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Myocardial Sympathetic Denervation, Fatty Acid Metabolism, and Left Ventricular Wall Motion in Vasospastic Angina

¹ Department of Clinical Pharmacology, Niigata University of Pharmacy and Applied Life Sciences, Niigata, Japan
² Radioisotope Center, Niigata University School, Niigata, Japan
³ Division of Cardiology, Tsubame Rosai Hospital, Niigata, Japan
⁴ First Department of Internal Medicine, Niigata University School of Medicine, Niigata, Japan
⁵ Daiichi Radioisotope Laboratories, Ltd., Chiba, Japan

Although various noninvasive methods have been used to detect vasospasm, none of them are sensitive enough for patients with sporadic attacks. Because abnormal fatty acid metabolism and cardiac adrenergic neuronal damage are observed in ischemic myocardium, ¹²³I-15-(p-iodophenyl)-3-R,S-methyl pentadecanoic acid (BMIPP) and ¹²³I-metaiodobenzylguanidine (MIBG) have recently been proposed as useful tracers for detection of myocardial damage. This study investigated the relationships among the coronary vasospastic regions, abnormal left ventricular regional wall motion, fatty acid metabolism, and sympathetic nerve functions and their changes during treatment in patients with vasospastic angina. Methods: We evaluated 50 patients with vasospastic angina (25 with clinically documented vasospasm [group A] and 25 with vasospasm induced by ergonovine provocation [group B]) and 25 control subjects who had chest pain but had normal coronary arteries without ergonovine provocation of spasm. Sixteen patients in group A were reevaluated 6 mo after medical treatment. The territorial regions of the vasospasm-induced coronary artery, wall motion determined by left ventriculography, and BMIPP and MIBG uptake were compared. Results: Regions exhibiting a positive reaction to the ergonovine provocation were observed in the right coronary artery in 41 patients, the left anterior descending artery in 33, and the left circumflex artery in 21. Provocation occurred in multiple vessels in 29 patients (58%). Reduction of wall motion was observed in 19 patients (38%). Sensitivity and specificity for the identification of vasospastic angina were 86% (43/50 patients) and 88% (22/25 control subjects), respectively, for BMIPP scintigraphy and 100% (50/50 patients) and 56% (14/25 control subjects), respectively, for MIBG scintigraphy. In the region exhibiting a reduction in left ventricular wall motion, BMIPP or MIBG uptake was decreased. The sensitivity and specificity of determination of vasospasm-induced coronary arteries were 71% (67/95 arteries) and 95% (71/75 arteries), respectively, for BMIPP scintigraphy and 96% (91/95 arteries) and 55% (41/75 arteries), respectively, for MIBG scintigraphy. After 6 mo, during treatment, vasospasm was reinduced by ergonovine provocation in 6 patients (group I) and was not reinduced in 10 patients (group II). Improvements of decreased BMIPP and MIBG uptake were lower in group I (25% ± 4% and 16% ± 4%, respectively) than in group II (69% ± 4% and 50% ± 3%, respectively; both P < 0.01). The regions in which vasospasm was reinduced exhibited decreased BMIPP and MIBG uptake. Conclusion: Abnormal fatty acid metabolism and cardiac sympathetic denervation were observed more frequently than were wall motion abnormalities in the vasospastic region in patients with vasospastic angina. BMIPP and MIBG scintigraphy are highly accurate and noninvasive techniques for determining the presence and location of vasospasm.

Key Words: BMIPP • MIBG • fatty acid metabolism • sympathetic denervation • vasospasm

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