RESUMEN
BACKGROUND: Myocardial bridging (MB) is a congenital coronary artery anomaly that has limited molecular disease state characterization. Though a large portion of individuals may be asymptomatic, the myocardial ischemia caused by this anomaly can lead to angina, acute coronary syndrome, coronary artery disease, and sudden cardiac death in patients. OBJECTIVE: This study aims to summarize and consolidate the current literature regarding the genomic associations of myocardial bridge development and, in doing so, prompt further investigation into the molecular basis of myocardial bridge development. METHODS: We performed a systematic literature review of myocardial bridging using the key search terms "Myocardial Bridging" AND ("Gene" OR "Allelic Variants" OR "Genomic") in the databases of PubMed, CINAHL, EMBASE, and Cochran. We then performed a detailed review of the resulting abstracts and a full-text screening, summarizing these findings in this report. RESULTS: In total, we identified eight articles discussing the associated genomics behind MB development. Studies included review articles, case reports and genomic studies that led to the discussion of several genes: DES (E434K), FBN1 (I1175M), and COMMD10; MACROD2, SLMAP, MYH7 (A1157G), and DPP6 (A714T); MYH7 (A862V); SCN2B (E31D); and NOTCH1 (R2313Q), and to the discussion of miRNAs (miR-29b, miR-151-3p, miR-126, miR-503-3p, and miR-645). CONCLUSIONS: Our study is the first to summarize the genes and molecular regulators related to myocardial bridges as they exist in the current literature. This work concludes that definitive evidence is lacking, warranting much broader genetic and genomic studies.