International Collaboration Study on the Racial Difference in Coronary Vasospasm

1. 我们已经证明rho激酶实质上参与了冠状血管痉挛的分子机制。我们已经证明rho激酶不仅参与心外膜血管痉挛的分子机制，也参与微血管痉挛的分子机制。我们已经证明，长期抑制rho激酶可导致冠状动脉硬化和冠状血管痉挛的消退。我们已经确定了rho激酶的新SNP， G930T在其催化区域，并证明了该SNP与rho激酶活性的增强有关。我们已经证明，t930等位基因在冠状血管痉挛患者中的频率明显高于没有痉挛或对照的患者。我们进一步证明，这种SNP在白种人心绞痛患者中不存在。综上所述，这些结果表明G930T相对较高的频率可以解释，至少部分地，日本和高加索人群在冠状动脉痉挛患病率上的种族差异。我们发表了关于rho激酶治疗重要性的英文综述。

1. We have demonstrated that Rho-kinase is substantially involved in the molecular mechanism for coronary vasospasm.2. We have demonstrated that Rho-kinase is substantially involved in the molecular mechanism fornot only epicardial vasospasm but also microvascular vasospasm.3. We have demonstrated that long-term inhibition of Rho-kinase causes a regression of both coronary arteriosclerosis and coronary vasospasm.4. We have identified the novel SNP of Rho-kinase, G930T in its catalytic domain and have demonstrated that this SNP is associated with an enhancement of Rho-kinase activity.5. We have demonstrated that the frequency of the T930allele is significantly higher in patients with coronary vasospasm than in those without the spasm or controls. We have further demonstrated that this SNP is not noted in Caucasian patients with angina pectoris.6. Taken together, those results suggest that the relatively higher frequency of G930T could explain, at least in part, the racial difference in the prevalence of coronary vasospasm between Japanese and Caucasian populations.7. We have published the English review regarding the therapeutic importance of Rho-kinase.