Case Report and Brief Review

Myocardial Infarction Induced by Myocardial Bridging: Report
of Successful Percutaneous Therapy and Review of the Literature

Branislav Schifferdecker, MD and *Joseph Benotti, MD
Branislav Schifferdecker, MD and *Joseph Benotti, MD
Case Report. A 56-year-old male patient presented one hour after the onset of severe, substernal chest pain at rest. Physical examination revealed moderate distress secondary to chest pain. His blood pressure was 135/80 mmHg, his heart rate was 76 beats per minute and he had a respiratory rate of 22 per minute. The patient’s lungs were clear bilaterally, and there was no murmur, rub or gallop. The initial electrocardiogram showed ST-segment elevations in leads V1 to V3 that resolved with nitrate, aspirin and beta-blocker therapy. Eight hours after the onset of pain, his creatine kinase was 832 mg/dL and troponin I was 7.6 ng/mL. The patient developed another episode of angina with ST-segment elevations on electrocardiogram despite therapy with aspirin, clopidogrel, low-molecular weight heparin, beta-blocker and nitroglycerin. Emergent catheterization revealed no fixed obstructive coronary artery disease (CAD). Myocardial bridging (MB) caused a 71% systolic compression in the 24 mm long middle segment of the left anterior descending artery (Figure 1). A ventriculogram showed anteroapical hypokinesis, with an overall left ventricular ejection fraction of 45%. Drug-eluting stents were not yet available at the time of this procedure. A 3.0 x 18 mm NIR Elite® bare metal stent (Boston Scientific Corp., Natick, Massachusetts) was deployed in the tunneled artery at 14 atm. This closed-cell, slotted tube, stainless steel stent with uniform strut cell design was selected due to its strong radial stiffness and equal distribution of wall stress induced by MB and stent deployment forces. Residual mild milking effect at the proximal edge of the first stent persisted and worsened after intracoronary therapy with 100 mg of nitroglycerin. A second 3.5 x 8 mm bare metal Multi-LinkPenta® coronary stent (Guidant Corp., Indianapolis, Indiana) was therefore deployed at 14 atm proximal to the first stent, with approximately 3 mm of overlap (Figure 2). The final angiogram showed complete disappearance of the milking effect. The patient presented 9 weeks later with crescendo angina. A repeat catheterization showed Mehran type 2 in-stent restenosis (Figure 3) which was treated with a 3 x 10 mm Cutting Balloon® (Boston Scientific) at a maximal inflation pressure of 10 atm. Brachytherapy was performed using a 60 mm BetaCath® device (Novoste Corp., Norcross, Georgia) to deliver 23 Gy over 4 minutes. The patient remains asymptomatic at 3-year follow-up on beta-blocker and aspirin therapy, having fully returned to his previous activities. Discussion A myocardial bridge is a band of myocardial tissue overlying a segment of epicardial coronary artery — tunneled artery. MB is a congenital abnormality that is almost exclusively localized in the mid-segment of the left coronary artery. The incidence of MB ranges between 15–85% in autopsy studies,1,2 and 0.5–16% in angiographic series.3 This usually benign condition4 has been associated with stable and unstable angina,5 myocardial infarction,6 myocardial stunning,7 atrioventricular nodal block,8 ventricular tachycardia9 and sudden death.10 Factors associated with increased risk of symptomatic MB include its length, thickness and location, severity of systolic arterial compression, presence of left ventricular hypertrophy, increased heart rate, low systolic blood pressure and concomitant coronary vasospasm.11 By an unclear mechanism, MB seems to protect the tunneled artery against atherosclerosis. Ge et al. found no atherosclerotic lesions in tunneled or distal coronary arteries in 8 patients, while 12 of 14 patients had atherosclerotic plaques proximal to a MB.12 Diagnosis. Atypical chest pain may be a presenting symptom in up to 45% of patients with MB.5 Sensitivity of exercise stress testing and perfusion imaging studies in patients with MB is comparable with that seen in patients with single-vessel coronary disease.11 MB with a minimal lumen diameter reduction of 70% during systole and 35% during diastole is considered to be hemodynamically significant.13 The intracoronary Doppler flow velocity profile within MB shows early diastolic flow acceleration — the “finger-tip” phenomenon, followed by a plateau phase and early systolic flow reversal in the proximal tunneled artery.11 Coronary flow reserve is reduced in patients with MB to less than 3.14 However, coronary flow reserve is not site-specific and both concomitant atherosclerotic lesions, and microvascular disease can overestimate the severity of a MB. Intravascular ultrasound helps to delineate the extent of MB. Provocation tests with intracoronary nitroglycerin or intravenous dobutamine uncover angiographically silent MB if the characteristic intravascular ultrasound (IVUS) “half-moon” phenomenon is present.14 IVUS also identifies significant atherosclerotic stenoses at the edges of the tunneled artery and may be particularly useful in MB stenting. Therapy. Therapeutic options in symptomatic patients with MB are similar to therapy for atherosclerotic coronary artery disease. Medical Treatment. Beta-blockers and calcium channel blockers improve myocardial perfusion by prolonging diastole. Rate-independent anti-ischemic properties of beta-blockers seem to be mediated by reduced systolic and diastolic vascular compression.13 Calcium channel blockers may be particularly useful in patients with MB-associated vasospasm. Nitrates may worsen symptoms of MB due to increased vessel compression and should be used with caution.15 Antiplatelet agents counteract possible enhanced platelet aggregation in patients with MB. Surgical Treatment. Coronary artery bypass grafting in symptomatic MB is currently used if: 1. There are other indications for cardiac surgery. 2. Patient failed medical therapy and prefers surgical treatment. 3. Patient failed medical and percutaneous therapy (unsuccessful stenting, recurrent in-stent restenosis). Minimally invasive, supra-arterial myotomy may become the preferred surgical therapy if its safety can be documented.16,17 Magnetic resonance imaging or intraoperative epicardial echocardiography18 may then provide necessary information regarding the MB thickness and intramyocardial vessel course. Percutaneous Intervention. Treatment of a tunneled artery with balloon angioplasty is not effective. MB leads to almost complete early arterial recoil. Stent placement is currently the only effective percutaneous therapy. IVUS helps in stent size selection and guides stent deployment to achieve maximal luminal area to prevent clinical in-stent restenosis. The radial strength of balloon-expandable stents seems to be sufficient to overcome compressive forces of the MB. Self-expanding stents have not been used in percutaneous therapy of symptomatic MB, and are unlikely to be useful due to their relatively low radial strength and potential recoil during periods of increased MB contractions. Stents with thin struts seem to induce less vessel wall injury and lead to lower rates of restenosis. However, they also seem to have lower radial strength. New metal alloys such as cobalt chromium overcome this limitation. Closed-cell design stents provide better radial strength than those with open-cell design and are therefore likely better suited for stenting in symptomatic myocardial bridging.19,20 Recurrent symptoms after percutaneous intervention were usually related to in-stent restenosis due to neointimal proliferation rather then stent strut compression.21 Percutaneous therapy appears to be safe. Reported complications include tamponade requiring emergent thoracotomy with venous patching of the coronary perforation and coronary dissection leading to a coronary fistula into the right ventricular outflow tract that resolved spontaneously within 3 months.6 Recurrent symptoms due to in-stent restenosis after percutaneous therapy on a symptomatic MB have been reported, but its frequency remains unknown.22 Conclusion Myocardial bridging is a common, usually benign coronary artery anomaly that can (rarely) cause angina, myocardial infarction, malignant arrhythmia and sudden death. Noninvasive stress testing, quantitative coronary angiography, intracoronary ultrasound and intracoronary Doppler can identify patients at risk. Both percutaneous stent therapy and bypass surgery appear to be safe and effective therapies for MB and should be considered in patients who fail medical therapy with aspirin, beta-blockers and/or calcium channel blockers. Both percutaneous stent therapy and bypass surgery have been utilized in the treatment of symptomatic MB and may be considered in patients who fail medical therapy with aspirin, beta-blocker and/or calcium channel blocker.
References
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