Myocardial Infarction Secondary to Myocardial Bridging

Swartzel, Gina DiAntonio; Neltner, Kurt MD; Dick, Michael MD

doi: 10.1097/01.EEM.0000443059.63820.ef
The Case Files

Ms. DiAntonio Swartzel is a fourth-year medical student at the Ohio State University College of Medicine. Dr. Neltner is a clinical assistant professor of emergency medicine at the Ohio State University Wexner Medical Center. Dr. Dick is a clinical professor of emergency medicine at the Ohio State University Wexner Medical Center.

Article Outline

A 49-year-old male smoker with a past medical history of hypertension and transient ischemic attack presented to the emergency department with a one-day history of severe, persistent substernal chest pain. He had been seen in the emergency department two weeks prior to this visit for elevated blood pressure secondary to medication noncompliance, and he was not complaining of chest pain and had a nonspecific ECG at that time.

He had been having intermittent, brief, nonexertional chest pain every two to three days after that encounter, and it became constant and severe on the morning of presentation. His blood pressure was 209/115 mm Hg with a heart rate of 84 bpm, and oxygen saturation of 98%. His lung exam revealed clear breath sounds bilaterally with no rales, and cardiovascular exam showed regular rate and rhythm with no murmurs, rubs, gallops, or edema.

He denied dyspnea, nausea, vomiting, palpitations, lightheadedness, and syncope. An ECG revealed ST elevation in leads V1-V5 and ST depression in leads II, III, and aVF, and labs revealed a troponin I level of 11.06 ng/ml. He was transported to the catheterization lab for a left heart catheterization, which showed no acute epicardial coronary occlusions but did demonstrate a significant muscular bridge in the mid-LAD with complete obliteration of the lumen during systole.

Myocardial bridging, defined as a band of muscle overlying the intramyocardial segment of an epicardial coronary artery, was initially described in 1737 by Reyman during autopsy. (J Am Coll Cardiol 2003;41[3]:351; Eur Heart J 2005;26[12]:1159; J Cardiovasc Dis Res 2012;3[2]:176.) Compression of the tunneled artery occurs during systole, but no clinical repercussions occur in the vast majority of patients. It is often considered a benign normal variant of coronary anatomy, but it has been rarely linked to myocardial ischemia, infarction, and sudden cardiac death. Prevalence during autopsy has been described in multiple studies, varying widely from five to 85 percent, but most studies cite myocardial bridging prevalence between 20 and 55 percent. (Heart 1998;80[1]:91; BMC Cardiovasc Disord 2002;2:15; Intern Med 2004;43[12]:1097.) Bridging visualization on angiography is much less, with a prevalence of 0.5 to 2.5 percent (J Am Coll Cardiol 2003;41[3]:351; J Cardiovasc Dis Res 2012;3[2]:176), which is likely due to most bridges being small and causing minimal compression. The prevalence is higher in patients who have undergone heart transplantation and patients with hypertrophic obstructive cardiomyopathy (HOCM). (Eur Heart J 2005;26[12]:1159.)

The most common location for a myocardial bridge is the middle segment of the left anterior descending coronary artery (LAD). (J Am Coll Cardiol 2003;41[3]:351; Eur Heart J 2005;26[12]:1159.) Interestingly, the tunneled segment of the artery is usually free from atherosclerotic plaque while the section of artery proximal to the bridge often has plaque formation. The myocardial bridge causes coronary narrowing or occlusion during systole, and bridges should theoretically have no negative effect on coronary perfusion because coronary filling occurs during diastole. A milking effect of the bridge on the coronary artery can, in fact, prolong the period of occlusion into diastole — interfering with approximately 26 percent of the diastolic period on average — leading to a decrease in coronary perfusion and myocardial ischemia. As a patient's heart rate rises, diastolic filling time is shortened even more, which can lead to further ischemia. Other factors that may lead to ischemia are increased intramyocardial depth and length of the tunneled portion of the coronary artery, hypotension, increased heart rate and contractility, endothelial dysfunction, and coronary artery vasospasm. A variety of serious consequences have been described with myocardial bridging including angina, myocardial infarction, left ventricular dysfunction, life-threatening arrhythmias, and sudden cardiac death, though these sequelae are rare.

The typical patients presenting with symptomatic myocardial bridges are men who are five to 10 years younger than most patients with coronary artery disease who present with angina. The angina can be typical, atypical, or at rest, and it is often severe. Coronary angiography is the diagnostic gold standard for myocardial bridging, but new imaging techniques like intravascular ultrasound can be useful in evaluating myocardial bridges. Treatment options range from medication like beta-blockers and calcium channel blockers to stents and surgical correction with myotomy or bypass grafts. Despite the presumable high prevalence of myocardial bridging, most patients do not experience symptoms or serious complications; however, it is important to consider myocardial bridging as a potential cause of angina-like chest pain or ECG changes in patients at low risk of atherosclerotic disease or at high risk for bridging, such as heart transplant recipients and patients with hypertrophic obstructive cardiomyopathy.

An echocardiography performed in our patient after the left heart catheterization revealed a normal ejection fraction with severe left ventricular hypertrophy and grade II diastolic dysfunction. Cardiac stress MRI showed a recent ischemic post-infarct scar in the territory of the LAD. Cardiothoracic surgery evaluated the patient, and he underwent cardiac surgery to unroof the LAD with resection of fibrous tissue. His post-operative course was complicated by hypertension and LAD spasms, and he was discharged home 10 days after initial presentation.

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