Unappreciable myocardial bridge causing anterior myocardial infarction and postinfarction angina. (Case Report).

Abstract: We report a case of anterior myocardial infarction in a middle-aged man without risk factors for atherosclerosis in whom myocardial bridge was diagnosed several years later. An abnormal wall motion during acute myocardial infarction masked the characteristic angiographic findings of myocardial bridge and rendered it unappreciable during the initial angiographic study.

Key Words: etiology, myocardial infarction, nonatherosclerotic coronary artery disease 

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Approximately 6% of patients with myocardial infarction have no evidence of coronary atherosclerosis by angiography or at autopsy. (1) Myocardial bridge is thought to be the responsible cause in some of these patients. Myocardial bridge is a common finding during an autopsy. The prevalence of greater than 50% has been reported consistently in most autopsy series. (6) In contrast, only a few cases of myocardial infarction from myocardial bridge have thus far been reported. (2-5)

Clinically, the diagnosis of myocardial bridge in an individual patient is primarily based on an angiographic finding of systolic narrowing of the coronary arterial lumen that normalizes during diastole. The ability to detect myocardial bridge angiographically can be influenced by medications affecting vascular tone or contractile state of the ventricle. Administration of intravenous isoproterenol or intracoronary nitroglycerine has been shown to enhance the detection rate. (7) Intravenous [beta]-blocker, however, has been shown to attenuate a systolic luminal reduction as well as ischemia in these patients. (8)

It is well known that during an acute myocardial infarction, an affected region of the ventricle typically becomes akinetic or dyskinetic. Therefore, it is conceivable that the myocardial bridge may become unrecognizable on angiogram during acute phase of myocardial infarction caused by this condition. We report a case of a middle-aged man without major risk factors for atherosclerosis who presented with acute anterior wall myocardial infarction but the myocardial bridge was not diagnosed until a few years later.

Discussion

In our patient, the myocardial bridge of the middle portion of LAD was not diagnosed at the initial coronary angiography during an acute phase of anterior wall myocardial infarction but was detected on a subsequent study. We believe that the myocardial bridge was present at the initial study but was unrecognizable because of the coexisting severe systolic dysfunction of the anterior wall from severe ischemia. The patient, however, underwent a successful mechanical reperfusion early in the course of his infarction. Thus, it is likely that a significant amount of myocardium was salvaged and some degree of regional contractile function subsequently returned once myocardial stunning resolved.

Myocardial bridge is more common in cardiac diseases associated with left ventricular hypertrophy. (7, 9) A recent report retrospectively reviewing coronary angiographic studies in children with hypertrophic cardiomyopathy detected the myocardial bridge in 40% of the cases. (10) Its incidence was also related to the severity of left ventricular hypertrophy. In this patient, the distal LAD was the site of total occlusion, although an intraluminal thrombus was detected in the proximal LAD at the initial angiography. Consequently, the area of major injury is limited to the apex and distal portion of anterior wall as confirmed by the left ventriculography on the subsequent study. Left ventricular remodeling after a myocardial infarction is known to lead to hypertrophy of the noninfarcted region. Since the bridged segment is located in the middle rather than distal portion of the anterior wall, this compensatory change may render the myocardial bridge more angiographically recognizable. Our patient, however, expe rienced recurrences of his chest pain shortly after the myocardial infarction and there was no clinical indication of severe left ventricular hypertrophy. Thus, we strongly feel that myocardial bridge was present before the initial MI rather than resulted from it.

Moreover, we believe that myocardial bridge may be responsible for the initial cardiac event in this patient. Our patient did not have any major risk factors for coronary atherosclerosis, any clinical evidence of hypercoagulability or conditions associated with coronary embolism. Coronary thrombotic occlusion has been reported in patients with myocardial bridge who present with acute MI.(3-6) The majority of these cases did not have angiographic evidence of significant coronary atherosclerosis. Similarly, we found no evidence of coronary artery disease from multiple angiographies in our patient. However, the limitations of coronary angiography to detect atherosclerosis are well appreciated. Atherosclerotic plaques proximal to the bridge have been demonstrated by intravascular ultrasound studies in 86% of the patients with myocardial bridge and ischemic symptoms despite the absence of coronary artery disease angiographically in most of them. (11) Endothelial injury due to an excessive shear stress associated w ith an abnormal flow characteristic proximal to and within the bridge is felt to be responsible for plaque formation in these patients. We believe that the same mechanism is likely responsible for plaque rupture and thrombus formation in our patient.

Our case demonstrated that the myocardial bridge can be under recognized during acute phase of an MI. We were able to detect myocardial bridge in our patient because contractile function of the bridge segment had returned. It is conceivable that in those patients whom a permanent dysfunction of the anterior wall occurs as a result of either an unsuccessful or a markedly delayed reperfusion, a preexisting myocardial bridge may be completely unrecognizable unless the patient undergoes open-heart surgery. As a result, the association between myocardial bridge and myocardial infarction may be clinically underappreciated.

Conclusion

Myocardial bridge maybe underappreciated during acute phase of myocardial infarction. This condition may be responsible for some of the cases of anterior MI with angiographically normal coronary artery. A subgroup of these patients, particularly those with recurrent chest pain following an anterior MI, may require a careful evaluation for the myocardial bridge.

Accepted December 2, 2002.

References

(1.) Antman EM, Braunwald E. Acute myocardial infarction, in Braunwald E, Zipes DP, Libby P (eds): Heart Disease: A Textbook of Cardiovascular Medicine. Philadelphia, W.B. Saunders, 2001, ed 6, pp 1114-1218.

(2.) Laifer LI, Weiner BH. Percutaneous transluminal coronary angioplasty of a coronary artery stenosis at the Site of myocardial bridging. Cardiology 1991;79:245-248.

(3.) Vasan RS, Bahi VK, Rajani M. Myocardial infarction associated with a myocardial bridge. Int J Cardiol 1989;25:240-241.

(4.) van Brussel BL, van Tellingen C, Ernst MP, Plokker HW. Myocardial bridging: A cause of myocardial infarction? Int J Cordial 1984;6:78-82.

(5.) Ciampricotti R, el Gamal M. Vasospastic coronary occlusion associated with a myocardial bridge. Cathet Cardiovasc Diagn 1988;14:118-120.

(6.) Ramos SG, Montenegro AP, Felix PR, Kazava DK, Rossi MA. Occlusive thrombosis in myocardial bridging. Am Heart J 1993;125:1771-1773.

(7.) Ishimori T, Raizner AE, Chahine RA, Awdeh M, Luchi RJ. Myocardial bridges in man: Clinical correlations and angiographic accentuation with nitroglycerin. Cathet Cardiovasc Diagn 1977;3:59-65.

(8.) Schwarz ER, Klues HG, vom Dahl J, Klein I, Krebs W, Hanrath P. Functional, angiographic and intracoronary Doppler flow characteristics in symptomatic patients with myocardial bridging: Effect of short-term intravenous [beta]-blocker medication. J Am Coil Cardiol 1996;27:1637-1645.

(9.) Irvin RG. The angiographic prevalence of myocardial bridging in man. Chest 1982;81:198-202.

(10.) Mohiddin SA, Begley D, Shih J, Fananapazir L. Myocardial bridging does not predict sudden death in children with hypertrophic cardiomyopathy but is associated with more severe cardiac disease. J Am Coll Cardiol 2000;36:2270-2278.

(11.) Ge J, Erbel R, Rupprecht HJ, Koch L, Kearney P, Gorge G, et al. Comparison of intravascular ultrasound and angiography in the assessment of myocardial bridging. Circulation 1984;89:1725-1732.

RELATED ARTICLE: Case Report

The patient was a 47-year-old Hispanic man without any major risk factors for atherosclerosis who initially presented with acute anterior ST segment elevation myocardial infarction (MI). There was no history of drug abuse, past history of thromboembolism or family history of premature atherosclerosis. An emergent cardiac catheterization with coronary angiography was performed. This study revealed a relatively large intraluminal filling defect in the proximal left anterior descending artery (LAD) which was completely occluded in its distal segment (Fig. 1). Akinesis of the mid to distal anterior wall of the left ventricle was also noted. However, there was no atherosclerotic plaque detected in any coronary arteries. A percutaneous transluminal coronary angioplasty was subsequently performed. This resulted in complete resolution of the intraluminal thrombus in the proximal LAD and complete restoration of normal antegrade flow in the distal segment. The proximal LAD at the site of thrombus did not appear to hav e any significant atherosclerosis. The patient left the hospital several days later after an uncomplicated hospital course.

Shortly after his MI, the patient began to experience recurrences of the chest pain. The characteristic of his chest pain was typical for angina pectoris except that it was not related to exertion. Over the following two years, he underwent multiple diagnostic workups including two additional coronary angiographies and endoscopy but no definitive diagnosis could be discerned. Because of rather disabling pain, the patient visited emergency rooms multiple times and received various empirical treatments but none was truly beneficial.

He subsequently presented to us and coronary angiography was again performed. The left ventriculogram showed akinetic apex with rather hypercontractile basal and mid portion of the anterior wall. More importantly, a myocardial bridge was detected in the middle portion of LAD (Figs. 2 and 3). The proximal and distal LAD as well as the other coronary territories had no evidence of atherosclerosis. Reviewing of two previous coronary angiograms after his myocardial infarction also showed a myocardial bridge in the same location but somewhat less noticeable. Medical treatment, which included a high dose [beta]-blocker, was prescribed but his symptoms did not significantly improve. The patient subsequently underwent a surgical release of myocardial bridge. Postoperatively, he reported a marked improvement of his chest pain and was able to return to work without any significant limitations.

From the Division of Cardiology, Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX.

Reprint requests to S. Lane Cox, MD, Division of Cardiology, Department of Internal Medicine, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430-0001. Email: [e-mail]

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