摘要
当冠状动脉粥样硬化性心脏病发生时,动脉内的粥样硬化导致狭窄并使局部心肌血流量减少,这种缺血的过程可导致心肌细胞的收缩及舒张功能受损,并逐渐出现运动状态异常,进而呈现室壁节段性运动异常。这种病理生理过程在冠脉三支血管病变中应表现得更为明显,继而表现为心室壁节段运动的异常。但在部分患者中,其心室壁运动反而呈现出正常运动。结合冠心病的危险因素及其病理生理改变,考虑冠脉三支血管病变但心室壁运动正常的原因有:缺血预适应及侧枝循环的形成等。冠脉三支血管病变患者是一种较普通冠心病更为广泛、弥散,更为严重的病变,当超声心动图提示心室壁节段运动正常,便容易在就诊时导致诊断上的疏漏,并最终造成个人家庭及社会的严重损失,因此,此类病变应引起我们的高度重视。
目的:探讨冠状动脉三支血管病变合并心室壁运动正常的病例的临床特点;及与心室壁运动异常病例相对照,探寻可能导致心室壁运动正常的因素。
方法:自2011年01月01日至2011年12月31日期间就诊于我院并行冠状动脉造影术的病例中筛出冠状动脉三支血管病变病例141例,其中,心室壁运动正常的有47例(A组),心室壁运动异常的有94例(B组)作为对照,记录两组冠心病患者的临床因素,并结合Gensini评分系统,运用SPSS17.0软件分别对其临床因素进行总体及分层对比,分析冠脉三支病变的临床特点及两组病例的差异对比。
结果:两组患者的各年龄段百分比仍然不存在统计学差异(P=0.749)。其中心室壁运动正常组(A组)与心室壁运动异常组(B组)患者中年龄位于30-49岁的患者比例分别为16.6%vs.14.9%。而在50-69岁年龄段,A组与B组的比例分别为63.8%vs.58.5%。。两组患者首次发生心绞痛时间的构成比例存在统计学差异(P<0.05)。A组患者中发病24小时以内的比例大于B组患者(25.5%vs10.5%)两组EF值分段构成的比较中,A组患者EF值多位于正常范围(76.6%vs.57.4%),而B组的患者中,EF值轻度下降的比例较正常组大(35.1%vs14.9%)。A组患者的侧枝循环形成率的在Gensini积分位于100-149分时更高(75%vs.16.7%,P<0.05);而在积分100-149分时B组患者的吸烟率更高(25%vs.83.3%,P<0.05)。
结论:
室壁运动正常的三支血管病变患者,其超声心动图的EF值更易表现为正常。存在侧枝循环的或不吸烟的严重三支血管病变患者,其超声心动图更易表现为室壁节段运动正常。
As the occurrence of coronary atherosclerotic heart disease, atherosclerosis within theartery leads to stenosis and regional myocardial blood flow reduction. The process ofischemia can result in impaired systolic and diastolic function of the myocardial cells, andthe gradual emergence of movement abnormal state, thus showing regional wall motionabnormality. This pathophysiological process in the coronary tri-vessel disease should bemore obvious, and then ventricular wall motion abnormalities perform. However, in somepatients, ventricular wall motion shows a normal movement. To associate with coronaryheart disease risk factors and pathophysiological changes, consider the reason to thecoronary tri-vascular disease with normal ventricular wall motion may: the limitations of thecolor Doppler Echocardiography, ischemic preconditioning and the formation of cardiaccollateral circulation. coronary tri-vessel disease proves a kind of more widely dispersed, andmore serious disease, but binding with normal performance of the ventricular wallmovement in echocardiography, it seems more likely to result in diagnostic omissions, andeventually lead to serious losses for individuals, their families and society, and thereforesuch a disease should be worthy of being paid our much more attentions.
Objective: To investigate the clinical features of cases with coronary tri-vessel diseasecombined with normal ventricular wall motion; and contrast with the ventricular wall motionabnormality cases, to explore the factors may result in normal ventricular wall motion.Methods: Screen out141cases with coronary tri-vessel disease from January1,2011to31December2011, including47patients with normal ventricular wall motion (group A), andventricular wall motion abnormalities94cases (group B) as a control. Record two groups ofpatients with clinical characteristics, combined with the Gensini score system, to deal withthe clinical factors by the overall and stratified contrast with SPSS17.0software, analyzeclinical features of coronary three-vessel disease, and the reasons that causing the differencesof these two groups.
Results: The percentage of all ages of the patients were no significant difference (P=0.749). the proportions in normal wall motion group (group A) and abnormal ventricularwall motion group (B) at30-49years of age were16.6%vs.14.9%, in the50-69years agegroup, the proportions were63.8%vs.58.5%, respectively. For the composition ratio of the first time angina pectoris, in group of less than24hours of onset, the proportion of patientsin group A was larger than that in group B patients (25.5%vs10.5%,P<0.05). A comparisonof two groups’ EF value composition ratio, patients’ EF values in group A were most locatedin the normal range (76.6%vs.57.4%), while the proportion of EF value that slightlydecreased in group B was higher than normal group (35.1%vs14.9%, P<0.05). Cardiaccollateral circulation rate in group A was higher than group B in the Gensini score of100-149points (75%vs.16.7%, P<0.05); and group B had a higher smoking rates in100-149points than group A(25%vs.83.3%, P <0.05).
Conclusion: For the patients of severe triple-vessel disease with cardiac collateralcirculation or non-smoking, their cardiac ventricular wall motion is more inclined to performnormal. EF values in patients with normal cardiac ventricular wall motion are more likely toshow normal.
引文
[1] Hamm CW, Bassand JP, Agewall S, et al. ESC Guidelines for the management of acutecoronary syndromes in patients presenting without persistent ST-segment elevation[J].Eur Heart J,2011,32(23):2999-3054.
[2] Murray CJ, Lopez AD. Alternative projections of mortality and disability by cause1990–2020: Global Burden of Disease Study [J]. Lancet1997;349:1498–1504.
[3] Roberts KB, Califf RM, Harrell Jr FE, Lee KL, Pryor DB, Rosati RA. The prognosis forpatients with new-onset angina who have undergone cardiac catheterization [J].Circulation1983;68:970.
[4] Wallentin L, Lagerqvist B, Husted S, et al. Outcome at1year after an invasive comparedwith a non-invasive strategy in unstable coronary-artery disease: the FRISC II invasiverandomised trial. FRISC II investigators. fast revascularisation during instability incoronary artery disease[J]. Lancet2000;356:9.
[5] Andersen HR, Nielsen TT, Rasmussen K, et al. A comparison of coronary angioplastywith fibrinolytic therapy in acute myocardial infarction[J]. N Engl J Med2003;349:733.
[6]张维东,吕树铮,吴学思,等.642例冠心病患者冠脉造影结果分析[J].心肺血管病杂志,2002,21(2):78-79.
[7]田作军,邓宇,陆亚琴等,影响灌装动脉粥样硬化的程度及病变支数的常见危险因素[J].广东医学,2010,31(22):2903-2906.
[8]牛海芳,车京津,邵元霞,等.早发严重冠状动脉三支病变患者冠心病危险因素的分布及聚集[J].中华心血管杂志,2011,39:41-42.
[9]鄢盛恺.冠心病的危险因素及其临床应用价值[J].中华检验医学杂志,2001,24(6):384-386.
[10]Kitler ME. Differences in men and women in coronary artery disease, systemichypertension and their treatment [J]. Am J Cardiol,1992,70(11):1077-1080.
[11]Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint NationalCommittee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure:the JNC7report [J]. JAMA,2003,289(19):2560-2572.
[12]杜保民,陆宗良,武阳丰,等.中国冠心病二级预防研究一老年高血压人群的干预结果分析[J].中华老年心脑血管病杂志,2006,8(2):82-86.
[13]Hammound T, Tanguay JF, Bourassa MG. Management of coronary artery disease:therapeutic options in patients with diabetes [J]. J Am Coll Cardiol.2000;36:355-365.
[14]Bonow RO, Gheorghiade M. The diabetes epidemic: a national and global crisis[J]. AmJ Med.2004;116(suppl5A):2S-10S.
[15]Creager MA, Luscher TF, Cosentino F, Beckman JA. Diabetes and vascular diseasepathophysiology, clinical consequences, and medical therapy: part I.[J]. Circulation.2003;108:1527-1532.
[16]Lee CD, Folsom AR, Pankow JS, Brancati FL; Atherosclersosis Risk in Communities(ARIC) Study Investigators. Cardiovascular events in diabetic and nondiabetic adultswith or without history of myocardial infarction [J]. Circulation.2004;109:855-860.
[17]Haffner SM, Lehto S, Ronnemaa T, Pyorala K, Laakso M. Mortality from coronary heartdisease in subjects with type2diabetes and in nondiabetic subjects with and withoutprior myocardial infarction[J]. N Engl J Med.1998,(339):229-234.
[18]Sprafka JM, Burke GL, Folsom AR, McGovern PG, Hahn LP. Trends in prevalence ofdiabetes mellitus with myocardial infarction and effect of diabetes on survival: theMinnesota heart survey [J]. Diabetes Care.1991;14:537-543.
[19]Mak KH, MoliternoDJ, Granger CB, et al; GUSTO-I Investigators. Influence of diabetesmellitus on clinical outcome in the thrombolytic era of acute myocardial infarction [J]. JAm Coll Cardiol.1997;30:171-179.
[20]Waller BF, Palumbo PJ, Lie JT, et al. Status of the coronary arteries at necropsy indiabetes mellitus with onset after age30years: analysis of229diabetic patients with andwithout clinical evidence of coronary heart disease and comparison to183controlsubjects [J]. Am J Med.1980;69:498-506.
[21]Lemp GF, Vander Zwaag R, Hughes JP, et al. Association between the severity ofdiabetes mellitus and coronary arterial atherosclerosis [J]. Am J Cardiol.1987;60:1015-1019.
[22]Ledru F, Ducimetiere P, Battaglia S, et al. New diagnostic criteria for diabetes andcoronary artery disease: insights from an angiographic study [J]. J Am Coll Cardiol.2001;37:1543-1550.
[23]Burchfiel CM, Reed DM, Marcus EB, et al. Association of diabetes mellitus withcoronary atherosclerosis and myocardial lesions: an autopsy study from the HonoluluHeart Program [J]. Am J Epidemiol.1993;137:1328-1340.
[24]Goraya TY, Leibson CL, Palumbo PJ, et al. Coronary atherosclerosis in diabetesmellitus: a populationbased autopsy study [J]. J AmColl Cardiol.2002;40:946-953.
[25]Woodfield SL, Lundergan CF, Reiner JS, et al; GUSTO-I Angiographic Investigators.Angiographic findings and outcome in diabetic patients treated with thrombolytictherapy for acute myocardial infarction: the GUSTO-1experience [J]. J Am Coll Cardiol.1996;28:1661-1669.
[26]Mak KH, Faxon DP. Clinical studies on coronary revascularization in patients with type2diabetes [J]. Eur Heart J.2003;24:1087-1103.
[27]Moreno PR, Murcia AM, Palacios IF, et al. Coronary composition and macrophageinfiltration in atherectomy specimens from patients with diabetes mellitus [J].Circulation.2000;102:2180-2184.
[28]Abaci A, Oguzhan A, Kahraman S, et al. Effect of diabetes mellitus on formation ofcoronary collateral vessels[J]. Circulation.1999;99:2239-2242.
[29]Hermiller JB, Tenaglia AN, Kisslo KB, et al. In vivo validation of compensatoryenlargement of atherosclerotic coronary arteries [J]. Am J Cardiol.1993;71:665-668.
[30]Vavuranakis M, Stefanadis C, Toutouzas K, et al. Impaired compensatory coronaryartery enlargement in atherosclerosis contributes to the development of coronary arterystenosis in diabetic patients: an in vivo intravascular ultrasound study [J]. Eur Heart J.1997;18:1090-1094.
[31]Pipe A L,Papadakis S,Reid R D. The role of smoking cessation in the prevention ofcoronary artery disease[J]. Curr Atheroscler Rep,2010,12(2):145-150.
[32]赵菁,胡大一,丁荣晶,等.青年吸烟冠心病患者冠状动脉病变特点和术后控烟干预[M].第十五届全国控制吸烟学术研讨会.2011;237-238.
[33]Genest J.Liporotein disorders and cardiovascular risk [J]. Inherit Metab Dis,2003,26(2-3):267-287.
[34]王薇,赵冬,孙佳艺,等.中国11省市队列人群危险因素与不同类型心血管病发病危险的比较[J].中华心血管病杂志,2006,34(12):1133-1137.
[35]Feron O, Dessy C, Moniotte S, et al. Hypercholesterolemia decreases nitric oxideproduction by promoting the interaction of caveoli and endothelial nitric oxide synthase[J]. J Clin Invest,1999,103:897-905.
[36]Sasayama S, Fujita M. Resent Insight into coronary collateral circulation [J]. Circulation,1992,85:1197-1204.
[37]Abdulmassih S,Iskandrian,Jaekyeong H.Identification of high-risk patients with leftmain and three-vessel coronary artery disease using stepwise discriminant analysis ofclinical,exercise,and tomographic thallium data [J].American Heart Journal,1993,125(1):221-225.
[38]Gaitonde RS, Sharma N, Ali-Hasan S, et al. Prediction of significant left main coronaryartery stenosis by the12-lead electrocardiogram in patients with rest angina pectoris andthe withholding of clopidogrel therapy [J]. Am J Cardiol2003;92:846–848.
[39]Kosuge M, Kimura K, Ishikawa T,et al. Predictors of left main or three-vessel disease inpatients who have acute coronary syndromes with non-ST-segment elevation [J]. Am JCardiol2005;95:1366–1369.
[40]Nikus KC, Eskola MJ, Virtanen VK, et al. ST-depression with negative T waves in leadsV4-V5—a marker of severe coronary artery disease in non–ST elevation acute coronarysyndrome: a prospective study of angina at rest, with troponin, clinical, electroca-rdiographic, and angiographic correlation [J]. Ann Noninvasive Electrocardiol2004;9:207.
[41]Nikus KC, Eskola MJ, Sclarovsky S, et al. Electrocardiographic presentations of leftmain or severe triple vessel disease in acute coronary syndromes—an overview [J].Journal of Electrocardiology.2006,(39):S68–S72.
[42]杨光,李飞.异常Q波对非急性期冠脉三支病变的诊断价值[J].中华心血管病杂志2005,(33).
[43]Shen ZQ, Palma A, Rajachandran M, et al. Prediction of single and multivesselcoronary disease in patients after myocardial in farction according to quantitativeultrasound wall2motion analysis[J]. Am Heart J,1993,125(4):949.
[44]Braunwald E, Kloner RA The stunned myocardium prolonged, postischemic ventriculardysfunction. Circulation,1992;66:1146-1149.
[45]Rahim.The hibernating myocardium1[J].Am Heart J,1989,117:21-26.
[46]Murry CE,Jennings RB,Rerimer KA. Preconditioning with ischemia: a delay of lethalcell injury in ischemic myocardium [J].Circulation,1996,75:1124.
[47]Murry CE,Richard VJ,Jennings RB,et al. Myocardial protection is lost beforecontractile function recorers from ischemic preconditioning[J]. Am J Physicol,2005,260:796.
[48]Przyklenk K, Kioner RA. Ischemic preconditioning: exploring the paradox [J]. ProgCardiovas c Dis,1998,40:517-547.
[49]Hirait T,Fujita M,Yeshida N,et al.Importance of ischemic preconditioning andcollateral circulation for left ventricular functional recovery in patients with successfulintracoronary thrombolysis for acute myocardial infarction [J]. Am Heart J,2003,126(4):828.
[50]张敬,付研,李田昌,等.缺血预适应在急性心肌梗死溶栓和PTCA中心肌保护作用的对比研究[J].中华急诊医学杂志2002,11(6):392-403.
[51]Pasceri V, Lanza GA, Patti G, et al. Preconditioning by transient myocardial ischemiaconfers protection against ischemia induced ventricular arrhythmias in variant angina [J].Circulation,1996,94(8):1850-1856.
[52]Speechly ME, Grover GJ, Yellon DM. Does ischemic preconditioning in the humaninvolve protein kinase C and the ATP-dependent K+channel? Studies of contractilefunction after simulated ischemic in an atrail in vitro model [J]. Circ Res,1995,77:1030-1035.
[53]赵娜.心肌缺血预适应对急性心肌梗死患者影响的临床研究[J].实用心脑肺血管病杂志2012,20(3):473-474.
[54]Walker DM, Yellon DM. Ischemic preconditioning: from mechanisms to exploitation [J].Cardipvasc Res,1992,26:734-739.
[55]Ninomiya H, Otani H, Lu K, et al. Complementary role of extracellular ATP andadenosine in ischemic preconditioning in the rat heart [J]. Am J Physiol Heart CircPhysiol,2002,282(5): Hl810.
[56]陈宏伟.心肌缺血预适应及冠脉侧支循环对急性心肌梗塞患者的保护[J].心血管康复医学杂志.2011,20(1):22-25.
[57]Masatoshi F, Izuru N, Yasuki K, et al. Determinants of collateral development inpatients with acute myocardial infarction[J]. Clin Cardiol,1999,22:595.
[58]王新房.超声心动图学[M].第三版.北京:人民卫生出版社,1999.528.
[59]Berne RM, Levg MN. Cardiavascular physiology.1996,197-207.
[60]Schaper W, Ito WD.Molecular mechanisms of conronary collateral vessel growth [J].Circ Res,1996,79:911-915.
[61]Fogarty JA, Muller-Delp JM, Delp MD, et al. Exercise training enhances vasodilationresponses to vascular endothelial growth factor in porcine coronary arterioles exposed tochronic coronary occlusion [J]. Circulation,2004,109:664-670.
[62]Clayton JA, Chalothorn D, Faber JE. Vascular endothelial growth factor—A specifiesformation of native collaterals and regulates collateral growth in ischemia [J]. Circ Res,2008,103:1027-1036.
[63]Sager HB,Middendorff R,Rauche K,et al. Temporal patterns of blood flow and nitricoxide synthase expression affect macrophage accumulation and proliferation duringcollateral growth [J]. J Angiogenes Res,2010,2:18.
[64]Couffinhal T, Kearney M, Witzenbichler B, et al. Vascular endothelial growthfactor/vascular permeability factor(VEGF/VPF) in normal and atherosclerotic humanarteries[J]. Am J Pathol,1997,150(5):1.
[65]Pick J J, van Liebergen RA, Koeh KT, et al. Clinical angiographic and hemodynamicpredictors of recruitable collateral flow assessed during balloon angioplasty coronaryocclusion [J]. J Am Coll Cardiol,1997,29:275-282.
[66]霍海洋,李杰,胡健,等.冠心病患者冠状动脉侧枝循环形成的影响因素[J].中国动脉硬化杂志,2003,11(4):355-358.
[67]Pellinen TJ, Virtanen KS, Toivonen L, et al, Coronary collateral circulation [J]. ClinCardiol,1991,14(2):111-118.
[68]Heil M, Ziegelhoeffer T, Mees B, et al. A different outlook on the role of bone marrowstem cells in vascular growth: bone marrow delivers software not hardware [J]. Circ Res,2004,94:573-574.
[69]Werner GS, Ferrari M, Heinke S, et al. Angiographic assessment of collateral connectioncomparison with invasively determined collateral function in chronic coronary occlu-sions [J].Circulation,2003,107(15):1972-1977.
[70]Pohl T, Hochstrasser P, Billinger M, et al. Influence on collateral flow of recanalisingchronic total coronary occlusions: a case-control study [J]. Heart,2001,86(4):438-443.
[71]吴伟力,傅向华,马宁,等.缺血预适应及侧支循环对缺血再灌注心肌的保护作用[J].中华心血管病杂志,2004,32(8):717-722.
[72] Regieli JJ,Jukema JW,Nathoe HM, et al.Coronary collaterals improve prognosis inpatients with ischemic heart disease [J]. Int J Cardiol,2009,132:257-262.
[73]Grollier G,commeau P, Foucault JP, et al. angioplasty of chronic totally occludedcoronary arteries:usefulness of retrograde opacification of the occluded vessel viathecontralateral coronary artery[J]. Am Heart J,1987,114:1324-1328.
[74]Habib GB, Heibig J, Forman SA, et al. Influence of coronary col-lateral on myocardialinfarction size in humans: results of phase1thrombolysis in myocardial infarction(TIMI) trial [J]. Circulation,1991,83(3):739-746.
[75]Sabia PJ, Powers ER, Ragosta M, et al. An association between collateral blood flowand myocardial viability in patients with recent myocardial infarction[J]. N Engl J Med,1992,327(26):1825-1831.
[76]Fukai M, Li M, Nakakoji T, et al. Angiographically demonstrated coronary collateralpredict residual viable myocardium in patients with chronic myocardial infarction: aregional metabolic study[J].J Cardio,2000,35(2):103-111.
[77]Sasayama S, Fujita M. Resent Insight into coronary collateral circulation[J]. Circulation,1992,85:1197-1204.
[78]刘蔚,齐国先,贾大林,等.冠心病冠状动脉病变特点及与临床表现的对比分析[J].中国实用内科杂志,1996,16(5):291.
[79]Aronow WS, Epstein S, Koenigsberg M. Usefulness of echocar diographic leftventricular ejection fraction and silent myocardial in ischemia in predicting newcoronary events in elderly patients with coronary artery disease or systemic hypertension[J]. A m J Cardiol,1990,65(11):811.
[80]Romano S, Dagianti A, Penco M, et al.Usefulness of echocardiography in the prognosticevaluation of non-Q-wave myocardial infarction[J]. Am J Cardiol,2000(86):43-45.
[81]吴雅峰,张桂珍.实用心脏超声诊断学[M].北京:中国医药科技出版社,1996:70.
[82]Peteiro J, Monserrat L, Fabregas R, et al. Comparison of two dimensionalechocardiography and pulsed doppler tissue imaging during dobutamine atropine stresstesting to detect coronary artery disease [J].Echocardiography,2001,18(4):275.
[83]孙红光,李澄,於晓平,等.应用超声心动图左室壁运动异常节段推测冠心病相关狭窄血管-与冠脉造影对比研究[J].中国医学计算机成像杂志,2006,12(2):96-98.
[84]马长生,盖鲁粤,张奎俊,等.介入心脏病学[M].1998:240.
[85]Schiller NV, Shah PM, Gawford M, et al. Recommendations for quantitative of the leftventricle by two-dimensional echocardiography[J]. J Am Soc Echocardiography,1989,2:358~367
[86]中国成人血脂异常防治指南制订联合委员会.中国成人血脂异常防治指南[J].中华心血管病杂志,2007,35(05):390一419.
[87]Rentrop KP, Thornton JC, Feit F, et al. Determinants and protective potential ofcoronary arterial collaterals as assessed by an angioplasty model [J]. Am J Cardiol,1988,61(4):677-684.
[88]Leaman DM, Brower RW, Meester GT,et al.Coronary artery atherosclerosis: Severity ofthe disease, severity of angina pectoris and compromised left ventricular function[J].Circulation.1981,63:285–299.
[89]Gensini GG. A more meaningful scoring system for determining the severity of coronaryheart disease[J]. Am J Cardiol1983;51:606.
[90]Guidelines for coronary angiography: A report of the American College ofCardiology/American Heart Association Task Force on Assessment of Diagnostic andTherapeutic Cardiovascular Procedures [J]. J Am Coll Cardiol1987;10:935–950.
[91]Gang H, Jiang LZ, Huan D. Coronary Score Adds Prognostic Information for PatientsWith Acute Coronary Syndrome[J].Circ J.2010;74:490–495.
[92]Ng MK, Wu J, Chang E, et al. A central role for nicotinic cholinergic regulation ofgrowth factor-induced endothelial cell migration[J]. Arterioscler Thromb Vasc Biol,2007,27:106-112.
[93]Kornowski R. Collateral formation and clinical variables in obstructive coronary arterydisease: the influence of hypercholesterolemia and diabetes mellitus [J]. Coron ArteryDis,2003,14:61-64.
[94]Kperselmam J, De JP, Verhaar MC, et al. Coronary collateral circulation: the effects ofsmoking and alcohol[J]. Atherosclerosis,2007,191:191-198.
[95]Sze L, Attenhofer Jost CH, Amann FW,et al. Stress echocardiography: analysis of resultsin100coronary angiography patients[J]. Schweiz Med Wochenschr.2000,130(23):878-888.
[96]Chandraratna PA, Kuznetsov VA, Mohar DS, Comparison of Squatting StressEchocardiography and Dobutamine Stress Echocardiography for the Diagnosis ofCoronary Artery Disease[J]. Echocardiography,2012, xx:1-5.