Myocardial Bridge Causing Anterior Myocardial Infarction
Myocardial Bridge Causing Anterior Myocardial Infarction
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.
Approximately 6% of patients with myocardial infarction have no evidence of coronary atherosclerosis by angiography or at autopsy. 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. In contrast, only a few cases of myocardial infarction from myocardial bridge have thus far been reported.
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. Intravenous
-blocker, however, has been shown to attenuate a systolic luminal reduction as well as ischemia in these patients.
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.
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.
Approximately 6% of patients with myocardial infarction have no evidence of coronary atherosclerosis by angiography or at autopsy. 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. In contrast, only a few cases of myocardial infarction from myocardial bridge have thus far been reported.
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. Intravenous
-blocker, however, has been shown to attenuate a systolic luminal reduction as well as ischemia in these patients.
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.