Echo diagnosis of ruptured aortic valve leaflet.

artery, and it has been suggested that these patients should be treated by bypass surgery. The mechanism for sudden death is not known. Theories include kinking of the anomalous artery2 and occlusion by a flap-like closure of the ostium as the aorta expands.3 However, sudden death, infarction, and ischemia may occur without regard to the course of the anomalous left coronary artery.4 In the past six years there have been nine cases of an anomalous left coronary artery from the right sinus of Valsalva or right coronary artery out of 7,893 adult cardiac catheterizations performed course of the anomalous artery varied-posterior to the aorta, anterior to the aorta, and anterior to the pulmonary artery. In only one case, posterior to the aorta, did the patient have a previous in-farction by ECG and abnormal ventriculogram in the distribution supplied by the anomalous artery in the absence of any demon-strable fixed obstruction. The entire spectrum of the nonatherosclerotic anomalous left coronary artery, regardless of its course, presents a difficult clinical decision in the patient with chest pain. Chaitman et al.4 summarize the dilemma best by suggesting lactate studies during pacing, coronary sinus blood flow during exercise and exercise testing of these patients. complication of anomalous left coronary origin from the anterior sinus of Valsalva. angiographic, and hemodynamic findings in patients with anomalous origin of the coronary arteries. Circulation 53: 122, 1976 The author replies: To the Editor: We have no basic disagreement with Dr. Rossner's letter. In our discussion' of the hemodynamic significance of origin of the left coronary artery (LCA) from the right aortic sinus with subsequent passage between the aorta and right ventricular infundibulum, we reviewed the study by Cheitlin et al.2 which incontrovertibly proved the clinical danger of such anomalies. Like Dr. Rossner, we alluded to the paper by Chaitman et al.3 which documented the occurrence of myocardial infarction in two patients without coronary athero-sclerosis whose LCA also arose from the right aortic sinus but which passed either anterior to the pulmonary artery or posterior to the aorta, rather than between the two great arteries. The case described by Rossner, in which a patient with previous myocardial infarction but no coronary atherosclerosis was found to have a LCA originating from the right aortic sinus and passing behind the aorta, would appear to be a third example of this phenomenon. The etiology of the infarcts in these cases is certainly …