A New Marker of Myocardial Bridge?

Myocardial Bridging-Induced Acute Coronary Syndrome: A Bridge Too Far

“…Additionally, there is an intricate milieu of vasoactive compounds such as endothelial nitric oxide synthase (eNOS), endothelin-1, and angiotensin-converting enzyme (ACE) in the proximal segment, which impact smooth muscle cell proliferation and atheroma formation. The presence of cardiovascular risk factors such as hypertension (HTN), diabetes mellitus (DM), and dyslipidemia (HLD) has been shown to amplify CAD proximal to the MB [15]. The MB segment is usually spared from atherosclerotic disease due to a thinner intima absence of smooth muscle cells and foam cells, which are integral in atherogenesis [7,10].…”

“…In contrast, within the MB, they exhibit a helical orientation, typically associated with laminar flow and high shear stress. The alteration in shear stress, the frictional force to flow, is proatherogenic and pro-inflammatory, leading to endothelial dysfunction and atherosclerosis development [ 15 ]. Additionally, there is an intricate milieu of vasoactive compounds such as endothelial nitric oxide synthase (eNOS), endothelin-1, and angiotensin-converting enzyme (ACE) in the proximal segment, which impact smooth muscle cell proliferation and atheroma formation.…”