Genetics and Sinus Node Dysfunction

Abstract

Sinus node dysfunction (SND) is commonly encountered in the clinic. The clinical phenotype ranges from asymptomatic sinus bradycardia to complete atrail standstill. In some cases, sinus bradycardia is associated with other myocardial conditions such as congential abnormalities, myocarditis, dystrophies, cardiomyopathies as well as fibrosis or other structural remodeling of the SA Node. Although there are many etiologies for symptomatic slow heart rates, the only effective treatment available today is the implementation of a pacemaker. The predominant ion channel currents contributing to the pacemaker activity in the sinoatrail node (SAN) include currents flowing through hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels, L- type Ca, T- type Ca, delayed rectifier K, and acetylcholine (ACh)-activated channels