Asian Cardiovasc Thorac Ann 2000;8:158-160
© 2000 Asia Publishing EXchange Pte Ltd
Surgical Approach in Symptomatic Myocardial Bridge
Ali Rahman, MD,
Oktay Burma, MD,
Ihsan Sami Uyar, MD,
Ilgin Karaca, MD1,,
Erdogan Ilkay, MD1,,
Ahmet Çekirdekçi, MD
Department of Thoracic and Cardiovascular Surgery
1 Department of Cardiology
Firat University Medical Faculty
Elazi , Turkey
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For reprint information contact: Ali Rahman, MD Tel: 90 424 238 8080 Fax: 90 424 238 8096 email: alirahman33{at}hotmail.com Department of Thoracic and Cardiovascular Surgery, Firat University Medical Faculty, Elazi 23200, Turkey.
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Abstract
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Between 1996 and 1998, surgery was carried out in 4 patients with myocardial bridging who had angina refractory to medical therapy. Two patients were treated by supraarterial myotomy and 2 underwent coronary artery bypass grafting. One patient suffered a right ventricular perforation that was successfully repaired. Surgery is recommended for a grade-III myocardial bridge.
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Introduction
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Intramyocardial course of a coronary artery can arise from abnormal embryological development. Systolic compression of a coronary arterial segment by overlying myocardium is termed myocardial bridging; other terms that have been applied to this phenomenon include mural coronary artery, myocardial loop, and coronary artery over-bridging.1 It frequently involves the mid segment of the left anterior descending coronary artery (LAD).2 Symptomatic patients are most often middle-aged men with typical or atypical chest pain, either related or unrelated to exercise. The condition is usually benign, although cases associated with myocardial ischemia, infarction, and sudden death have been reported.3 Between 1996 and 1998, 4 patients with symptomatic myocardial bridges were treated surgically in our institute.
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Case Reports
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Case 1
A 58-year-old man presented with stable angina pectoris of 6 months' duration. He had hyperlipidemia and a family history of coronary heart disease. A treadmill test was performed according to the Bruce protocol but after the third step, he had chest pain and ST-segment depression (more than 2 mm) in leads V1 to V4. He underwent coronary angiography and the ventriculogram was normal except for a 24-mm length of the mid section of the LAD that was found to have a myocardial bridge causing 80% compression during systole (Figures 1A and 1B
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Figure 1. (A) Angiogram showing systolic narrowing (arrow) in the mid left anterior descending coronary artery in patient no. 1. (B) The same area (arrow) during diastole.
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Case 2
A 40-year-old male smoker who had hyperlipidemia and hereditary risk factors, presented with a history of exercise-induced angina for 2 years. After the second step in a treadmill test, he developed angina and 3-mm ST-segment depression in leads V1 to V6, so the test was stopped. Dyskinesia in the anteroseptal region, an atherosclerotic lesion in the proximal LAD, and an 18-mm myocardial bridge were observed during coronary angiography. There was 70% systolic compression in the mid LAD because of the myocardial bridge (Figures 2A and 2B).
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Figure 2. (A) Angiogram showing systolic narrowing in the mid left anterior descending coronary artery (large arrow) and a proximal atherosclerotic lesion (small arrow) in patient no. 2. (B) The same area during diastole; the proximal lesion (small arrow) remains but the systolic narrowing (large arrow) has disappeared.
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Case 3
A 38-year-old male smoker was admitted with unstable angina pectoris of 6 months' duration. He had suffered an anterior myocardial infarction 6 years previously and had been taking aspirin, atenolol, enalapril. Heparin and nitroglycerin were added to his treatment. Electrocardiography showed QS formation in leads V3 to V5. Ventriculography showed apical akinesia and anterolateral hypokinesia in the mid LAD and a myocardial bridge of 21 mm in length that caused 90% systolic compression.
Case 4
A 68-year-old man was admitted with unstable angina and a 16-year history of angina. His risk factors for coronary artery disease included hyperlipidemia, smoking, and hypertension but an electrocardiogram was normal. He was given aspirin, angiotensin-converting enzyme inhibitors, and nitroglycerin, which relieved his symptoms. On the 5th day after admission, a treadmill test was carried out. After the first step, he had chest pain and 2.1-mm ST-segment depression in leads V1 to V3. Coronary angiography showed an atherosclerotic lesion with 90% narrowing in the proximal LAD, a 14-mm myocardial bridge causing 70% systolic compression in the mid LAD, and an atherosclerotic lesion with 90% narrowing in the circumflex artery.
All 4 patients were treated by elective surgery. After a median sternotomy, aortic and atrial cannulation was carried out, and cardiac arrest was achieved with moderately hypothermic antegrade blood cardioplegia. Patients no. 1 and 3 underwent supraarterial myotomy over the compressed segment of the LAD, using a no. 15 blade. Left internal mammary artery-to-LAD bypass grafting was undertaken without myotomy in patients no. 2 and 4. An aorta-to-second obtuse marginal bypass graft using saphenous vein was performed concomitantly in patient no. 4. Right ventricular perforation occurred during vertical supraarterial myotomy in patient no. 3. The defect was repaired with 2/0 polypropylene suture pledgeted with vascular material.
The patients were followed up for 16, 8, 7, and 5 months, respectively. Angina was completely relieved in all 4 cases. In patient no. 3 who suffered right ventricular perforation, coronary angiography was carried out 3 months postoperatively and no LAD compression was observed.
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Discussion
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The prevalence of myocardial bridges in patients undergoing coronary angiography varies between 0.5% and 16%.2 Clinical manifestations include angina pectoris, arrhythmias, myocardial infarction, and sudden cardiac death.4 Myocardial bridges in vivo are recognized primarily by a decrease in blood flow (milking effect) due to systolic narrowing seen on coronary angiography.1 Myocardial bridges have been classified as: grade I, temporary systolic narrowing less than 50%; grade II, 50% to 75% narrowing; and grade III, more than 75% narrowing.1 Surgical correction has been recommended in symptomatic patients with grade-III myocardial bridges.5 Two of our patients without atherosclerotic lesions had symptomatic myocardial bridges and LAD compression of 80% and 90%.
Development of a thrombus in the bridged segment may lead to serious events such as myocardial infarction or sudden death.6 With the exception of one case report, there has been general agreement that it is unusual for atherosclerosis to involve the coronary arterial segment within a myocardial bridge.1 In one study, there was no atheroma in the bridged segments in 1102 consecutive coronary angiograms.2 Because tachycardia decreases the duration of coronary blood flow, it increases ischemia in the region of a myocardial bridge. The critical ventricular rate that causes ischemia or ventricular arrhythmias in severe myocardial bridging appears to be 150 beats•min–1. The critical heart rate may be lower during sympathetic stimulation due to exercise.4,7 This is supported by the finding of ST-segment depression that halted the exercise tests in 3 patients in this study.
In cases of grade-II myocardial bridging where symptoms are observed during exercise testing, beta-blockers may be suitable as the initial treatment.5 When systolic narrowing is less than 75% but the bridge causes arrhythmias, it is mandatory to attempt medical treatment before opting for a surgical approach. The combination of two drugs, amiodarone with its antianginal and antiarrhythmic properties and diltiazem with its antianginal properties, were reported to be effective treatment.4
In view of our experience, we recommend surgery as the best strategy for treating a grade-III myocardial bridge in a patient with angina pectoris. However, difficulty in finding the precise location of the bridged segment some-times arises during the operation. In such circumstances, Watanabe and colleagues8 demonstrated the effectiveness of intraoperative echocardiography for identifying the exact location of the bridge. Angina unresponsive to several months of medical therapy was completely relieved in all 4 of our patients. The only complication was right ventricular perforation in one case. In order to prevent this complication, it is suggested that myotomy should be performed at an angle of 45 from the left side of the LAD.5 When surgical treatment is indicated for atherosclerotic coronary artery disease in patients with myocardial bridges, the most suitable strategy is coronary artery bypass grafting, as performed in two of our patients. In those with atherosclerosis and myocardial bridging, supraarterial myotomy can be performed according to the preference of the surgeon. If there is no septal perforator or diagonal coronary artery between the segment with the atherosclerotic lesion and the segment with the myocardial bridge, it is wise to place a bypass graft distal to the stenosis.5 This procedure should be carried out under cardiopulmonary bypass with moderate hypothermia because of the risk of ventricular perforation.
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References
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Kracoff OH, Ovsyshcher I, Gueron M. Malignant course of a benign anomaly: myocardial bridging. Chest 1987; 92:1113–5.[Abstract/Free Full Text]
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Grondin P, Bourassa MG, Noble J, Petitclerc R, Dydra I. Successful course after supraarterial myotomy for myocardial bridging and milking effect on the left anterior descending artery. Ann Thorac Surg 1977;24:422–9.[Abstract]
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Ramos SG, Montenegro AP, Felix PR, Kazava DK, Rossi MA. Occlusive thrombosis in myocardial bridging. Am Heart J 1993;125:1172–3.[Medline]
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Sueda T, Matsuura Y, Ishihara H, Hamanaka Y, Shikata H, Nakagawa H, et al. Surgical repair of Wolff-ParkinsonWhite syndrome complicated with myocardial bridging. Ann Thorac Surg 1991;51:119–21.[Abstract]
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Watanabe G, Ohhira M, Takemura H, Tanaka N, Iwa T. Surgical treatment for myocardial bridge using intra-operative echocardiography. J Cardiovasc Surg 1989; 30:1009–12.[Medline]
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Abstract
Introduction
