Do age-associated changes of voltage-gated sodium channel isoforms expressed in the mammalian heart predispose the elderly to atrial fibrillation?

Core Tip

Core tip: Na_v1.8 has been implicated by multiple studies in producing the late sodium current, predisposing the cardiomyocyte to arrhythmogenic activity. Animal models have demonstrated an enhancement of this aberrant current in aged hearts. Human studies have identified a reduction of Na_v1.5 and an increase in Na_v1.8 in both heart failure and left ventricular hypertrophy, strongly suggesting that voltage-gated sodium channel expression plays a central role in the development of arrhythmia. Clinically, sodium channel blockade through Ranolazine has proved promising in terminating the arrhythmia. Prevention of atrial fibrillation should focus on lifestyle management, as well as targeting cardiac risk factors. Irbesartan has been demonstrated to slow atrial remodelling, prevent atrial fibrillation in animal models, as well as avert the arrhythmia in human subjects.