[Remodeling of the aging heart : Sinus node dysfunction and atrial fibrillation]

Area of Science:

• Cardiology
• Electrophysiology
• Molecular Biology

Background:

• Sinus node dysfunction (SND) and atrial fibrillation (AF) are common arrhythmias that increase with age.
• Both SND and AF are frequently associated with cardiovascular diseases and share underlying pathomechanisms.
• These pathomechanisms include structural remodeling (e.g., fibrosis) and functional remodeling (e.g., altered calcium handling).

Purpose of the Study:

• To explore the shared pathophysiological mechanisms between SND and AF.
• To investigate the role of Ca2+/calmodulin-dependent protein kinase II (CamKII) in the remodeling processes associated with these arrhythmias.
• To discuss the controversial relationship between SND and AF, specifically whether one causes the other.

Main Methods:

• Review of existing literature on SND, AF, cardiac remodeling, and CamKII.
• Analysis of pathomechanisms including structural changes (fibrosis) and functional changes (calcium handling, delayed afterdepolarizations).
• Discussion of the potential role of CamKII in mediating these remodeling processes.

Main Results:

• SND and AF share common aging-related incidence and pathophysiological pathways.
• Both conditions involve structural and functional cardiac remodeling, with CamKII implicated in these processes.
• Remodeling in the sinus node can lead to bradycardia or tachycardia, while atrial remodeling contributes to AF triggers like delayed afterdepolarizations.

Conclusions:

• SND and AF may represent different clinical manifestations of related underlying pathophysiological mechanisms.
• CamKII plays a significant role in the structural and functional remodeling observed in both SND and AF.
• The precise causal relationship between SND and AF remains an open question requiring further investigation.