913-114 Abnormal Cardiac Sympathetic Nervous System in Patients with Coronary Spastic Angina; Assessment with Iodine-123 Metaiodobenzylguanidine Myocardial Scintigraphy

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We have shown that dysregulation of autonomic nervous system plays an important role in the mechanism(s) of coronary artery spasm. To assess regional abnormalities in cardiac sympathetic nervous system in the mechanism(s) of coronary artery spasm, twenty-eight patients with coronary spastic angina and 10 control subjects were examined with MIBG myocardial tomographic imaging (SPECT) which is a non-invasive and useful method evaluating regional cardiac sympathetic nervous activity. The patients included in this study had neither organic coronary stenosis nor myocardial infarction. MIBG-SPECTwas examined at rest and was avoided to perform during anginal attack. Coronary spasm was documented by coronary angiography during the anginal attack induced by intracoronary injection of acetylcholine in all of the patients. MIBG-SPECT was performed at the time period when spontaneous attack frequently occurred. Regional reduction of MIBG uptake was observed in 30 of 42 areas perfused with coronary arteries having spasm (sensitivity 71%). whereas it was observed in 12 of 73 areas perfused with coronary arteries not having spasm in patients with coronary spastic angina and in control subjects (specificity 84%). Sensitivity for detecting coronary arteries with spasm in the LAD was 69% (9/13 arteries) and that in RCA was 81% (13/16 arteries) and that in LCX was 62% (8113 arteries). MIBG-SPECT was again performed in 7 patients at 4 months after complete suppression of the anginal attack by treatment with calcium antagonists and nitrates without b blocker. The re-studies showed that reduction of MIBG uptake was still observed in the same scintigraphic areas having MIBG uptake reduction at the initial studies in all patients tested. The results show that MIBG-SPECT is a feasible and high sensitive method for predicting the coronary arteries with spasm without provocation of coronary spastic anginal attacks, and sympathetic nervous dysfunction continues for several months after complete suppression of myocardial ischemia, suggesting that sympathetic nervous dysfunction may not be the ischemic effect but playa possible role in the cause of coronary artery spasm.