Study on the Pathogenesis of Coronary Artery Spasm

本研究阐明了以下几点关于冠状动脉痉挛的发病机制.冠状动脉痉挛的发作最常发生在午夜至清晨，通常不是由白天的运动引起的。冠状动脉内注射乙酰胆碱（ACH），副交感神经系统的神经递质和内皮依赖性血管扩张剂，导致扩张血管造影正常的冠状动脉在年轻的受试者，而它收缩了大多数血管造影正常的冠状动脉在老年受试者。几乎所有不规则或狭窄的冠状动脉（明显的动脉粥样硬化）都会对ACh产生反应。冠状动脉痉挛患者多为冠状动脉内注射ACh引起的冠状动脉痉挛。因此，本研究有力地表明，大多数成年受试者的冠状动脉参与动脉粥样硬化，即使他们出现正常的血管造影。本研究还表明冠状动脉粥样硬化是冠状动脉痉挛发生的先决条件. Mg（1.0-8.0 mm）可剂量依赖性地扩张离体人冠状动脉。但其作用方式与钙拮抗剂地尔硫卓或硝酸甘油不同。变异型心绞痛患者24小时镁潴留率显著高于对照组（6221%比3114%，P<001）。提示变异型心绞痛患者中存在镁缺乏，镁缺乏可能参与了部分变异型心绞痛患者冠状动脉痉挛的发病机制。静脉输注镁0.54mEg/kg对20例变异型心绞痛患者中14例（70%）的过度通气发作有抑制作用（P < 0.01）。因此，Mg可用作冠状动脉痉挛的治疗剂或预防剂。

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.