor in conduction tissue
↑ Gi, ↑ GIRK, ↓ ICa,L
Anti-M2 receptor Chagas’ disease Agonist-liked activity on M2 receptor
↓cAMP, ↑ IKACh, ↓ ICa,L
Anti-Ro/SSA Systemic lupus erythematosus ↓ICa,L, ↓ICa,T
Congenital Complete Heart Block Anti-Ro/SSA Neonatal lupus syndrome Cross-reaction with α1C subunit of L-type Ca2+ channels → L-type Ca2+ channel internalization → [Ca2+]i dysregulation → cell death → inflammation → fibrosis
↓ ICa,L

ICa,L, L-type calcium currents; ICa,T, T-type calcium currents; IKACh, acetylcholine-activated potassium currents; M2 receptor, muscarinic cholinergic type 2 receptor; Gi, inhibitory G protein; GIRK, G-protein activated inward rectifier K+ channel