Kim Jin Won, Park Chang Gyu, Suh Soon Yong, Choi Cheol Ung, Kim Eung Joo, Rha Seung-Woon, Seo Hong Seog, Oh Dong Joo
Cardiovascular Center, Korea University, Guro Hospital, Seoul, Republic of Korea.
Am J Cardiol. 2007 Oct 1;100(7):1083-6. doi: 10.1016/j.amjcard.2007.05.030. Epub 2007 Jul 18.
The longstanding compression-relaxation effects of myocardial bridging may produce endothelial dysfunction by direct stress on the endothelium. We tested the hypothesis that myocardial bridging induces endothelial dysfunction and subsequently increases the risk of coronary spasm and investigated the symptomatic response to medication in patients with documented myocardial bridging and coronary spasm. In 81 patients with myocardial bridging (44 men; mean age 57.2 years) and 195 control patients without bridging and atherosclerotic lesions confirmed by angiography (97 men; mean age 58.4 years), spasm provocation testing was done by incremental acetylcholine infusion into the left coronary artery. Spasm was documented in 62 of 81 patients with bridging and in 31 of 195 controls (p <0.001). A focal spasm was limited to the bridging segments compared with controls (p <0.001). In conclusion, the results of this study showed that myocardial bridging increased the risk of coronary spasm by endothelial dysfunction in the bridging segment.
心肌桥长期的压迫-舒张效应可能通过对内皮的直接应力而导致内皮功能障碍。我们检验了心肌桥诱发内皮功能障碍并随后增加冠状动脉痉挛风险这一假说，并研究了有记录的心肌桥和冠状动脉痉挛患者对药物治疗的症状反应。在81例心肌桥患者（44例男性；平均年龄57.2岁）和195例经血管造影证实无桥接及动脉粥样硬化病变的对照患者（97例男性；平均年龄58.4岁）中，通过向左冠状动脉递增注入乙酰胆碱进行痉挛激发试验。81例有桥接患者中有62例出现痉挛，195例对照中有31例出现痉挛（p<0.001）。与对照组相比，局灶性痉挛局限于桥接节段（p<0.001）。总之，本研究结果表明，心肌桥通过桥接节段的内皮功能障碍增加了冠状动脉痉挛的风险。
