Resolution of Myocardial Bridge-Related Wall Motion Abnormality and Associated Myocardial Perfusion Defect with Beta-Blocker The

Case Report. A 67-year-old female was referred to our center due to chest pain. She had no prior history of ischemic heart disease; however, in the last 6 months, she began experiencing exertional chest discomfort. Cardiac risk factors included untreated dyslipidemia, a family history of premature coronary artery disease and a remote history of tobacco use. Cardiac gated single photon emission computed tomography (SPECT) imaging indicated a fixed perfusion defect involving 14% of the left ventricular myocardium in the anteroseptal region extending from mid-ventricle to apex, and evidence of significant ischemia in the right coronary artery distribution. Post-stress left ventricular ejection fraction (EF) was markedly reduced at 22%. Coronary angiography demonstrated a myocardial bridge in the mid-portion of the left anterior descending artery (LAD). The right coronary artery (RCA) had a 70% ostial stenosis. The left ventriculogram in the RAO projection demonstrated inferior wall hypokinesis from apex to base, and anterior wall akinesis from mid-ventricle to apex, with a calculated EF of 34%. The initial clinical decision was to evaluate the anterior wall for viability and to treat the cardiomyopathy with diuretics, ACE inhibitors and beta-blockers. A 6-hour thallium redistribution study did not demonstrate viability of the anterior wall distal to the site of the LAD myocardial bridge. After optimization of the patient’s antianginal and heart failure regimen, her symptoms markedly improved. Repeat coronary angiography was therefore performed with the intention of intervening on the RCA lesion. Coronary angiography demonstrated resolution of the LAD myocardial bridge, and the anterior wall motion abnormality was no longer present on the left ventriculogram. The ostial RCA stenosis was stented using a 3.0 x 13 mm Ultra stent (Guidant Corporation, Indianapolis, Indiana) after pretreatment of the lesion with rotational atherectomy. Three months following the percutaneous coronary intervention, a repeat cardiac gated SPECT study demonstrated no evidence of ischemia, infarction or wall motion abnormality, with a post-stress EF of 51–55%. The patient has remained asymptomatic with no adverse cardiac events. Discussion. Myocardial bridging is the tunneling of an epicardial coronary artery through the myocardium. It is characterized angiographically by systolic compression, also known as the “milking effect”. Most commonly, the mid-portion of the LAD is involved.¹ Although myocardial bridges are often seen as an incidental and benign angiographic finding, they have been associated with myocardial ischemia and infarction.^2,3 The mechanism for ischemia with systolic compression of the artery when the preponderance of myocardial perfusion occurs during diastole is unclear. A potential explanation is abnormal coronary flow physiology. Systolic compression of the artery leads to an alteration in the ratio of systolic and diastolic flow.There is reduced systolic antegrade flow, which leads to an increased diastolic/systolic velocity ratio (as high as 3.0, compared with values of 1.8 in normal controls).^4,5 Retrograde systolic flow has also been demonstrated and can be provoked with intracoronary nitroglycerin.⁴ These abnormalities in flow, along with a persistent decrease in diastolic lumen diameter, are associated with decreased coronary flow reserves (1.5–2.5 baseline flow with vasodilation).^4,6 Intracoronary Doppler flow wires may show the “finger-tip phenomenon”, which is a sharp acceleration of flow in early diastole followed by immediate deceleration and mid-diastolic plateau in flow. These alterations in flow make the determination of a hemodynamically significant myocardial bridge challenging. The measurement of diastolic fractional flow reserve (FFR), as compared to the more traditional mean FFR with inotropic challenge, has been advocated.⁷ The compressed segment of the artery rarely shows significant atherosclerosis.⁸ However, the segment of the coronary artery proximal to the bridge is typically affected by atherosclerosis (up to 90% of the time),⁴ possibly due to increased shear force.⁹ Usually, this is not flow-limiting. Coronary stenting has been shown to resolve clinical symptoms6 and flow abnormalities, but there is a high rate of restenosis.⁵ Beta-blockers have been advocated as treatment for symptomatic myocardial bridges and are generally thought to be the first-line therapy.⁵ The mechanism involves a decrease in external compression by decreasing intramural pressures through their negative inotropic effects, and an increase in the time of diastole by their negative chronotropic effects.¹⁰ Intravenous beta-blockers have been shown to decrease vascular compression and maximal flow velocities and to alleviate signs and symptoms of myocardial ischemia acutely.¹¹Conclusion. Myocardial bridging can result in substantial alterations in normal coronary flow hemodynamics, with the present case illustrating that significant wall motion abnormalities, as well as perfusion defects on noninvasive imaging studies, can occur as a result of these alterations. Treatment with beta-blockers resulted in resolution of the myocardial bridge and the associated cardiomyopathy. Whether the improvement in left ventricular systolic function and resolution of the abnormalities seen on left ventriculography were a direct result of eliminating the hemodynamic consequences of the bridge, or were a result of treating the underlying cardiomyopathy, is difficult to ascertain. The resolution of the anterior wall perfusion defect on gated cardiac SPECT imaging with treatment of the LAD myocardial bridge lends support to the hypothesis that the myocardial bridge played a substantial role in the alteration of coronary flow in the affected territory.

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