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

Kenichi Watanabe, MD1, Toshihiro Takahashi, PhD2, Seiichi Miyajima, MD3, Yoichi Hirokawa, MD4, Naohito Tanabe, MD4, Kiminori Kato, MD4, Makoto Kodama, MD4, Yoshifusa Aizawa, MD4, Shusaku Tazawa, PhD5 and Minoru Inoue, PhD5

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



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FIGURE 1. BMIPP scintigrams of vasospastic angina before and after medical treatment of 50-y-old man (patient 1 in group II). Patient had spontaneous vasospastic attacks, and coronary vasospasm was induced in LAD, LCX, and RCA by ergonovine provocation. Decreased BMIPP uptake was seen in anterior, interventricular septum, inferior, and apex regions (BMIPP-1). TDS of BMIPP was 19. Decreased MIBG uptake was observed in anterior, lateral, and inferior regions (MIBG-1). TDS of MIBG was 21. After 6 mo of medical treatment, anginal attacks were completely suppressed and vasospasm was not reinduced by ergonovine provocation. TDS and percentage improvement of BMIPP were 4 and 79% (BMIPP-2). Regions of decreased MIBG uptake were alleviated 6 mo after treatment, except in inferior region (MIBG-2). TDS and percentage improvement of MIBG were 10 and 52%. A, B, C, and D indicate basal short-axis, midventricular short-axis, vertical long-axis, and horizontal long-axis images, respectively.

 


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FIGURE 2. BMIPP scintigrams of vasospastic angina before and after medical treatment of 58-y-old man (patient 1 in group I). Patient had spontaneous vasospastic attacks, and coronary vasospasm was induced in LAD, LCX, and RCA by ergonovine provocation. Decreased BMIPP uptake was observed in anterior and inferior regions (BMIPP-1). TDS of BMIPP was 16. Decreased MIBG uptake was seen in anterior, lateral, inferior, and apex regions (MIBG-1). TDS of MIBG was 34. Although anginal attacks were completely suppressed after 6 mo of medical treatment, vasospasm was reinduced in 3 coronary arteries by ergonovine provocation. TDS and percentage improvement of BMIPP were 11 and 31%. TDS and percentage improvement of MIBG were 24 and 29% (BMIPP-2 and MIBG-2). Patient’s percentage improvements of both tracers were lower than those in group II (Fig. 1)

 





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