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Myocardial ischemia with normal coronary arteries can be due to anatomic or functional reasons. The more severe congenital coronary anomalies in the adulthood are the origin of the left main of the left coronary artery from the right aortic sinus, with a course between the aorta and the pulmonary trunk, and the origin of the left main from the pulmonary trunk. Both these anomalies can cause sudden death, usually associated with physical exertion. The coronary vasomotion of epicardial vessels depends on the interaction of several neurohumoral substances. We report the hemodynamic, angiographic and stress test data of 30 patients affected by chest pain, with myocardial ischemia and normal coronary arteries. In 8 patients the response of epicardial coronary arteries to intracoronary infusion of acetylcholine was evaluated.

Myocardial infarction and normal coronary arteries is not a rare event in the ischemic heart disease. Even if the patients with acute myocardial infarction and angiographically normal coronary arteries represent a small percentage (reported incidence varies from 1% to 12%) of all patients with acute ischemic attacks, they might be useful to highlight the pathogenetic mechanisms of this syndrome. To improve the understanding of this clinical entity, we reviewed our experience of 18 patients with myocardial infarction and normal coronary arteries. They were compared with a control group of patients with similar clinical characteristics (gender, age, infarct location) and residual coronary artery stenosis. The myocardial damage was less extensive in patients without residual stenosis (peak CK-MB: 56.1 +/- 71.9 vs 126.5 +/- 87.9 IU/I, p < 0.05), with a better left ventricular function either global (ejection fraction: 64 +/- 11 vs 55 +/- 13%, p < 0.05) and regional (SD/chord: -1.36 +/- 1.20 vs -2.42 +/- 1.04, p < 0.02). These findings probably reflect a more prompt and complete reperfusion of the infarct related artery. Myocardial necrosis may occur without obstructive coronary artery disease by the interaction of multiple factors such as abnormal platelet aggregation, thrombus formation and localized or diffuse changes of coronary vascular tone.

Doppler left ventricular inflow time-velocity curves have been extensively used to evaluate left ventricular filling. The reproducibility of the technique, however, has been rarely assessed, its temporal variability being, presently, unknown. In order to define the temporal reproducibility of Doppler parameters of left ventricular filling, 10 normal subjects were studied at 3 different times (baseline, after 24 hours, and after 1 week). No parameter changed significantly during 1 week follow-up. When variability, however, was expressed as percent changes relative to baseline, values ranging from 5.7% to 25% were found, the largest variability being associated with acceleration-deceleration parameters (p less than 0.001). In conclusion temporal variability of parameters obtained from Doppler diastolic mitral time-velocity curves is acceptable in homogeneous groups of subjects. When the technique, however, is used for serial evaluation of ventricular filling in a single patient, the specific temporal variability of the parameter considered must be taken into account before any variation can be ascribed to real hemodynamic changes.