Case Report

Coronary Artery Occlusion and Myocardial Infarction Caused by Vasospasm within a Myocardial Bridge

Lori Vales, MD, Yumiko Kanei, MD, John Fox, MD
Lori Vales, MD, Yumiko Kanei, MD, John Fox, MD
ABSTRACT: Myocardial bridging is a common congenital coronary anomaly that is clinically silent in the majority of cases. Case reports suggest myocardial ischemia and infarction can be caused by myocardial bridging. The proposed mechanisms by which myocardial bridging causes myocardial ischemia include compromised coronary blood flow, endothelial dysfunction, thrombus formation and a strong association with coronary vasospasm. We reported a case of myocardial infarction caused by both myocardial bridging and coronary vasospasm. We reviewed the literature and suggest that coronary stenting may have a role in treating myocardial ischemia due to myocardial bridging and coronary spasm that is refractory to medical management. J INVASIVE CARDIOL 2010;22:E67–E69
Myocardial bridging is a congenital coronary anomaly defined as the tunneling of a segment of a major epicardial artery that travels intramurally through the myocardium beneath a muscle bridge. Its prevalence has been reported to range between 5.4 and 85% in autopsy series and 0.5–29.4% on coronary angiography.1 Since 85% of coronary blood flow occurs during diastole, the systolic “milking” compression characteristically associated with myocardial bridging is often thought to have little clinical significance.2 Nevertheless, case reports have linked myocardial bridging to myocardial ischemia and infarction and even sudden cardiac death.2 The mechanism by which myocardial bridging can cause these adverse clinical events remains unclear, but coronary spasm at the bridging segment has been proposed as a possible contributory factor. Provocative testing using spasm-inducing agents supports a connection between myocardial bridging and coronary vasospasm. 3–5 Documentation of clinically important, but unprovoked spasm at the site of a myocardial bridge, however, remains limited. This case report demonstrates unprovoked spasm within a myocardial bridging segment associated with myocardial infarction. Case Report. A 53-year-old male with a history of hypertension and dyslipidemia was found to have an abnormal electrocardiogram (ECG) during a routine medical visit. The ECG showed sinus rhythm at 64 beats per minute, with prominent ST-elevations and T-wave inversions in all the precordial leads and Q-waves in leads V1–V3. The patient denied symptoms of acute chest pain or shortness of breath. Family and social history were non-contributory, and his physical examination was normal. Given the significantly abnormal ECG, the patient was referred for cardiac catheterization. Initial contrast dye injection to the left coronary arteries revealed subtotal occlusion of the mid-left anterior descending artery (LAD) with thrombolysis in myocardial infarction (TIMI) 1 flow (Figure 1A). Subsequent images showed spontaneous resolution of the total occlusion with TIMI 3 flow throughout the LAD. The occlusion site showed evidence of myocardial bridging with systolic compression of the artery (Figures 1B and 1C). There was an apical aneurysm on the left ventriculogram indicative of previous myocardial infarction. A positron emission tomography (PET) viability study was conducted subsequent to the angiogram showing a degree of viability in the infarcted segment. Repeat angiography was performed after 1 week of treatment with a calcium channel-blocker and a beta-blocker. Again, complete obstruction of flow was initially observed in the mid-LAD. Flow completely normalized with injection of intracoronary nitroglycerin. A segment of myocardial bridging was again evident at the previous site of occlusion. The segment was successfully stented, and the patient was discharged in stable condition. His ECG and cardiac function improved. After 1-year follow up, the patient continues to do well and denies chest pain or cardiac symptoms. Follow-up noninvasive nuclear stress testing revealed no residual reversible ischemia, a significantly smaller area of infarct and significantly improved left ventricular function. Discussion. Given the high frequency of the anomaly at autopsy, myocardial bridging is likely clinically silent in the vast majority of cases. Proposed mechanisms linking myocardial bridging to coronary ischemia in select cases include systolic compression of the bridging segment affecting coronary blood flow and extending into early diastole, induced endothelial dysfunction and thrombus formation at the site of the myocardial bridge and a strong association with coronary vasospasm. 1,2,6 Normally, only 15% of coronary blood flow occurs during systole and because myocardial bridging is a systolic event, its clinical significance is unclear. It has been proposed, however, that the presence of tachycardia could unmask the ischemic effect of myocardial bridging by shortening the diastolic period and increasing the reliance on systolic blood flow for coronary perfusion.2,7 Pichard et al showed that in a patient with angina pectoris, myocardial bridging and otherwise normal coronary arteries during tachycardia induced by rapid atrial pacing, there was decreased regional blood flow to the area perfused by the bridged area.8 This demonstrates that in the presence of myocardial bridging, overall coronary perfusion was compromised during tachycardia despite the relatively small proportion of coronary blood flow in systole normally. Even in the absence of tachycardia, intravascular ultrasonography has shown that the cross-sectional area in myocardial bridging segments is reduced during systole and that this reduction continues into early diastole.9,10 There are multiple proposed effects of myocardial bridging on endothelial function. It has been proposed that the milking of myocardial bridging segments causes increased shear stress.5 Furthermore, thrombus formation in myocardial bridging segments has been reported in patients with myocardial-bridging-related cardiac events. These reports suggest that turbulent shear stress and intimal trauma predispose the vessel toward thrombus formation.4 Increased shear stress associated with myocardial bridging also appears to reduce the production of vasoactive agents such as endothelial nitric oxide synthase, endothelin-1 and angiotensin-converting enzyme within the bridging segment.6 Consequently, the increased shear stress and high intravascular pressure in myocardial bridging appears to negatively affect endothelial function and significantly affects endothelium-dependent vasorelaxation.11,12 These effects could potentially predispose patients with myocardial bridging to coronary vasospasm. Increasing reports have suggested a significant association between myocardial bridging and coronary spasm in coronary ischemic events.3,13 In fact, Teragawa et al has shown myocardial bridging to be an independent predictor of spasm caused by spasm-inducing agents, acetylcholine and methylergotamine. 4 In 114 patients who underwent coronary angiography and spasm-provocation testing, coronary spasm was induced in 73% with myocardial bridging versus 40% without myocardial bridging (p = 0.0006), the majority of whom had no other risk factors.4 A similar study by Kim et al demonstrated that 77% of 81 patients with myocardial bridging compared to 16% of 195 matched controls, had induced coronary vasospasm by incremental acetylcholine spasm provocation testing.14 Furthermore, Herrmann et al found pharmacologically-induced spasm occurring at the site of myocardial bridging in 90% of patients with bridging exposed to acetylcholine.5 The fact that myocardial bridging may cause dynamic obstruction in the form of coronary vasospasm, in addition to mechanical obstruction, should be considered when choosing a treatment strategy for patients with symptomatic myocardial bridging. Therapies that have been attempted clinically for myocardial bridging include beta-blockers, calcium channel-blockers, stents and surgical myotomy. 1 Though it is generally thought that nitrates should be avoided because they angiographically exacerbate myocardial bridging, they often appear to alleviate coronary vasospasm. The negative chronotropic effect of beta-blockers increases diastolic coronary perfusion time and theoretically decreases compression of coronary arteries in myocardial bridging. Patients with myocardial bridging and coronary spasm are often treated with varying combinations of nitrates, calcium channel-blockers and beta-blockers with improvement of symptoms. 14 Successful treatment using angioplasty and stenting has been reported in patients who were refractory to medical management.v 3 In our case, treatment with stenting improved angiographic outcomes as well as electrocardiographic and functional evidence of ischemia and the patient has done well at 1-year follow-up. Stenting may therefore be considered in patients with myocardial bridging and vasospasm who are refractory to medical therapy. Conclusion. Myocardial bridging is a common congenital coronary anomaly. Cases reporting myocardial ischemia and infarction implicating myocardial bridging have been published. The multiple proposed mechanisms by which myocardial bridging causes myocardial ischemia include its strong association with coronary vasospasm. We reported a case of myocardial infarction caused by both myocardial bridging and coronary vasospasm and reviewed the literature. This case suggests coronary angioplasty and stenting may have a role in treating myocardial ischemia due to myocardial bridging and coronary spasm that is refractory to medical management.

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_________________________________________________ From the Beth Israel Medical Center, The Heart Institute, New York, New York. The authors report no conflicts of interest regarding the content herein. Manuscript submitted July 28, 2009, provisional acceptance given August 10, 2009, final version accepted October 14, 2009. Address for correspondence: Lori Vales, MD, Beth Israel Medical Center, The Heart Institute, 1st Avenue at 16th Street, Baird Hall — 5th Floor, New York, NY 10003. E-mail: lvalesmd@gmail.com