Case Report

Acute Anterior Myocardial Infarction Secondary to a Myocardial Muscular Bridge

*Emre Gurel, MD, *Nihal Ozdemir, MD, §Cihan Cevik, MD, *Cihangir Kaymaz, MD
*Emre Gurel, MD, *Nihal Ozdemir, MD, §Cihan Cevik, MD, *Cihangir Kaymaz, MD
Author Affiliations: From *Kartal Kosuyolu Heart and Research Hospital, Department of Cardiology, Istanbul, Turkey, and §Texas Tech University Health Sciences, Lubbock, Texas . The authors report no conflicts of interest regarding the content herein. Manuscript submitted July 15, 2008, provisional acceptance given September 8, 2008 and final version accepted September 16, 2008. Address for correspondence: Emre Gurel MD, Tervuursestraat 117/12, B-3000, Leuven, Belgium. E-mail:


J INVASIVE CARDIOL 2009;21:E12-E15 Myocardial bridge (MB) is an anatomical anomaly characterized by segmental narrowing of an epicardial coronary artery within the myocardium during systole. It is encountered in 0.5–2.5% of routine coronary angiograms,1 and may alter the hemodynamics of the coronary circulation in susceptible individuals. Although it is considered a benign anomaly, it may lead to serious complications such as acute myocardial infarction (AMI), ventricular tachycardia, syncope, atrioventricular block and sudden cardiac death.2–4 Here we present a case of AMI secondary to a MB and its evaluation with eligible diagnostic methods. Case Report. A 46 year-old-male presented to our emergency unit complaining of typical severe chest pain that had started 5 hours previously. He had no history of coronary artery disease or other cardiovascular risk factors except for smoking. The electrocardiogram (ECG) revealed 3 mm ST-segment elevation in the precordial leads. His vital signs were within normal limits (blood pressure 130/80 mmHg, and pulse rate 92). He had no signs or symptoms of pulmonary congestion. The patient was admitted to the intensive care unit with a diagnosis of acute anterior MI. After admission, 5000 IU intravenous heparin, 300 mg oral acetyl salisylic acid (ASA) and 600 mg oral clopidogrel were given. Subsequently, he was taken to the catheterization laboratory for emergent coronary intervention. Coronary angiography revealed that the mid segment of the left anterior descending (LAD) artery was obstructed, demonstrating pulsatile contrast hanging, a “milking effect” in the septal arteries and thrombolysis in myocardial infarction (TIMI) grade 0 flow (Figure 1). Metoprolol 5 mg was administered intravenously because of ongoing tachycardia. After metoprolol administration, there was TIMI grade 2–3 flow in the LAD, with narrowing in every systole secondary to MB. There was no sign of thrombus formation (Figure 2). Because of the presence of TIMI 3 flow and relieved chest pain, no further intervention was considered. The patient was transferred back to the intensive care unit and the ECG revealed complete resolution of the ST-segment elevation. Oral metoprolol 100 mg was added to his medications. The patient did not report any chest pain in the following days and the echocardiogram showed hypokinesia at the anterior and apical segments. The patient’s global ejection fraction was 45%. In order to evaluate the MB in detail, we performed an intravascular ultrasound (IVUS) study. IVUS demonstrated the characteristic “half-moon phenomenon” within the bridge segment (Figure 3), small eccentric plaques at the segment proximal to the MB (Figure 4) and a delay in relaxation after systolic compression. The cross-sectional area of the MB was measured as 3.19 mm² and the percent of angiographic luminal stenosis was measured as 65% (Figure 5). Additionally, we performed fractional flow reserve (FFR) measurement to investigate the presence of ischemia after beta-blocker therapy. We detected abnormal intracoronary pressure distal to the MB. Therefore, surgical therapy (myotomy) was considered and suggested to the patient. The patient was discharged after the surgery with medications including ASA 300 mg, clopidogrel 75 mg, metoprolol 100 mg, atorvastatin 40 mg and ramipril 2.5 mg daily. Discussion. Coronary arteries and their major branches are usually located subepicardially. MB occurs when a band of cardiac muscle overlies an intramural segment of a coronary artery, the intramural segment being referred to as a “tunneled” artery. The incidence of MB has been reported to be between 15% and 85%.5 However, the incidence ranges from 0.5–2.5% in angiographic series.6,7 MB is most commonly located in the middle segment of the LAD artery and a high prevalence has also been reported in patients with hypertrophic obstructive cardiomyopathy and in heart transplant recipients.8,9 Several studies have shown that phasic systolic vessel compression of the coronary artery persists as a vessel diameter reduction into diastole.10 This incomplete relaxation of the bridge during diastole results in increased intracoronary flow velocities, reduced diastolic coronary flow, retrograde coronary flow and a reduction in coronary flow reserve.10,11 Coronary atherosclerosis in association with MB has primarily been studied in the LAD. The segment proximal to the bridge frequently shows atherosclerotic plaque formation, although the tunneled segment is typically spared, similar to our case.11 Studies on cellular and ultrastructural levels showed that in contrast to proximal and distal segments, foam cells and modified smooth muscle cells were missing in patients’ tunneled segments.12 Hemodynamic forces may also explain atherosclerotic plaque formation in the origin of the tunneled segment. Although most patients are asymptomatic, common symptoms associated with MB can range from angina pectoris to MI, ventricular tachycardia and sudden death.2,3 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.13 Induction of ischemia by a MB has been demonstrated with different underlying mechanisms such as thrombus formation, vasospasm, endothelial dysfunction or impaired coronary flow reserve.14 The current gold standard for diagnosing MB 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.15 With the use of IVUS, intracoronary Doppler ultrasound and intracoronary pressure devices, morphological and functional features of MB can be identified.16,17 The “half-moon” phenomenon16 is the characteristic IVUS finding, but its physiology and anatomy are not fully understood. IVUS-based frame-by-frame analysis of lumen area during the entire cardiac cycle can also be used to quantify the delay after systolic compression.17 However, some IVUS studies supported the absence of atherosclerosis within tunneled segments, although approximately 90% of patients showed plaque formation proximal to the bridge.16 We can also use FFR for the hemodynamic assessment of MB. Symptomatic patients with MB should be treated. Medical therapy is considered as the first-line therapy and should include beta-blocker, calcium channel-blocker and antiplatelet agents, with the objective of relieving myocardial ischemia and protecting against future coronary adverse events.18 Nitrates increase the milking effect on angiography mainly secondary to coronary and systemic vasodilation, increased heart rate and reduced coronary pressure distal to the bridged segment.19 The management of symptomatic patients despite medical therapy is controversial. Stables et al20 reported coronary stenting as an interventional treatment for severe MB that is refractory to medical therapy. Nevertheless, in one study, at 7 weeks after stent implantation, 46% of patients required revascularization as a result of in-stent restenosis.21 Similarly, another observational study of 25 patients who received coronary stents for MB reported a 50% restenosis or major periprocedural complication rate.22,23 As another therapeutic option, surgical myotomy improves clinical symptoms and is associated with the reversal of local myocardial ischemia and an increase in coronary flow.24 However, an unpredictable intramural course of the coronary artery may require deep incision of the ventricular wall, which may lead to subsequent ventricular wall aneurysm. Alternatively, internal mammary artery anastomosis to the LAD may be another surgical therapeutical option in symptomatic patients who have accompanying diffuse coronary artery disease.21 In our case, acute anterior MI probably resulted from a tachycardia-induced delay in myocardial relaxation after systolic compression by the MB and/or marked vasospasm in both the tunneled segment and proximal to the bridging segment. We diagnosed this anomaly with coronary angiography, analyzed the plaque formation and the bridging segment in detail with IVUS, used FFR for hemodynamic assessment of the MB and defined the abnormal intracoronary pressure distal to the bridge. Intracoronary stenting was not considered because of the long bridging segment (> 25 mm) and the relatively high risk of in-stent restenosis. Surgical therapy was considered and recommended to the patient.


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