Key result
Electrical remodeling and genetic mutations are now recognized as important processes in the pathophysiology of sinoatrial node dysfunction, alongside traditional factors like age-related fibrosis.
This review highlights that sinoatrial node dysfunction is driven by electrical remodeling and genetic mutations, rather than solely by age-related fibrosis or ischemia.
Electrical remodeling and genetics warrant consideration in SND beyond fibrosis; leaves open targeted interventions pending prospective trials.
The sinoatrial node (SAN) is the normal pacemaker of the heart and SAN dysfunction (SND) is common, but until recently the pathophysiology was incompletely understood. It was usually attributed to idiopathic age-related fibrosis and cell atrophy or ischaemia. It is now evident that changes in the electrophysiology of the SAN, known as electrical remodelling, is an important process that has been demonstrated in SND associated with heart failure, ageing, diabetes, atrial fibrillation and endurance exercise. Furthermore, familial SND has been identified and mutations have been characterised in key pacemaker genes of the SAN. This review summarises the current evidence regarding SAN function and the pathophysiology of SND.
No takes yet. Share an insight, caveat, or question.
Choudhury et al. (2015) conducted a review in Sinoatrial node dysfunction (SND). Electrical remodeling and genetic mutations are now recognized as important processes in the pathophysiology of sinoatrial node dysfunction, alongside traditional factors like age-related fibrosis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: