the Role of Ivabradine in Causing AF in Patients With Chronic Coronary Syndrome

AF - Atrial Fibrillation

This study is aiming to detect the possibility of Ivabradine's role in the development of atrial fibrillation in chronic coronary syndrome patients with No structural heart disease.

Ivabradine is a heart rate-lowering agent best characterized by its negative chronotropic effect on the sinoatrial node. Its unique mechanism selectively blocks the pacemaker funny channels, which are responsible for spontaneous depolarization in the sinoatrial node that regulates heart rate during sinus rhythm. It has been well established that controlling the heart rate is the main target when treating coronary artery disease and heart failure and is associated with a beneficial effect on mortality and morbidity. According to the European Society of Cardiology guidelines for Chronic coronary syndrome, ivabradine should be considered as an anti-anginal agent in patients with sinus rhythm and heart rate of ≥70 BPM in combination with beta-blockers or when beta-blockers are not tolerated. The If current, which is affected by ivabradine, was found to be present in the pulmonary vein myocardial sleeves, the well-recognized triggers for AF. This may explain the risk of AF in patients receiving this drug. However, AF is commonly associated with HF and ischemic heart disease, the current two clinical indications for the use of ivabradine, hence AF in this patient population may be an association rather than a drug-induced effect. Previously, ivabradine's heart rate reduction was thought to be exclusively due to inhibition of If channels in the sinoatrial node. However, emerging data have shown channels that maintain the If current in the free wall of both atria. These findings support the idea that the If current plays a role in the pathophysiological procedure that initiates and maintains AF.

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