Myocardial bridging of coronary arteries

Myocardial bridging is a common congenital anomaly of the coronary arteries where a coronary artery courses through the myocardium.

Epidemiology

It is found approximately in 20-30% of the adult population in autopsy studies. The incidence in coronary angiograms is between 2-15% and can be easily seen at coronary CT angiography. It occurs more frequently in patients with hypertrophic cardiomyopathy (HCM), and is associated with :

Pathology

Normally major coronary arteries follow an epicardial course throughout their length, but in some cases, segments of the coronary arteries may course intramurally into the myocardium (tunnelled artery).

Myocardial bridging may be described as:

  • superficial (incomplete)
  • deep (complete)
Location

Bridging is typically described for left anterior descending artery (LAD), with the mid segment of the LAD considered the most common location ; however, other major coronary arteries can also be involved .

Clinical presentation

Myocardial bridging does not produce any symptoms in the majority of patients. However, conditions which increase the amount of systolic compression (e.g. hypertrophic cardiomyopathy) and/or decrease diastolic filling disproportionately (e.g. rapid heart rates) may exacerbate the myocardial oxygen supply/demand mismatch, resulting in troponin positive ischemic chest pain with complications such as :

Radiographic features

CT and angiography
  • both angiography and coronary artery MDCT can detect LAD myocardial bridging
    • angiographic diagnosis is by demonstrating an indirect sign called milking effect
    • coronary artery MDCT directly shows a portion or all of the artery in a intramyocardial location
    • coronary artery MDCT is often better at detecting RCA myocardial bridging
  • the bridged segment often appears to be free of atherosclerosis
Cardiac MRI including perfusion and MDE sequences
  • Regional wall motion abnormality
  • Perfusion defect pertaining to the affected vascular territory (correlates with MPS perfusion abnormality)
  • T2 hyperintensity and mild T1 delayed myocardial enhancement within affected vascular territory.

Treatment and prognosis

Some reports are suggesting the efficacy of calcium channel blockers in symptomatic patients .

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