A Case of Acute Myocardial Infarction due to Coronary Spasm in the Myocardial Bridge

Daisuke Fujibayashi, MD, Yoshihiro Morino, MD, Yuji Ikari, MD, PhD
Daisuke Fujibayashi, MD, Yoshihiro Morino, MD, Yuji Ikari, MD, PhD
Coronary arteries are usually located on the surface of the cardiac muscle. Myocardial bridges have been described in a variable number of autopsy cases ranging from 5.4% to 85.7% of cases examined, depending on the population sampled.1,2 In contrast, identification of myocardial bridging during diagnostic angiography was reported to be between 0.5% and 16% of sampled populations.3,4 The majority of such abnormalities were found in the left anterior descending coronary artery, whereas those in the circumflex or the right coronary artery (RCA) were relatively rare.2 Briefly, a myocardial bridge has been considered a “benign” structural variation since it predominantly compresses a coronary artery in the systolic phase. Because coronary circulation is physiologically dominant in the diastolic phase, segmental compression of coronary arteries by bridging the myocardium is rarely associated with significant myocardial ischemia. However, several clinical studies have shown that myocardial bridging occasionally causes acute myocardial infarction (AMI).5–12 A coronary artery wall surrounded by myocardial bridges is unlikely to be a cause of progressive atherosclerotic plaques; thus, other mechanisms may be at play in the development of acute coronary syndrome besides the common causes like plaque rupture and/or erosion. In this report, we describe a case of AMI in which the culprit lesions were located at sites distal to the RCA within the myocardial bridge, and present the assessments and the relevant angiographic tests to investigate its potential causes.

Case Report. A 68-year-old Japanese man with essential hypertension that had been treated with nifedipine, 10 mg every 12 hours for over 10 years, visited our hospital due to a slight precordialgia that lasted for 8 hours. During the 3 months prior to his admission, precordialgia had occurred once a month for 30–60 seconds in the early morning. There was no episode of exertional chest symptoms. His coronary risk factors included hypertension and smoking (20 cigarettes per day for 40 years). On admission, the electrocardiogram (ECG) showed abnormal Q-wave and ST-segment elevation in inferior wall leads II, III and aVF (Figure 1). A blood test showed a WBC of 13,100/mm3, a GOT of 31 U/l, a GPT of 21 U/l, an LDH of 223 U/l, and myocardial troponin I of 2.18 ng/ml. Creatine kinase (CK) was high, at 216 U/l, and the maximum value was observed at 20 hours after the onset (maximum CK:386 U/l; CK-MB:10.2%). An echocardiogram showed nonobstructive hypertrophy of the interventricular septum at the outflow, with normal chamber size and inferior wall hypokinesis. ST-elevation AMI was diagnosed, and the patient underwent emergency catheterization. However, his chest pain was relieved with nitroglycerin in the catheterization laboratory. Amazingly, there were no stenoses of the coronary arteries, but coronary compression due to the myocardial bridge was observed in the middle of the posterior descending branch. The compression caused 75% stenosis in the systolic phase (Figure 2). A left ventriculogram showed contraction abnormality of the left ventricular inferior wall, where it was identified with the perfused segments downstream of the compression site of the posterior descending branch.
Enhanced heart magnetic resonance imaging showed subendocardial enhancement in the inferior wall, and the T2 weighted image showed a high signal at the same site, which was considered to be myocardial edema caused by infarction (Figure 3).
One week after the first emergency catheterization, we performed a spasm provocation test using intracoronary acetylcholine. Infusion of 20 µg of acetylcholine into the RCA provoked total occlusion in the middle of the posterior descending branch that was identical to the position of the muscle compression. ST-segment elevation was observed in leads II, III and aVF. We confirmed the reproducibility of the phenomenon by a second provocation test using 50 µg of acetylcholine. After infusion of 5 mg of isosorbide dinitrate, coronary spasm disappeared, but the muscle compression was evident (Figure 4). His symptoms did not recur with administration of oral nifedipine (10 mg every 12 hours) and isosorbide mononitrate (20 mg every 12 hours).

Discussion. Here we report a case of AMI at the myocardial bridge that was caused by coronary spasm. The mechanism of ischemia at the myocardial bridge has not been clarified. Recent studies suggest that a high degree of milking effect of the coronary flow induced by the myocardial bridge can be the cause of myocardial ischemia if tachycardia and/or long-distance bridging exist.1,4,12,13 Intimal thickening was observed in intravascular ultrasound in the area of coronary spasm,14 but significant plaques were not found in the bridging area and distal to that area.3,15–17 Recently, a number of cases were reported in which coronary spasm was provoked at the myocardial bridge.5,6,18–20 Coronary spasm is vascular smooth muscle contraction that causes myocardial ischemia. Many factors are considered to participate in the spasm such as endothelial dysfunction, smoking, alcohol, lipid metabolic disorders, gene expression, race, oxidative stress, intimal thickening and decreased nitric oxide (NO).14,21–27 In a porcine model, repeated endothelial denudation can cause coronary spasm.28 Coronary squeezing by a myocardial bridge may cause mechanical endothelial denudation. Therefore, coronary spasm is a conceivable cause of myocardial ischemia at the myocardial bridge.
In terms of treatment for these patients, stent placement or coronary bypass has rendered satisfactory results.29 The recommended medical treatment for the ischemia associated with myocardial bridges is beta-blockers.30 However, if coronary spasm is the cause of ischemia, one should avoid the use of beta-blockers because it is contraindicated for coronary spasm.27 Our patient was successfully stabilized with a calcium antagonist without beta-blockers.
In conclusion, we report a case of AMI due to coronary spasm that coincided with an area of myocardial bridging. A provocation test of coronary spasm should be considered in patients with myocardial ischemia at a myocardial bridge, because it is useful to determine the appropriate medical treatment, which may be a beta-blocker or a calcium antagonist.






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