冠状动脉心肌桥的检出率及临床分析

目的:分析冠状动脉心肌桥的检出率及其临床特点。方法:回顾性分析冠状动脉造影检测出的53例心肌桥病例的临床资料。结果:冠状动脉造影发现心肌桥的检出率为3.29%(53/1610),心肌桥患者并发冠心病的发生率约为26.4%,孤立性心肌桥与心肌桥并发冠心病在传统的冠心病易患因素方面无统计学差异(P0.05),但在收缩期壁冠状动脉狭窄程度与心肌桥长度方面差异有显著统计学意义(P0.01)。结论:经冠状动脉造影,心肌桥的检出率为3.29%,心肌桥患者心肌桥长度与收缩期壁冠状动脉狭窄程度可能是心肌桥并发冠心病的危险因素。     

冠状动脉心肌桥与缺血性心脏病

目的　探讨冠状动脉心肌桥 (心肌桥 )的特征和心肌桥与缺血性心脏病 (IHD)的关系。方法　回顾性分析接受冠状动脉造影的 2 398例患者 ,其中共检出心肌桥 2 2例。结果　心肌桥检出率为 0 92 % ;心肌桥最常出现在左前降支 ;心肌桥段冠状动脉收缩期狭窄是最主要征象 :心肌桥近段冠状动脉粥样硬化检出率为 5 4 5 % ;有心肌桥患者临床均表现出不同程度心绞痛和心肌梗死。结论　冠状动脉收缩期狭窄是心肌桥最主要征象 ;冠状动脉心肌桥可导致缺血性心脏病。     

冠状动脉心肌桥造影特点及临床意义

目的　分析心肌桥在冠状动脉造影中的表现特征并探讨其临床意义。方法　对 870例选择性冠状动脉造影检出的冠状动脉心肌桥的患者临床资料进行回顾性分析。结果　 870例中共检出冠状动脉心肌桥 10例 ,发生率为 1.15 % ,其中 9例为左前降支心肌桥 ,1例在左回旋支 ,收缩期狭窄程度 >5 0 %的有 7例 ,均有心绞痛症状 ,心电图提示有 ST段下移及 T波改变等心肌缺血表现 ,2例合并冠状动脉粥样硬化性心脏病 ,1例合并有心室壁肥厚 ,6例为单纯性心肌桥。结论　冠状动脉造影中心肌桥的检出率较低 ,冠状动脉心肌桥的存在可能导致缺血性心脏病 ,引起心肌缺血及相应心电图改变 ,临床上对有症状的心肌桥患者应当给予积极治疗。     

心肌桥临床特点分析

目的:观察分析心肌桥的临床特征,为临床上心肌桥的正确诊断与治疗提供参考。方法:采用选择性冠状动脉造影方法,检测心肌桥患者120例,男75例,女45例,年龄30~63岁。结果:120例具有胸闷,胸痛,心悸等症状。87例(72.5%)有不同程度的心电图异常;前降支肌桥114例(95%),回旋支肌桥6例(5%)。狭窄Ⅰ级:6例(5%),Ⅱ级:78例(65%),Ⅲ级:36例(30%)。120例中,药物治疗117例,置入支架3例。随访1年,大部分患者症状减轻,无恶化及死亡病例。结论:心肌桥并非罕见现象,随着年龄的增长可出现不同的临床症状,治疗应首选药物治疗。     

冠状动脉心肌桥55例临床分析

目的探讨行选择性冠状动脉造影人群中冠状动脉心肌桥的发生率、临床特点及治疗措施。方法我院2002年6月~2005年7月接受选择性冠脉造影3886例人群中发现冠状动脉心肌桥55例,分析其发生率、临床特点及治疗措施。结果冠状动脉心肌桥发生率为1·5%,除1例为右冠状动脉心肌桥外,其余均为左前降支心肌桥。男性发生率高于女性(P<0·01)。收缩期狭窄30%~99%,平均(55±18)%;肌桥长度15~30mm,平均(24·5±3·5)mm。12例有心绞痛症状,其收缩期狭窄均在75%以上。7例症状较重的患者,在其左前降支心肌桥内植入TAXUS支架后症状消失,其余有症状的病例使用β-受体阻滞剂可缓解心肌桥所致的心绞痛。12例随访1~3年,无一例新发心肌梗死、心脏性猝死及左心功能不全。结论冠状动脉肌桥多发生于左前降支,可致心肌缺血。β-受体阻滞剂可缓解心肌桥所致的心绞痛。冠状动脉内支架术可能是治疗冠状动脉心肌桥安全有效的办法。     

69例冠状动脉心肌桥临床分析

目的　分析冠状动脉造影病人中心肌桥的发生率以及临床特征。方法和结果　 1678例行选择性冠状动脉造影术的人群中 ,共检出心肌桥 69例 ,发生率为 4.11%。均为左冠状动脉前降支 ( L AD)心肌桥。位于 L AD近段 1例 ,中段 5 7例 ,远段 11例。伴有冠心病的心肌桥 13例 ,伴有瓣膜病 3例 ,伴有心肌病 3例 ,无伴随心脏病的孤立心肌桥5 0例。孤立心肌桥中收缩期冠状动脉狭窄程度≥ 70 % 2 5例 ,5 0 %～ 70 % 17例 ,<5 0 % 8例。孤立心肌桥中有胸痛症状 2 5例 ;心电图提示有 ST- T改变 18例 ;行运动负荷试验阳性 18例。 69例心肌桥中超声心动图或左心室造影提示有室壁肥厚 13例。结论　冠状动脉造影是心肌桥的可靠检出手段。心肌桥可伴随其他心脏病发生也可孤立存在。心肌桥引起冠状动脉收缩期的高度狭窄而导致心肌缺血症状、心电图 ST- T变化、运动负荷试验阳性 ,狭窄程度越重 ,上述表现越显著     

壁冠状动脉心肌桥的造影和临床分析

目的:观察、分析壁冠状动脉(冠脉)和心肌桥的临床特点与诊断、治疗方法。方法:观察、分析经冠脉造影确诊的96例109处心肌桥患者的心肌桥分布特点、临床症状、心电图、心肌酶谱、肌钙蛋白T、心脏超声,评价药物或支架治疗心肌桥的疗效。结果:心电图、临床症状、心肌酶谱、肌钙蛋白T和心脏超声对心肌桥的诊断均无特异性。造影发现93.7%的心肌桥发生于冠脉前降支(LAD)。心肌桥患者临床症状与收缩期狭窄程度有关。药物治疗、手术治疗均有一定疗效。结论:冠脉造影发现"收缩期狭窄"为目前确诊心肌桥的主要方法。心肌桥与心绞痛、动脉粥样硬化、心肌梗死的发生有密切关系。药物治疗可选用肾上腺素β受体阻滞剂和Ca2+拮抗剂。     

33例冠状动脉心肌桥临床分析(英文)

目的:观察分析冠状动脉心肌桥患者的临床特征,探讨其治疗方法。方法:回顾性分析2011年1月至2013年1月在我院接受选择性冠状动脉造影340例患者的临床资料。结果:在340例行冠状动脉造影患者中,发现冠状动脉心肌桥33例(9.70%),其中29例为孤立性心肌桥患者,4例伴有冠状动脉粥样硬化样改变。31例(93.9%)位于左前降支(LAD),1例(3.03%)位于第一对角支(D1),1例(3.03%)位于左回旋支(LCX)。按Noble狭窄程度分级:1级有19例(57.6%),2级有12例(36.4%),3级有2例(6.06%)。16例(48.5%)有典型心绞痛症状,15例(45.5%)为胸闷,2例(6.06%)表现为心悸。19例(57.6%)心电图或/和动态心电图有ST-T或T波改变。所有患者均应用β-受体阻滞剂或/和非二氢吡啶类钙通道阻滞剂治疗,29例(87.8%)患者症状改善。结论:心肌桥的临床症状表现多种多样,非二氢吡啶类钙离子拮抗剂及β-受体阻滞剂可缓解大多数心肌桥引起的临床症状。     

35例心肌桥心电图的临床分析

目的探讨心肌桥的冠状动脉造影特点和心电图的变化。方法回顾性分析冠状动脉造影中35例心肌桥的临床表现及冠状动脉造影和心电图的特点。结果冠状动脉造影心肌桥的检出率为1％，均位于左前降支，其中1级狭窄5例，2级狭窄12例，3级狭窄18例，16例病人伴有冠状动脉粥样硬化样改变。金部病例均有临床症状，23例有心电图ST-T改变，运动试验阳性8例，可疑阳性5例，3例病人出现与相关心肌桥无关的下壁心肌梗死。16例病人随访0．5～3年，无1例发生与相关血管有关的急性心肌梗死、心源性猝死和急性心衰。结论冠状动脉心肌桥可能导致心肌缺血，引起心绞痛，但预后良好。     

冠状动脉造影检查对心肌桥的诊断价值

目的 探讨冠状动脉造影检查对心肌桥诊断的应用,研究心肌桥和冠状动脉粥样硬化的相关性.方法 收集1523例患者冠状动脉造影检查资料,分析心肌桥检出率,观察心肌桥的发生位置、壁冠状动脉收缩期狭窄程度、心肌桥血管合并粥样斑块的位置、斑块处管腔狭窄程度.结果 全部1523例患者中,201例患者检查结果正常,1225例患者检出粥样斑块,231例患者检出心肌桥.心肌桥检出率为15.2％,共检出心肌桥235处.心肌桥位置：右冠状动脉1处,左主干1处,旋支1处,对角支3处,左前降支229处,以左前降支中段多见,壁冠状动脉收缩期轻度狭窄为主.纯心肌桥97例.134例患者心肌桥血管合并粥样斑块144处,斑块位置：心肌桥近端111处,心肌桥段19处,心肌桥远端14处.心肌桥近端血管粥样硬化较心肌桥段、心肌桥远端发生率高,但粥样斑块的形成与壁冠状动脉收缩期的狭窄程度无显著相关（P＞0.05）.结论 心肌桥多见于左前降支中段血管,壁冠状动脉收缩期多为轻度狭窄,血管合并粥样硬化,多见于心肌桥前端,但粥样斑块的形成与壁冠状动脉收缩期狭窄程度无明显相关性.冠状动脉造影检查对心肌桥及心肌桥合并粥样硬化的诊断有重要价值.     

冠状动脉心肌桥及其临床意义

目的　探讨冠状动脉造影的病人中心肌桥的发生率及其临床意义。方法和结果　 2 557例行冠状动脉造影术的人群中 ,共检出心肌桥 1 7例 ,发生率为 0 665% ,均为左前降支心肌桥。收缩期狭窄程度 >50 %的有 1 4例 ,均有心绞痛症状 ,心电图提示有ST段移位、T波改变等心肌缺血表现 ;5例行心肌核素显像的病人提示有前壁心肌缺血。有 1例患者为陈旧前壁心肌梗塞 ,心肌桥于收缩期致 1 0 0 %血流阻断。 1 7例病人中有 3例左心室造影提示有室壁肥厚。结论　冠状动脉造影中的心肌桥现象并非罕见。心肌桥的存在可引起心肌缺血及相应的心电图、核素心肌显像缺血改变 ,严重的心肌桥压迫可引起心肌梗塞。     

心肌桥和心肌桥近端合并严重动脉粥样硬化病变的介入治疗疗效观察

目的通过与心肌桥本身介入治疗疗效的比较,观察心肌桥近端血管严重动脉粥样硬化病变的介入治疗疗效。方法试验组选择心肌桥近端动脉粥样硬化并严重狭窄（≥70％）者28例（A组）,对照组选择有症状的单纯心肌桥改变且收缩期严重狭窄（≥195％）者16例（B组）和单纯前降支动脉粥样硬化严重狭窄（≥70％）者54例（C组）,应用普通冠状动脉支架介入治疗。结果三组均成功行介入手术,三组支架置入后的血管内径及支架长度比较差异无统计学意义。A组6个月内4例（14．3％）再狭窄,B组6个月内7例（43．7％）出现再狭窄,C组8例（14．8％）再狭窄,A组和c组的再狭窄率差异无统计学意义,但均显著低于B组（P〈0．05）。三组中再狭窄患者均再次接受介入治疗。结论心肌桥近端严重动脉粥样硬化病变的介入治疗疗效未受心肌桥近端异常血流动力学的影响。但心肌桥病变本身的介入治疗远期再狭窄率较高。     

Myocardial bridge - congenital anomaly of coronary vasculature.

Coronary artery lumen compression during systole by a myocardial bridge can cause myocardial ischemia and even necrosis. Myocardial bridges represent a variant of norm or congenital anomaly of coronary vasculature. They belong to relatively frequent autopsy findings (5.4-85.7%) and are most often located over left anterior descending artery. Main angiographic sign of myocardial bridging is effect of contrast medium pushing out during narrowing of intramural part of a coronary artery during systole. In most cases systolic coronary artery narrowing not associated with any symptoms and bridging is just accidentally found at angiography. However some bridges produce clinical manifestations such as angina pectoris or myocardial infarction which require drug treatment. Therapy failures are managed by stenting or surgery. Under certain conditions systolic coronary artery narrowing can cause sudden death therefore all patients with clinically overt myocardial bridges should be under continuous medical surveillance. A case of clinically successful open heart supracoronary myotomy in a patient with myocardial ischemia due to a bridge causing 80% systolic narrowing of the left anterior descending coronary artery is presented.     

Clinical and angiographic profile and follow-up of myocardial bridges: a study of 21 cases

Myocardial bridging describes an angiographic entity, which is any degree of systolic narrowing of a coronary artery observed in at least one angiographic projection. Among the cineangiograms of 3200 patients reviewed, there were 21 cases (19 males) of myocardial bridges--incidence of 0.6 percent. Of these, seven had hypertrophic cardiomyopathy, six had atherosclerotic coronary artery disease and remaining eight had no evidence of either. All 21 patients had myocardial bridges in proximal or mid left anterior descending coronary artery. In addition, one case of hypertrophic cardiomyopathy had whole posterior descending coronary artery under a myocardial bridge. Another case of hypertrophic cardiomyopathy had a short normal segment of 5 mm inside a long myocardial bridge of 35 mm (tandem myocardial bridges). The length of the bridges varied from 10 to 35 mm (mean 24.5 +/- 4.5 mm) and diameter stenosis during systole varied from 40-90 percent (mean 70 +/- 8%). Two patients had large saccular coronary aneurysms proximal to the muscle bridge. Four of the eight patients who had neither hypertrophic cardiomyopathy nor coronary artery disease presented with acute anterior wall myocardial infarction and three of them had regional wall motion abnormality of left descending territory. Of the six patients who had coronary artery disease, one had 60 percent left descending artery lesion and two had recanalized segments proximal to the bridge. Five of the above six patients had significant stenosis of other coronary vessels. Four patients were lost to follow-up (mean period 3.4 +/- 2 years). In the coronary artery disease group, one patient underwent coronary artery bypass graft surgery for 3-vessel disease including graft to left descending artery and one developed inferior wall myocardial infarction. The patients in the hypertrophic cardiomyopathy group and "no hypertrophic cardiomyopathy-no coronary artery disease" group were free of events at last follow-up. Long-term prognosis of isolated myocardial bridges appears to be excellent. Degree of systolic narrowing or length of myocardial bridge does not correlate with event rates on follow-up.     

CT冠状动脉成像在诊断心肌桥及壁冠状动脉中的价值

目的探讨64排螺旋CT（64SCT）冠状动脉成像在诊断心肌桥及壁冠状动脉的应用价值。方法回顾性分析64SCT冠状动脉成像患者230例,统计心肌桥的检出率、部位、厚度、壁冠状动脉狭窄程度,分析其与临床症状的关系。结果在230例进行64SCT冠状动脉成像患者中,发现心肌桥53例（共60处）,检出率为23．04％（53／230）,与CAG的检出率（5．2％）比较差异有统计学意义（P〈0．05）,64SCT中仅有13支与CAG发现的14支心肌桥一致。浅表型肌桥和深在型肌桥在厚度、壁冠状动脉狭窄程度及临床症状均有统计学差异（P〈0．05）。结论64SCT冠状动脉成像是一种无创、较为准确诊断心肌桥的手段。     

Myocardial bridges in man: Clinical correlations and angiographic accentuation with nitroglycerin

Little is known of the clinical significance of myocardial bridges, which may be recognized angiographically as systolic coronary artery narrowing (SCAN). A retrospective review of a 1 year's experience (313 consecutive coronary arteriograms) revealed 5 patients with SCAN, an incidence of 1.6%. SCAN involved the proximal and/or middle segments of the left anterior descending coronary artery in all patients. It is of particular note that the administration of nitroglycerin noticeably accentuated the SCAN phenomenon in each of 3 patients to whom it was administered. Four of the 5 patients had left ventricular hypertrophy due to hypertrophic car-diomyopathy (2), aortic stenosis (1), and hypertension (1). All 5 patients with the SCAN phenomenon had anginal chest pains, and critical obstructive coronary atherosclerosis was observed in only 2 cases. The other 3 patients showed, otherwise, normal coronary arteriograms. Thus, myocardial bridges appear to be angiographically manifest predominantly in patients with cardiac hypertrophy. Nitroglycerin, which accentuates SCAN, might be useful as a provocative test to enhance the angiographic recognition of this phenomenon. The possible role of myocardial bridges in the production of myocardial ischemia warrants further investigation.     

心肌桥对冠状动脉粥样硬化的作用

目的:探讨心肌桥与冠状动脉粥样硬化病变之间的关系。方法:回顾性分析冠脉造影术中检出的心肌桥患者92例的冠脉病变与临床资料。结果:1500例冠脉造影患者检出心肌桥92例,检出率6.1%;心肌桥近段冠状动脉粥样硬化病变发生率71.7%,远段冠状动脉粥样硬化病变发生率10.9%,两者差异有显著性（P<0.01）。结论:心肌桥可能导致冠状动脉心肌桥近段冠脉粥样硬化病变。     

Myocardial bridge of the left anterior descending coronary artery and myocardial infarction: does coronary spasm play a part?]

The association of a myocardial bridge of the left anterior descending (LAD) coronary artery and myocardial infarction is rare. The mechanisms by which the myocardial bridge could predispose to myocardial infarction are tachycardia (reducing the duration of diastolic coronary filling), thrombosis at the site of the myocardial bridge, and coronary spasm which, however, has never been demonstrated in the context of infarction. The aim of this study was to detect coronary spasm by provocative ergometrine testing in 4 patients, all male, aged 21 to 49 years, average 39 years old, who had anterior myocardial infarction associated with myocardial bridging of the LAD artery without atheromatous coronary stenosis. The ergometrine tests were performed during (2 cases) or after coronary angiography (2 cases). The systolic narrowing due to the myocardial bridge ranged from 25 to 95% (average 70%). The ergometrine test was strongly positive in 1 patient and negative in the other 3. Repermeabilisation of a thrombus was suggested in these 3 patients by the recording of an accelerated idioventricular rythm in the acute phase of infarction (2 cases) or by the demonstration of abnormal platelet aggregation (1 case). This is the first report of coronary spasm in a patient with myocardial bridging associated with infarction. However, it is not possible to determine the respective roles of spasm and myocardial bridging in the genesis of the infarct. We suggest systemic provocative ergometrine testing in this situation to orientate the most appropriate treatment.