Abstract
A 46-year-old male presented with acute chest pain, monomorphic ventricular tachycardia, and non–ST-segment elevation myocardial infarction. He was found to have myocardial bridging of the mid left anterior descending coronary artery on coronary angiography and mildly reduced left ventricular ejection fraction with anteroseptal and apical hypokinesia. The patient was treated with antiplatelet therapy, guideline-directed medical therapy for heart failure, and had improvement in symptoms and left ventricular function 1 month later. The case highlights the complex way myocardial bridging may present and its potential to cause major adverse cardiovascular events.
Key Words: acute coronary syndrome, congenital heart defect, coronary vessel anomaly, myocardial infarction, systolic heart failure, ventricular tachycardia
Graphical Abstract
Case Summary
A 46-year-old male with type 2 diabetes mellitus, hypertension, and hyperlipidemia presented to the emergency department with chest pain. He felt heavy chest pressure that awoke him from sleep and lasted several hours. On presentation, he was afebrile, his heart rate was 83 beats/min, his blood pressure was 133/98 mm Hg, and his oxygen saturation was normal. Cardiopulmonary examination was normal. High-sensitivity troponin T was 16 ng/mL (normal ≤19 ng/mL) and electrocardiogram (ECG) demonstrated monomorphic ventricular tachycardia with a right bundle branch block pattern and rate of 127 beats/min (Supplemental Figure 1). No antiarrhythmic therapy was given because the patient remained asymptomatic and hemodynamically stable, and ECG 2 hours later showed normal sinus rhythm without ST-segment abnormalities. Cell counts and serum electrolyte concentrations were normal.
Take-Home Messages
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Myocardial bridging is a congenital anomaly that can rarely lead to major adverse cardiovascular events such as acute coronary syndrome and ventricular arrhythmia.
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Currently, there are no professional guidelines on the clinical management of MB, and further studies are needed to guide evidence-based recommendations.
On hospital day 1, his chest pain recurred in association with troponin T elevation to 908 ng/mL and 838 ng/mL 1 hour later. ECG showed anterior infarct pattern and anterolateral T-wave inversions (Supplemental Figure 2). He underwent cardiac catheterization, which revealed myocardial bridging (MB) of the mid left anterior descending artery, with length and depth approximately 8 mm and 9 mm, respectively (Figure 1). The clinical diagnosis was non–ST-segment elevation myocardial infarction related to coronary spasm in the setting of MB. Dual antiplatelet therapy was started because plaque erosion could not be excluded. Left ventricular ejection fraction by echocardiography was 45%-50% with hypokinesis of the anteroseptum and apex. He had several episodes of nonsustained ventricular tachycardia but no further chest pain and was discharged on day 3 with guideline-directed medical therapy. One month later, cardiac magnetic resonance imaging showed normal biventricular function and a small area of subendocardial ischemia in the apical septum.
Figure 1.
MB on Coronary Angiography
Coronary angiography showed evidence of MB in the middle segment of the LAD coronary artery. In the right anterior oblique cranial projection, narrowing of this segment occurs in systole (A) and is reversed in diastole (B). In the left anterior oblique cranial projection, narrowing is also seen in systole (D) with reversal in diastole (E). Left ventriculography (C, F) showed ejection fraction was approximately 50% with apical hypokinesis. Angiography of the right coronary artery (not shown) showed no significant coronary artery disease or evidence of MB. LAD = left anterior descending; MB = myocardial bridging.
Discussion
MB is a congenital anomaly in which a segment of the epicardial coronary artery traverses within the myocardium. MB can occur in any coronary artery, and most commonly involves the left anterior descending artery.1 MB can produce a supply-demand mismatch in oxygen that is exacerbated by adrenergic stimulation due to epicardial coronary vasoconstriction, reduced diastolic filling time, and increased myocardial contraction.2 MB-associated ischemia can also result from atherosclerosis just proximal to the tunneled segment, the development of which is accelerated by endothelial dysfunction due to shear stress, and localized epicardial coronary artery spasm.3 On coronary angiography, a characteristic “milking effect” with ≥70% reduction in minimal luminal diameter during systole and ≥35% reduction during diastole may be seen.2
Currently, there are no major cardiovascular society guidelines on the management of MB. Generally, symptomatic patients are treated with pharmacologic therapy, with beta-blockers considered first-line due to their negative chronotropic, negative inotropic, and sympatholytic effects.2 Despite their antispasmodic effects, vasodilators such as nitroglycerin should be used with caution because they may worsen systolic compression of the tunneled artery and cause reflex tachycardia.2 Risk factors for atherosclerosis should be aggressively treated, and antiplatelet therapy may be considered when atherosclerosis is detected.2 For patients with refractory symptoms, percutaneous coronary or surgical interventions such as coronary artery bypass grafting and supra-arterial myotomy/“unroofing” may be considered based on patient anatomy, likelihood of symptomatic relief, and available expertise.2
Visual Summary.
Timeline
| Date | Events |
|---|---|
| Reference point | 44-year-old male develops chest pain. Stress testing shows exercise-induced diffuse TWI. |
| 4 mo later | Coronary angiography shows no significant CAD, and no MB is recognized. |
| 2 y later | Develops acutely worsened chest pain with normal troponin and ECG with slow monomorphic VT. Admitted for further evaluation. |
| Hospital d 1 | Chest pain recurs and troponin now elevated, concerning for NSTEMI. Coronary angiography reveals mid-LAD MB. Started on DAPT and beta-blocker. |
| Hospital d 2-3 | Episodes of NSVT. Echocardiography shows mildly reduced LV ejection fraction. Started on GDMT. Chest pain improves. |
| 1-mo posthospitalization | Cardiac MRI shows normal LV ejection fraction, small area of subendocardial apical and septal ischemia, no scar or inflammation. Cardiac rehabilitation therapy and experiencing Canadian Cardiovascular Society grade 1 angina. CCBs are added while avoiding nitrates. |
CAD = coronary artery disease; CCB = calcium channel blocker; DAPT = dual antiplatelet therapy; ECG = electrocardiogram; GDMT = guideline-directed medical therapy; LAD = left anterior descending; LV = left ventricular; MB = myocardial bridging; MRI = magnetic resonance imaging; NSTEMI = non–ST-segment elevation myocardial infarction; NSVT = non sustained ventricular tachycardia; TWI = T-wave inversions; VT = ventricular tachycardia.
Funding Support and Author Disclosures
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Footnotes
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Appendix
For supplemental figures, please see the online version of this paper.
Appendix
References
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