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Ann Thorac Surg 1999;68:244-246
© 1999 The Society of Thoracic Surgeons


Case Reports

Supraarterial decompression myotomy for myocardial bridging in a child

Neal D. Hillman, MDa,b, Constantine Mavroudis, MDa,b, Carl L. Backer, MDa,b, C. Elise Duffy, MDa,b

a Division of Cardiovascular-Thoracic Surgery, Children’s Memorial Hospital, Chicago, Illinois, USA
b Departments of Cardiothoracic Surgery and Pediatrics, Northwestern University Medical School, Chicago, Illinois, USA

Address reprint requests to Dr Mavroudis, Division of Cardiovascular-Thoracic Surgery, M/C #22, Children’s Memorial Hospital, 2300 Children’s Plaza, Chicago, IL 60614
e-mail: c-mavroudis{at}nwu.edu


    Abstract
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 Abstract
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A 10-year-old boy presented with a history of exertional chest pain. An electrocardiogram demonstrated an inferior apical myocardial infarction. Cardiac catheterization revealed myocardial bridging of the left anterior descending coronary artery with evidence of intramyocardial obstruction during systole. The patient underwent successful treatment with supraarterial decompression myotomy and remains symptom free at 1 year.


    Introduction
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Myocardial bridging is often considered a congenital anomaly with little clinical significance. However, recent reports of unstable angina, arrhythmia, myocardial infarction, and sudden death emphasize the hemodynamic importance of myocardial bridging in some patients [1]. Hemodynamically significant obstruction to coronary blood flow combined with reduced coronary flow reserve result in the occurrence of clinical symptoms [2]. Although ß-blockade therapy and coronary artery bypass have been advocated, supraarterial decompression myotomy corrects the anatomic defect, thereby eliminating the need for lifetime ß-blockade or future redo coronary artery bypass grafting [1].

A 10-year-old boy presented with a 2-year history of exertional chest pain that resolved with rest. Over the last 6-month time period, the chest pain was induced with decreasing levels of activity and was now associated with palpitations. He also had a single episode of syncope while climbing three flights of stairs. A resting electrocardiogram (ECG) demonstrated right and left ventricular hypertrophy, right atrial hypertrophy, and nonspecific ST changes. Echocardiogram revealed mild inferior apical hypokinesis. Cardiac catheterization and ventriculography demonstrated hypokinesia at the apex of the septum and free wall. The left anterior descending coronary artery was torturous with myocardial bridging present in the middle and distal thirds of the artery. A "milking" effect was noted during systole with 90% luminal narrowing. Dobutamine stress echocardiogram demonstrated wall motion abnormality in the left ventricular free wall and anterior apical territory. Thallium scan revealed a corresponding region of reversible myocardial ischemia.

At operation, the distal two-thirds of the left anterior coronary artery was intramyocardial. There was discoloration and fibrosis in the area of the septum in the mid portion of the left anterior descending artery (LAD), which was consistent with previous myocardial infarction. Aortobicaval cardiopulmonary bypass was instituted with cooling to 28°C. Cold antegrade blood cardioplegic arrest was induced. A 6-cm myotomy along the course of the LAD to the apex was performed with a beaver blade (R. Beaver Inc, Waltham, MA) using standard coronary artery dissection techniques. The deepest level of the myotomy penetration was 2 mm at the mid-portion of the course of the LAD. At completion, the entire course of the LAD from its origin to the apex was identified. The patient was separated from cardiopulmonary bypass without difficulty.

Five days postoperatively, dobutamine thallium stress test demonstrated no perfusion abnormalities. There was new anterior septal dyskinesis, improved anterior wall motion with stress, and persistent hypokinesis of the septum. Cardiac catheterization and repeat coronary angiography showed definite improvement by demonstrating the elimination of systolic arterial constriction as compared with the preoperative angiogram. The patient was discharged to home on the sixth postoperative day. He had a normal exercise test (Bruce protocol, Level III, stopped at 10 minutes due to fatigue without electrocardiographic ST-T changes) at 1 year postoperatively. The thallium perfusion study was normal.


    Comment
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Myocardial bridging occurs when a band of myocardial muscle overlies a segment of the coronary artery resulting in mechanical stenosis due to systolic compression. Angiographically, the incidence of myocardial bridging ranges from 0.5% to 12%, while autopsy studies report an incidence of 5% to 86% [3, 4]. This difference has been attributed to the insensitivity of angiography in identifying this congenital abnormality. The left coronary artery is most frequently involved, however, there are reports of involvement of the right coronary artery [3]. Many authors feel myocardial bridging is an angiographic curiosity characterized by a "milking" effect during systole that is of little hemodynamic or clinical significance. Because the predominance of coronary blood flow occurs during diastole, it is postulated that systolic compression of the coronary artery would not result in ischemic changes [4]. However, recent reports of arryhthmias, myocardial infarction, and sudden death highlight the importance of this lesion.

Kramer and associates divided patients with angiographic evidence of myocardial bridging into three groups based on the degree of systolic compression (group 1: 0%–30%, group 2: 31%–50%, group 3: 51%–100%) [5]. In group 1, there was no evidence of ischemia on ECG or exercise thallium. Twenty-five percent of patients in group 2 had ECG abnormalities suggestive of ischemia; all had normal stress thallium studies. In group 3, ECG abnormalities were found in 30% of patients and positive stress thallium was identified in 33%. Using intracoronary Doppler and quantitative angiography, Schwartz and associates showed that, at rest, peak intracoronary blood flow velocity was higher within the myocardial bridge when compared with proximal and distal flow [2]. During atrial pacing, these differences were increased. During systole, there was characteristic luminal narrowing, however, during early diastole, diameter gain was delayed and there was persistent mid-diastolic diameter reduction of > 30%. Therefore, the major hemodynamic abnormality occurs during early and mid diastole, the phase of the cardiac cycle when maximal myocardial blood flow occurs.

Our patient is similar in character to those in group 3. He had 98% narrowing of the LAD during systole, ECG changes consistent with ischemia and myocardial infarction, and a positive thallium stress test. His anginal symptoms occurred at times of stress during which time diastole is shortened and alterations in coronary blood flow at the site of the myocardial bridge are greatest. Our patient is unique because he developed symptomatic ischemia from the myocardial bridge during adolescence and is, to the best of our knowledge, the youngest patient to undergo this procedure. Although treatment with ß-blockade has been successful in the adult population, this requires life-long commitment to medical management. Surgical treatment with supraarterial myotomy has been successful in the treatment of myocardial bridging [1]. Supraarterial decompressive myotomy not only treats the physiologic abnormality of myocardial bridging, but corrects the congenital anatomic defect. We conclude that supraarterial decompressive myotomy is feasible in the pediatric population and is the treatment of choice when clinically significant myocardial bridging is identified.


    References
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 References
 

  1. Tauth J., Thompson-Sullebarger J. Myocardial infarction associated with myocardial bridging. Cathet Cardiovasc Diagn 1997;40:364-367.[Medline]
  2. Schwarz E.R., Klues H.G., vomDahl J., Klein I., Krebs W., Hanrath P. Functional characteristics of myocardial bridging. Eur Heart J 1997;18:434-442.[Abstract/Free Full Text]
  3. Vangpatanasin W., Willard J.E., Hillis L.D., Lange R.A., Landau C. Acquired myocardial bridging. Am Heart J 1997;133:463-465.[Medline]
  4. Culter D., Wallace J.M. Myocardial bridging in a young patient with sudden death. Clin Cardiol 1997;20:581-583.[Medline]
  5. Kramer J.R., Kitazume H., Proudfit W.L. Clinical significance of isolated coronary bridges; benign and frequent condition involving the left anterior descending artery. Am Heart J 1982;103:283-288.[Medline]
Accepted for publication December 8, 1998.


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This Article
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Constantine Mavroudis
Carl L. Backer
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