SUMMARY A 30-year-old female had an acute myocardial infarction complicated by congestive heart failure. Angiography demonstrated an aneurysm in the area of the left aortic sinus. The aneurysm compressed and displaced the main trunk of the left coronary artery and the proximal portion of the left anterior descending artery. This aneurysm was considered to be the cause of the infarction. Aortic valve replacement and removal of the aneurysm were performed. Postoperative studies revealed good function of the replaced valve, good antegrade filling of the left coronary artery, and improved left ventricular function.AN ANEURYSM of the aortic sinus is uncommon. The most frequent complications of the aneurysm of the aortic sinus are rupture and development of aortocardiac fistula, but until they occur, clinical manifestations are not usually recognized. Single aneurysms originating from the left aortic sinus are rare. An aneurysm of the left aortic sinus is usually combined with aneurysmal dilatation of other sinuses, as in Marfan's syndrome.Recently we treated a patient who had an aneurysm originating from the left aortic sinus. This aneurysm compressed and displaced the adjacent left coronary artery, which produced effort angina and resulted in acute myocardial infarction. Case ReportThe patient was a 30-year-old female who had been in good health until 1 year before this episode, when she first exhibited an abnormal chest x-ray on the routine physical check-up. Four months before, she had a single episode of precordial discomfort when she climbed up the stairs; she was otherwise asymptomatic. On March 23, 1982, after she had run about 100 meters, anterior chest pain, cold sweating, nausea and vomiting afflicted her suddenly. She consulted a local practitioner and her condition was diagnosed as acute myocardial infarction by the serial enzymatic and electrocardiographic changes ( fig. 1) ble, a grade 2/6 mitral regurgitant murmur was noted at the apex, and a blowing aortic regurgitant murmur was noted at the third left sternal border. Bilateral basal crepitant rales were present. Prolonged circulation time suggested the presence of congestive heart failure. Laboratory data revealed no abnormalities. Creactive protein and serologic tests for syphilis were also negative. A chest x-ray showed a localized prominent bulge at the upper portion of the left cardiac border and the pulmonary vascular markings were increased ( fig. 2)

Small coronary vessel disease Coronary blood flow Coronary vascular resistance Systolic narrowing Left ventricular muscle mass Exercise tolerance ATIENTS with hypertrophic cardiomyopathy (HCM) frequently develop chest pain and ST depression during exercise. These symptoms suggest myocardial ischemia, despite angiographically normal epicardial coronary arteries.1)-3) Recent studies4),5) have shown that coronary blood flow per Vol.28 No.3

To study the clinical significance of abnormal myocardial perfusion in patients with hypertrophic cardiomyopathy (HCM), we performed a computerized washout analysis of digital subtraction coronary arteriograms in 28 patients with HCM and 16 control subjects. The contrast disappearance half-life (T1/2) was calculated from a time-density curve generated in the four sectors of the myocardium perfused by the left anterior descending coronary artery and the mean T1/2 was calculated by averaging T1/2 values for these four sectors. Patients with HCM demonstrated longer T1/2 in the ventricular septal region than control subjects. Thirteen (46%) of the patients with HCM presented abnormally longer mean T1/2 values, suggesting impaired myocardial perfusion. Family histories of HCM were more frequent in patients with abnormal mean T1/2 values (92% vs 47%; p less than 0.05). On the exercise stress test, patients with abnormal T1/2 values presented significantly lower exercise tolerance with more frequent exercise-induced ST segment depression (62% vs 13%; p less than 0.05). However, there were no significant differences between the two groups with regard to ventricular wall thickness, left ventricular end-diastolic pressure, or the severity of systolic narrowing of the coronary arteries. These findings suggest that 13 (46%) of the patients with HCM have impaired myocardial perfusion, which may be a manifestation of intramural coronary artery disease in addition to left ventricular hypertrophy, elevated left ventricular end-diastolic pressure, or systolic narrowing of the coronary arteries. Additionally, significant association of the prolonged T1/2 with a familial occurrence of HCM and depressed exercise tolerance with ST segment depression imply that impaired myocardial perfusion could be an important inherent pathophysiological state leading to myocardial ischemia during exercise.

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