Study on the Pathogenesis of Coronary Artery Spasm

本研究就冠状动脉痉挛的发病机制明确了以下几点：冠状动脉痉挛的发作多发生在午夜至清晨，通常不是由白天的运动引起的。在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，在年轻受试者中引起血管造影正常的冠状动脉扩张，而在老年受试者中，它收缩了大多数血管造影正常的冠状动脉。几乎所有有不规则或狭窄（明显动脉粥样硬化）的冠状动脉在乙酰胆碱作用下收缩。冠状动脉内注射乙酰胆碱可引起冠状动脉痉挛。因此，本研究强烈表明，成人受试者的大多数冠状动脉参与动脉粥样硬化，即使它们在血管造影上表现正常。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）呈剂量依赖性地扩张离体人冠状动脉。但它的作用方式不同于钙拮抗剂地尔硫卓或硝酸甘油。变异性心绞痛患者24小时Mg潴留明显高于对照组（621.0% vs 31.14%, p<0.01）。这表明许多变异型心绞痛患者存在缺镁，提示缺镁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。20例变异性心绞痛患者中，静脉输注Mg 0.54 mEg/kg可抑制14例（70%）过度通气所致的心绞痛发作（p < 0.01）。因此，镁可作为治疗或预防冠状动脉痉挛的药物。

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.