1988 Fiscal Year Final Research Report Summary
Study on the Pathogenesis of Coronary Artery Spasm
| Project/Area Number |
62480218
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Kumamoto University |
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Principal Investigator |
YASUE Hirofumi Kumamoto University Hospital, 医学部附属病院 (40174502)
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| Co-Investigator(Kenkyū-buntansha) |
FUJII Hiromi Kumamoto University Hospital, 保健管理センター, 助手 (40199295)
MATSUYAMA Koshi Kumamoto University Hospital, 医学部附属病院, 助手 (00190546)
OGAWA Hisao Kumamoto University Hospital, 医学部附属病院, 助手 (50177135)
OKUMURA Ken Kumamoto University Hospital, 医学部附属病院, 講師 (20185549)
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| Project Period (FY) |
1986 – 1988
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| Keywords | Coronary Artery Spasm / Acetylcholine / Atherosclerosis / マグネシウム |
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| Research Abstract |
The present study clarified the following points concerning the pathogenesis of coronary artery spasm.
1. The attacks of coronary spasm occur most often from midnight to early morning and is usually not induced by exercise in the daytime. Intracoronary injection of acetylcholine (ACH), the neurotransmitter of the parasympathetic nervous system and an endothelium-dependent vasodilator, caused dilatation of angiographically normal coronary arteries in the younger subjects, whereas it constricted most of the angiographically normal coronary arteries in the older subjects. Nearly all coronary arteries with irregularities or stenoses (evident atherosclerosis) constricted in response to ACh. Intracoronary injection of ACh induced coronary spasm in most patients with coronary spasm. Thus, the present study strongly suggests that most of coronary arteries in adult subjects are involved in atherosclerosis even though they appear normal angiographically. the present study also indicates that coronary atherosclerosis is a prerequisite for the development of coronary spasm.
2. Mg (1.0-8.0 mm) dilated isolated human coronary arteries dose-dependently. But its mode of action was different from that of either diltiazem, a Ca antagonist, or nitroglycerin. Twenty four hour retention of Mg was significantly increased in patients with variant angina as compared with the control subjects (62 21% vs 31 14%, p<0.01). This indicates that mg deficiency exists in many patients with variant angina and suggests that Mg deficiency may be involved in the pathogenesis of coronary spasm in some patients with variant angina. Intravenous infusion of Mg 0.54 mEg/kg suppressed hyperventilation-incuced attacks in 14 (70%) of the 20 patients with variant angina (p < 0.01). Thus, Mg may be used as a therapeutic or preventive agent for coronary spasm.
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