Electrophysiological consideration on sick sinus syndrome

Area of Science:

• Cardiology
• Electrophysiology
• Cellular Biology

Background:

• Sick Sinus Syndrome (SSS) is characterized by abnormally prolonged Sinus Recovery Time (SRT).
• Understanding the underlying factors of prolonged SRT is crucial for managing SSS.
• Previous research has implicated autonomic nervous system influences on SRT.

Purpose of the Study:

• To investigate the factors contributing to abnormally prolonged SRT in SSS.
• To differentiate between neurogenic and intrinsic cellular factors affecting SRT.
• To explore the impact of pharmacological agents and aging on SRT.

Main Methods:

• Microelectrode technique was employed to study SRT in cardiac preparations.
• Vagal stimulation was used to assess the role of acetylcholine.
• Pharmacological agents like atropine, neostigmine, and verapamil were administered.
• Analysis of aged rabbit heart preparations with fibrosis and reduced SA nodal cells.

Main Results:

• Acetylcholine's effect on SRT was confirmed, but vagal stimulation alone did not replicate SSS-like prolonged SRT.
• SA entrance block at higher drive rates influenced overdrive suppression, highlighting the importance of SA junction properties.
• Verapamil (10(-7) g/ml) induced abnormal SRT, suggesting ionic derangements as a contributing factor.
• Aged rabbit preparations showed fibrosis and reduced SA nodal cells, correlating with abnormal SRT.

Conclusions:

• Prolonged SRT in SSS is multifactorial, involving autonomic influences, SA junction characteristics, ionic balance, and age-related cellular changes.
• Intrinsic factors, such as SA nodal cell reduction and fibrosis, appear to be significant contributors to pacemaker dysfunction and prolonged SRT in SSS.
• Further research is needed to fully elucidate the complex mechanisms underlying SRT abnormalities in SSS.