Ann Thorac Surg 2001;72:1369-1370
© 2001 The Society of Thoracic Surgeons
Case report
Ventricular septal rupture caused by myocardial bridging
René A. Tio, MDa,
Tjark Ebels, MDb
a Department of Cardiology, Thoraxcenter, University Hospital Groningen, Groningen, The Netherlands
b Department of Cardiopulmonary Surgery, Thoraxcenter, University Hospital Groningen, Groningen, The Netherlands
Accepted for publication November 13, 2000.
Address reprint requests to Dr Tio, Department of Cardiology, Thoraxcenter, University Hospital Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands
e-mail: r.a.tio{at}thorax.azg.nl
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Abstract
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A 70-year-old woman was referred to us with postinfarction angina. During cardiac catheterization the only coronary abnormality found was myocardial bridging in the mid and distal parts of the left anterior descending coronary artery, despite a large ventricular septal rupture. The pulmonary-to-systemic flow ratio was 2.5:1. Her operation was successful.
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Introduction
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Ventricular septal rupture is a well-known complication of myocardial infarction. Thrombotic occlusion followed by reperfusion of a coronary artery is the most common cause. The infarct-related vessel is usually open after the acute phase of the myocardial infarction. This case report describes a patient who developed a ventricular septal rupture after infarction, with myocardial bridging as the only abnormality.
A 70-year-old woman was referred to our hospital for angina pectoris 4 days after an anterolateral myocardial infarction. The electrocardiogram at referral showed small R-waves in leads V1 and V2 and pathologic q-waves in leads V3 and V4, and biphasic/negative T-waves in the lateral leads. An echocardiogram showed akinesia in the apicoseptal, apicoinferior, and apicoposterior regions of the left ventricle, with overall good residual left ventricular function. The maximum creatinine kinase was 760 with an MB-fraction of 100 (U/L; normal values < 170 and < 25, respectively). During anginal complaints the ST-segments and T-waves in the anterolateral leads showed dynamic changes, ranging from deep negative T waves to biphasic T waves with some ST-segment elevation.
For those reasons she was scheduled for coronary angiography on the fifth day after her infarction (Fig 1). The catheterization was expedited because she developed acute dyspnea that was misinterpreted as angina pectoris. During cardiac catheterization the only coronary abnormality found was myocardial bridging in the mid and distal parts of the left anterior descending coronary artery. Ventriculography showed a ventricular septal rupture and an akinetic distal anterior wall. Right heart catheterization showed a central venous pressure of 12 mm Hg, pulmonary pressure of 50/21 mm Hg, and pulmonary wedge pressure of 26 mm Hg. Oxygen saturations were 94% (aorta), 80% (pulmonary artery), and 58% (mixed venous). The systemic flow Qs was 4.1 L/minute and pulmonary flow Qp 10.6 L/minute. The ratio of pulmonary-to-systemic circulation was thus 2.5:1. She was successfully operated on using a previously described technique [1]. At operation the infarcted area extended from the mid-left anterior descending artery to the apex. An incision was made through the infarction in the left ventricular free wall. Through this incision, a small rupture located in the apical part of the septum was readily seen. A prosthetic patch was inserted on the left ventricular aspect of the rupture, and the right ventricular free wall was used to stabilize the rupture in a sandwich fashion. At the end of the procedure there was no difference between mixed venous and pulmonary oxygen saturations.
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Fig 1. Right anterior oblique angiogram of the left coronary artery showing the myocardial bridge. (A) Diastolic frame showing the normal caliber of the left anterior descending artery (LAD). (B) Systolic frame showing an almost complete collapse of the mid-left anterior descending artery during myocardial contraction (arrow).
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No postoperative complications occurred, except for prolonged weaning from ventilation, which took 6 days. She was discharged 20 days after the operation and is doing well now 16 weeks postoperatively.
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Comment
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The prevalence of myocardial bridges in anatomic studies varies from 5.4% to 85.7% depending on definition and method used (see reference 2 for a review). During angiography, systolic narrowing of a coronary artery segment is seen in 0.5% to 4.5% of patients, the most frequent site being the middle segment of the left anterior descending coronary artery. Although most myocardial bridges are presumed to be asymptomatic [2] in some cases they can cause angina pectoris [3], myocardial infarction [3], life threatening ventricular arrhythmias, or even death [4].
Because myocardial perfusion occurs mainly during diastole, the systolic narrowing per se is thought not to be able to cause ischemia. However, ischemia can be caused by other mechanisms. Endothelial cell damage might occur because of the continuous mechanical stress, which predisposes the vessel segment to vasospasm [5] and might explain why myocardial bridges can cause ischemia. Another mechanism might be premature arteriosclerosis at the site of the myocardial bridge, although arteriosclerosis is rare in coronary arteries that do not run subepicardially [6]. Apart from these mechanisms the fact that the patient had postinfarct angina could be explained by changes in wall tension caused by the infarction, because the other coronary arteries had only minor vessel wall irregularitites.
Although there was a 1% to 2% incidence of ventricular septal rupture in the prethrombolytic era, as a complication of myocardial infarction treated with thrombolysis it has recently been reported to be as low as 0.2% [7]. In that GUSTO-1 substudy, advanced age, anterior location of infarction, female sex, and history of nonsmoking are the most important predictors of ventricular septal rupture. Compared with the prethrombolytic era, ventricular septal rupture occurred earlier—on day 1 instead of day 3 to 5 [7]. In the present case the ventricular septal rupture occurred 5 days after anterior wall myocardial infarction. At coronary angiography the only abnormality found was myocardial bridging of the mid-left anterior descending artery. In addition, a left ventriculogram showed contrast in the right ventricle. Although failure of reperfusion of the infarct-related coronary artery is thought to be an important contributing factor in ventricular septal rupture, we found the left anterior descending artery to be patent in our patient. Recurrent ischemia caused by the bridging, presented as postinfarct angina, could have contributed to the rupture.
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Acknowledgments
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Dr Tio is financially supported by the Netherlands Heart Foundation, grant D95–019.
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References
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Faruqui A.M., Maloy W.C., Felner J.M., Schlant R.C., Logan W.D., Symbas P. Symptomatic myocardial bridging of coronary artery. Am J Cardiol 1978;41:1305-1310.[Medline]
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Kracoff O.H., Ovsyshcher I., Gueron M. Malignant course of a benign anomaly: myocardial bridging. Chest 1987;92:1113-1115.[Abstract/Free Full Text]
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Ciampricotti R., el Gamal M. Vasospastic coronary occlusion associated with a myocardial bridge. Cathet Cardiovasc Diagn 1988;14:118-120.[Medline]
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Crenshaw B.S., Granger C.B., Birnbaum Y., et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation 2000;101:27-32.[Abstract/Free Full Text]
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Abstract
Introduction
