Spontaneous coronary artery dissection and associated myocardial bridging: Current evidence from cohort study and case reports. (July 2019)

• Record Type: Journal Article
• Authors: Tajrishi, Farbod Zahedi; Ahmad, Asrar; Jamil, Adeel; Sharfaei, Sadaf; Goudarzi, Sogand; Homayounieh, Fatemeh; Pitliya, Anmol; Kahe, Farima; Chi, Gerald
• Is Part Of: Medical hypotheses. Volume 128(2019)
• Page Start: 50
• Page End: 53
• Publication Date: 2019-07
• Subjects: ACh acetylcholine -- LAD left anterior descending artery -- MB myocardial bridging -- SCAD spontaneous coronary artery dissection; Myocardial bridging -- Spontaneous coronary artery dissection -- Acute coronary syndrome -- Coronary vessel anomalies; Medicine -- Periodicals; Medicine -- Periodicals; Médecine -- Périodiques; Medicine; Periodicals; 610
• DOI: 10.1016/j.mehy.2019.05.012
• Languages: English
• ISSNs: 0306-9877

Abstract

Abstract: Spontaneous coronary artery dissection (SCAD) is a relatively uncommon and under-diagnosed disease characterized by the dissociation of intima and media of coronary artery wall due to an intimal tear or intramural hemorrhage. The exact pathophysiology of SCAD remains elusive and may involve multiple predisposing or precipitating factors including genetic abnormalities, inherited or acquired vasculopathies, hormonal influences, inflammation, intense exercise, emotional stress, and recreational drugs. Accruing reports, including five case reports and one cohort study, have recently addressed the concurrence of SCAD and myocardial bridging (MB), an anatomic variant in which a segment of the epicardial coronary descends and traverses in the myocardium. Among the patients with coexisting MB and SCAD, the left anterior descending artery was the only artery that harbors both pathologies, with SCAD locating either within the tunneled segment or distal to the MB. No other predisposing factors or precipitating stressors for SCAD were noted. It is hypothesized that the predilection for vasospasm, impaired endothelial function, and disturbed coronary flow dynamics associated with MB bridging could collectively contribute to the development of SCAD. Future studies are warranted to explore the mechanistic implications of MB in patients with SCAD.