• Lu Chen, Yan He, Ying Wang, Shijing Liu, Qing Li, Jiyu Chen, Zhiyun Peng, Qian Zhang, Chen Zeng, Na Li, Yan Zeng, Yun Xiong, Wei Li, and Haiyan Zhou.
• Department of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
• Brit J Hosp Med. 2024 Sep 30; 85 (9): 1131-13.

AbstractAims/Background Coronary heart disease (CHD) and atrial fibrillation (AF) exhibit a close relationship, yet the existing body of research predominantly relies on observational study methodologies, posing challenges in establishing causal relationships. The objective of our study is to investigate the causal linkages between coronary atherosclerosis (CAAs), angina pectoris, myocardial infarction (MI), and AF. Methods This study utilizes a two-sample Mendelian randomization (TSMR) methodology, leveraging genetic variation as a means of evaluating causality. Mendelian randomization is grounded in three primary assumptions: (1) the genetic variant is linked to the exposure, (2) the genetic variant is independent of confounding factors, and (3) the genetic variant influences the outcome solely through the exposure. Results The results of our study suggest a genetic predisposition in which CAAs, angina, and MI may enhance susceptibility to AF, while AF may reciprocally elevate the risk of CAAs. Conclusion In light of these findings, it is recommended that patients with CHD undergo regular cardiac rhythm monitoring, and that patients with AF receive anticoagulant and antiplatelet therapy whenever feasible. This study posits a practical implication for clinical practice.

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