ABSTRACT: Deciding how to treat acute myocardial infarction (MI) with myocardial bridge is difficult because stent fracture and early restenosis are frequently reported. We present a 50-year-old female patient with acute MI and myocardial bridge. Optical coherence tomography (OCT) and fractional flow reserve were used to reach a decision on treatment.
J INVASIVE CARDIOL 2012;24(2):E27-E29
Key words: cardiac arrest, STEMI, OCT, IVUS, FFR
Myocardial bridging is a potential cause of myocardial infarction (MI) and life-threatening arrhythmia.1-6 There is no consensus about the treatment of symptomatic myocardial bridge patients. We used several imaging modalities to evaluate the pathophysiological aspects of acute MI patients with myocardial bridge. Optical coherence tomography (OCT) is useful in detecting coronary plaque rupture and fractional flow reserve (FFR) is useful in assessing functional stenosis.8
A 50-year-old woman with a history of hypertension complained of chest pain 2 months prior to admission. On the admission day, she felt severe chest pain and collapsed in the waiting room upon arrival at the hospital. Her monitor electrocardiogram (ECG) showed ventricular fibrillation. We performed defibrillation 2 times and she recovered sinus rhythm. After recovery, her 12-lead ECG showed significant ST-elevation in the precordial leads (Figure 1). Transthoracic ECG showed anterior wall hypokinesis. We suspected anterior MI and performed emergent coronary angiography (CAG). CAG showed normal right coronary artery, left circumflex artery, and myocardial bridge at the mid-portion of the left anterior descending artery (Figures 2A and 2B). We had to confirm that the etiology of left ventricular wall motion abnormalities was not due to plaque rupture, but due to myocardial bridging, in order to decide further management. We applied OCT to render a decision. OCT showed smooth internal coronary artery wall at the bridge and its proximal segment with no evidence of plaque rupture (Figure 3). We considered the possible contribution of coronary artery spasm to the etiology of ventricular fibrillation. We injected nicorandil and diltiazem intracoronarily and started 4 mg/H nicorandil intravenous infusion. Twenty minutes after infusion, the bridge dilated slightly. FFR was also measured by intracoronary adenosine, which was 0.82. We diagnosed the patient with ventricular fibrillation caused by ST-elevation myocardial infarction (STEMI) due to myocardial bridging and focal spasm, with no clinically significant stenosis in the bridge lesion. We prescribed 200 mg Ca-antagonist, diltiazem, twice a day and 15 mg nicorandil 3 times a day. Clinical course, serial ECG findings, and late gadolinium enhancement MRI at day 5 were compatible with anterior STEMI (Figure 4D). Laboratory data were as follows: cardiac troponin T was 1.6 ng/mL on admission, and the peak serum creatine kinase level and creatine kinase MB isoenzyme were 421 IU/L and 47 IU/L, respectively, 10 H after symptom onset. Repeated coronary angiography at day 7 showed dilatation of the bridge (Figure 4A and 4B). Acetylcholine intracoronary injection induced focal stenosis at the same lesion without any symptoms and ECG changes (Figure 4C). We judged that no clinical ischemia could be induced with the medications. On day 8, the patient was discharged and remains well after 2 years.
Myocardial bridge. Myocardial bridging is deﬁned as a segment of a major epicardial coronary artery, the “tunnelled artery,” that passes intramurally through the myocardium beneath the muscle bridge. MI and malignant arrhythmias (like ventricular fibrillation and ventricular tachycardia) due to myocardial bridge have already been reported.9 There is no consensus about the treatment of such symptomatic myocardial bridge patients.10-12 There are some reports about the efficacy of intracoronary stent implantation in myocardial bridge. However, the frequency of in-stent restenosis requiring target vessel revascularization was high and some other complications such as stent fractures associated with myocardial bridging are also reported.13-16 Medical therapy, especially beta-blockers and Ca-antagonists, constitute the first-line treatment. In unresponsive patients, coronary bypass surgery or unroofing, which involves excision of the overlying muscle bridge band or coronary stenting, are available options.17
Etiology of myocardial infarction. Usually, acute MI is pathologically provoked by sudden rupture or ulcer formation of vulnerable plaque followed by subsequent thrombosis. Intravascular ultrasound reveals the atherosclerosis in the proximal segment of the bridge, but cannot visualize the intracoronary thrombus precisely. Takashi et al reported that OCT could visualize thrombosis in all STEMI patients examined.8 In our case, OCT did not show any findings of fibrous cap disruption, fibrous cap erosion, or thrombus that were compatible with plaque rupture. Recently, there have been some reports about the usefulness of OCT in the evaluation of the internal coronary artery wall of myocardial bridges.18 The tunneled segment has endothelial dysfunction, which could predispose coronary vasospasm. Nicorandil is especially useful because it dilates the bridge lesion efficiently. In our case, the patient had a morning chest pain episode 2 months prior to admission and anatomically, nicorandil and diltiazem could dilate the bridging lesion so coronary vasospasm might affect the MI.
Limitation of FFR in patients with myocardial bridge. A recent study has shown that FFR can detect functional stenosis clinically.7 We used FFR to evaluate the severity of functional stenosis at the bridge lesion. FFR was 0.82, which suggested non-significant stenosis. There is no cut-off point of FFR, especially in myocardial bridge patients. For example, Singh et al reported the limitation of FFR in myocardial bridge patients,19 suggesting that FFR might overestimate the ischemia. In our case, FFR was >0.80 so their theory was not applicable. Escaned et al suggested that diastolic FFR and dobutamine challenge are useful to assess the myocardial bridge.20 Dobutamine challenge might be an option to measure the correct FFR and diastolic FFR in our case. However, their study did not indicate that dobutamine challenge was useful in deciding to perform coronary intervention of myocardial bridge because coronary stenting is still controversial in this procedure due to its high restenosis rate. Therefore, deferring coronary stenting, especially when FFR >0.80, is one treatment option, even in patients with myocardial bridging. Finally, there is a possibility the FFR was overestimated because there may have been transient microvascular dysfunction in the setting of acute MI. However, in our patient, the low peak creatine kinase suggests that this was not a very large MI and so we did not need to consider the small amount of reversible microvascular dysfunction.
This is the first case report showing the usefulness of OCT and FFR to determine whether we should perform intervention of myocardial bridging that induced STEMI. FFR is useful to defer coronary intervention in myocardial bridge patients, especially when FFR is >0.80.
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From the Cardiovascular Center, St. Luke’s International Hospital, Tokyo, Japan.
The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted July 6, 2011, provisional acceptance given July 18, 2011, final version accepted August 22, 2011.
Address for correspondence: Atsushi Mizuno, MD, St. Luke’s International Hospital, 9-1, Akashi-cho, Chuo-ku, Tokyo, Japan. E-mail: firstname.lastname@example.org