Genetic associations between Rapid Eye Movement (REM) sleep behavior disorder and cardiovascular diseases

• Published in: PloS one 2024-05, Vol.19 (5), p.e0301112-e0301112
• Main Authors: Xu, Pengfei, Wei, Yitong, Wu, Haibo, Zhang, Li
• Format: Article
• Language: English
• Subjects: Apnea; Atherosclerosis; Behavior disorders; Biology and Life Sciences; Cardiovascular disease; Cardiovascular diseases; Cardiovascular Diseases - genetics; Cerebral infarction; Confounding (Statistics); Congestive heart failure; Consortia; Coronary artery disease; Coronary vessels; Datasets; Diagnosis; Eye; Eye movements; Genetic aspects; Genetic diversity; Genetic Predisposition to Disease; Genetic variance; Genome-wide association studies; Genome-Wide Association Study; Heart attacks; Heart diseases; Heart failure; Heart Failure - genetics; Humans; Ischemia; Medicine and Health Sciences; Mendelian Randomization Analysis; Movements; Myocardial infarction; Myocardial Infarction - genetics; Polymorphism, Single Nucleotide; REM sleep; REM Sleep Behavior Disorder - genetics; Risk Factors; Sleep; Sleep disorders; Stroke; Stroke - genetics; Vein & artery diseases
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0301112

Previous studies revealed that sleep disorders are potential risk factors for cardiovascular diseases, such as obstructive sleep apnea and rapid eye movement (REM) sleep behavior disorder (RBD). However, the causal associations between RBD and cardiovascular diseases remained unknown. We used the latest and largest summary-level genome-wide association studies of RBD, stroke and its subtypes, coronary artery disease (CAD), myocardial infarction (MI), and heart failure (HF) to select genetic variants as the instrumental variables. Mendelian randomization (MR) analysis was performed to test the causal associations between RBD and the cardiovascular diseases above. Inverse variance weighted method was used as the main analysis. After multiple comparisons, genetically predicted RBD was significantly associated with the risk of HF [odds ratio (OR) = 1.033, 95% CI 1.013-1.052, p = 0.001]. Leave-one-out analysis further supported the robustness of the causal association. Furthermore, we identified a suggestive association between genetically predicted MI and RBD (OR = 0.716, 95% CI 0.546-0.940, p = 0.016). However, in our study no associations were identified of RBD with CAD or stroke and its subtypes. Our study highlighted the potential associations between RBD and cardiovascular diseases at genetic level, including HF and MI. More studies were required to clarify the biological mechanisms involved the associations.