Open AccessBridging the Gap in a Rare Cause of Angina
Author(s) -
Sumanth Khadke,
Jovana Vidovic,
Vinod F. Patel
Publication year - 2021
Publication title -
european cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 12
eISSN - 1758-3764
pISSN - 1758-3756
DOI - 10.15420/ecr.2020.33
Subject(s) - cardiology , medicine , myocardial bridging , myocardial bridge , angina , stenosis , diastole , ischemia , coronary arteries , coronary atherosclerosis , artery , sudden cardiac death , cardiomyopathy , coronary artery disease , myocardial infarction , heart failure , blood pressure , coronary angiography
Myocardial bridging occurs when coronary arteries run intramurally. Episodes of tachycardia can cause a dynamic obstruction that extends into diastole, compromising coronary filling time, and subsequently leading to ischaemia. Myocardial ischaemia, acute coronary syndrome, coronary spasm, myocardial stunning, arrhythmia, takotsubo cardiomyopathy, and sudden cardiac death have all been reported with bridging. Atherosclerotic plaques develop proximally in the bridge due to low shear stress and high oscillatory wall-flow. Factors affecting atherosclerotic build-up include disrupted flow patterns (particularly flow recirculation, which exacerbates LDL internalisation), cell adhesion and monocyte adhesion to the endothelium. Endothelial health depends on arterial flow patterns, given that the vessel reacts differently to various flow types, as confirmed in 3D simulations. Medication is the first-line therapy, while surgical de-roofing and coronary bypass are reserved for severe stenosis. Distinguishing physiological arterial compression from pathological stenosis is essential. Deeper bridges correlating with recurrent angina with an instantaneous wave-free ratio ≤0.89 or fractional flow reserve ≤0.80 are treated.