In 5-12% of patients coronary artery Courses intramyocardial instead of coursing epicardially , this congenital coronary anomaly called Myocardial Bridging..Muscle overlying the intramyocardial segment of an epicardial coronary artery, first mentioned by Reyman in 1737, is termed a myocardial bridge, and the artery coursing within the myocardium is called a tunneled artery.
It is characterized by systolic compression of the tunneled segment, which remains clinically silent in the vast majority of cases.Coronary atherosclerosis in association with myocardial bridging has primarily been studied in the LAD. The segment proximal to the bridge frequently shows atherosclerotic plaque formation, although the tunneled segment is typically spare.
Hemodynamic forces may explain atherosclerotic plaque formation at the entrance to the tunneled segment. There, the endothelium is flat, polygonal, and polymorph, indicating low shear, whereas in the tunneled segment, the endothelium has a helical, spindle-shaped orientation along the course of the segment as a sign of laminar flow and high shear. Low shear stress may induce the release of endothelial vasoactive agents such as endothelial nitric oxide synthase (eNOS), endothelin-1 (ET-1), and angiotensin-converting enzyme (ACE). Their levels were significantly higher in proximal and distal segments compared with the tunneled segment. Thus, low shear stress may contribute to atherosclerotic plaque formation proximal to the bridge, whereas high shear stress may have a protective role within the tunneled segment. In addition, an increase in local wall tension and stretch may induce endothelial injury and plaque fissuring with subsequent thrombus formation in the proximal segment,which is supported by autopsy and clinical observations.
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Neither nonsignificant stenosis proximal to the bridge nor systolic compression of the tunneled segment alone can sufficiently explain severe ischemia and associated symptoms. Experimental LCX occlusion, initially during systole only and then during continuing occlusion extending increasingly into diastole, resulted in distinct shortening of inflow time with significant reduction of epicardial flow, subendocardial flow, and distal coronary pressure. After releasing the occlusion, diastolic flow increased in correspondence with an increasing duration of vessel occlusion, despite a decrease in mean flow. This increased diastolic/systolic flow ratio was later verified in patients. Consistent with clinical findings, the increase in diastolic flow could not fully compensate for the decrease in mean flow resulting in reduced coronary flow reserve, which could not be explained by impaired vasodilatory capacity of resistance vessel.
When arterial occlusion was limited to systole, phasic coronary blood flow and distal coronary pressure was observed to resume with considerable delay contributing to reduced myocardial oxygen consumption and increased coronary sinus lactate concentration. This delayed diastolic relaxation was later identified in humans as an important mechanism contributing to ischemia with frame-by-frame analysis of IVUS images.
Angina, myocardial ischemia, myocardial infarction, left ventricular dysfunction, myocardial stunning, paroxysmal AV blockade, as well as exercise-induced ventricular tachycardia and sudden cardiac death are accused sequelae of myocardial bridging.However, considering the prevalence of myocardial bridging, these complications are rare. Patients may present with atypical or angina-like chest pain with no consistent association between symptom severity and the length or depth of the tunneled segment or the degree of systolic compression.Resting ECGs are frequently normal; stress testing may induce nonspecific signs of ischemia, conduction disturbances, or arrhythmias.
The current gold standard for diagnosing myocardial bridges is coronary angiography with the typical “milking effect” and a “step down–step up” phenomenon induced by systolic compression of the tunneled segment . However, these signs provide little information on the functional impact at the myocardial level. In the presence of a proximal stenosis, myocardial bridging may only be identifiable after PTCA when higher intravascular pressures and reversed hypokinesis unmask myocardial bridging. In patients with thin bridges, the milking effect may be missed and new imaging techniques and provocation tests may be required to detect a bridge.
On the basis of the above mechanisms for ischemia, 3 treatment strategies have been explored: (1) negative inotropic and/or negative chronotropic agents, ie, β-blockers, and calcium antagonists; (2) surgical myotomy and/or CABG; and (3) stenting of the tunneled segment.
3- European Society of Cardiology4- Self- experienced data and notes
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