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作 者:严卫[1] 马建英[1] 王健生[1] 王齐兵[1] 葛均波[1] 陈灏珠[1]
机构地区:[1]复旦大学附属中山医院心内科,上海市心血管病研究所,上海200032
出 处:《老年医学与保健》2007年第3期163-164,171,共3页Geriatrics & Health Care
摘 要:目的探讨有症状心肌桥患者的若干促发因素。方法回顾性检索冠脉造影诊断的心肌桥患者。结果947例次心肌桥中,累及前降支(LAD)者97.88%,最常见的伴随性心脏疾病为高血压及冠心病。这两组患者的室间隔及左室后壁厚度与正常对照组之间的差别有统计学意义(P<0.001)。结论促发心肌桥患者产生症状的因素为血管内血液流变学改变(冠心病时心肌桥前段动脉狭窄及桥后段血流储备减少);血管外因素为室间隔肥大从背侧,左室肥厚从左侧挤压壁冠状动脉,高血压时则释放儿茶酚胺刺激心肌细胞蛋白质合成,血管紧张素Ⅱ及醛固酮还可使心肌细胞间的胶元组织增生,加重压迫壁冠状动脉,心肌桥细胞也可增生。Objective To investigate the risk factors of symptomatic myocardial bridging. Methods This is a retrospective study. Coronary artery angiography was used for evaluation of myocardial bridging. Results 947 cases/incidences of symptomatic myocardial bridging were diagnosed, and the LAD involvement was 97.88%. The most common concomitant diseases were hypertension and coronary heart disease (CHD). The thickness of septum and left ventricular rear wall of patients with hypertension and CHD were higher than that of normal control (P〈0.001). Conclusions The risk factors of symptomatic n, yocardial bridging include intravascular factors such as stenosis of proximal myocardial hridging and/or atherosclerosis, and extravascular factors such as left ventricular and/or septum hypertrophy from left and rear compressing mural coronary, artery. In hypertension, the release of catecholamine results in synthesis of protein in myocardial cells. Angioteusin II and aldosterone cause proliferation of collagen filament. These factors can aggravate the compression of mural coronm'y artery and proliferation of cells of myocardial hridging.
关 键 词:冠状血管畸形 高血压 冠状动脉疾病 冠状动脉狭窄
分 类 号:R541.1[医药卫生—心血管疾病] R544.1[医药卫生—内科学]
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