用户名: 密码: 验证码:
非急性心梗2型糖尿病患者血清cTnT升高的临床意义
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
目的探讨非急性心梗2型糖尿病(T2DM)患者血清心肌肌钙蛋白T(cTnT)升高的临床意义,为2型糖尿病心血管并发症的预防、早期诊断与治疗提供新的思路。
     方法参照24小时尿白蛋白排泄率选择T2DM患者180例,上述对象均剔除近3个月内急性心梗、自身免疫性疾病、血液系统疾病、甲状腺疾病、严重感染、风湿性心脏病、原发性心肌病、原发性肾病、严重肝脏疾病。第1次检测血清cTnT大于正常值的患者连续复查心电图、cTnT,排除入组时为急性心肌梗死病例。结合糖尿病肾病Mogensen分期标准将所纳入研究对象为三组:尿白蛋白<30mg/D组(A组)60例;尿白蛋白介于30~300mg/D组(B组)60例;尿白蛋白>300mg/D或Scr高于参考值组(C组)60例。三组间的性别构成差别无统计学意义。再根据cTnT值分为cTnT阳性组及cTnT阴性组。测定T2DM患者血清cTnT、随机血糖(RBG)、果糖胺(FA)、糖化血红蛋白(HbA1C)、肝肾功能、血脂、C反应蛋白(CRP)。随访120天,观察患者心血管事件及死亡事件的发生情况,分析其与cTnT的关系。
     结果(1)180例T2DM患者cTnT升高25例,其中尿白蛋白低于30mg/D组(A组,60例)cTnT升高1例;尿白蛋白介于30-300mg/D组(B组,60例)cTnT升高4例;尿白蛋白大于300mg/D或Scr高于参考值组(C组,60例)cTnT升高20例。(2)cTnT升高25例患者中发生心血管事件16例,死亡8例, 7例死于心血管事件; cTnT正常155例中发生心血管事件6例,死亡4例,其中1例死于心血管事件,两组比较差异有统计学意义(P<0.01)。(3)cTnT阳性组与阴性组比较: TG、TC、LDL-c、FA、HbA1c均数比较差异均无统计学意义;cTnT阳性组CRP水平明显高于cTnT阴性组(P<0.05);cTnT阳性组Hb水平明显低于cTnT阴性组(P<0.01),ALB水平也明显低于cTnT阴性组(P<0.05);cTnT阳性组患者多为老年患者,与cTnT阴性组相比,年龄差异有统计学意义(P<0.01)。
     结论(1)随着糖尿病肾病进展, cTnT升高阳性率增加。(2)2型糖尿病患者血清cTnT水平升高与心脏微血管病变导致的心肌损伤有关,可以预测患者病死率及心血管事件的发生率。(3)对于具有高度心血管危险水平的老年糖尿病患者,单纯严格的血糖控制并不能有效降低其大血管事件危险性。
Objective: To investigate the clinical significance of elevated cTnT in patients with type 2 diabetes mellitus whithout acute myocardial infarction . To provide a new thinking to prevent,early diagnose and to treat for the cardioascular complications of type 2 diabetes mellitus .
     Methods:Referering to the 24-hour urinary albumin excretion rates,the 180 patients with T2DM were choosed and the participants above-mentioned were without acute myo- cardial infarction, autoimmune diseases, blood systemic diseases, thyroid diseases, serious infection, of rheumatic heart disease, primary cardiomyopathy, primary nephro- pathy, severe hepatopathy during the past three months. The electrocardiogram and cTnT in the patients with serum cTnT beyond the scope of normal reference value in the first determination were determined repeatly to exclude the cases with acute myocardial infarction . According to the diabetes nephropathy Mogensen staging system,the diabetic patients researchede were devided into three groups: The group A was composed with the diabetic patients whose urinary albumin below 30mg/D(n:60). The group B was composed with the diabetic patients whose urinary albumin between 30 and 300mg/D group (n: 60). The group C was composed with the diabetic patients whose urinary albumin > 300mg/D or Cr above reference (n: 60). There was not statistically significance difference in gender constitute of the three groups. The diabetic patients researched were then divided into cTnT positive group and cTnT negative group according to determination values of cTnT.The serum cTnT,random blood glucose, fructose- amine, glycated hemoglobin,hepatic function,renal function,blood-fat, C reactive protein in all patients were determined. In 120-days follow-up, observe the incidence of cardiovascular events and death events in patients were observed,the relationship between the incidence and cTnT was analyzed.
     Results: (1)There were 25 patients with elevated cTnT among 180 cases of T2DM patients. Of them cTnT increased in one patient in group A whose Urinary albumin less than 30mg / D (60 cases) ; cTnT increased in 4 patients in group B(Urinary albumin between 30-300mg / D as group B,60 cases); cTnT increased in 20 patients in group C(Urinary albumin greater than 300mg / D or Scr higher than the reference value as C group,60 cases). (2)Of 25 patients with elevated cTnT 16 patients had cardiovascular events , 8 died and among the died patients 7 patients died of cardiovascular events. Among 155 patients with normal cTnT ,6 patients occurred cardiovascular events. Of them 4 died, 1 of which died of cardiovascular events. There was significant difference between wo groups (P <0.01). (3)CTnT positive and negative groups were compared as follows: there were not statistically significant differences in the means’comparative of TG, TC, LDL - c, FA and HbA1c ; cTnT positive group's CRP level was significantly higher than cTnT negative group (P < 0.05); cTnT positive group's Hb level was obviously lower than cTnT negative group (P < 0.01) and ALB level was also obviously lower than cTnT negative group's (P < 0.05); the majority of the patients in CTnT positive group were the aged, compared with cTnT negative group, the difference in age was statistically significant (P < 0.01).
     Conclusions: (1)With the progress of diabetic nephropathy, the positive rate of elevated cTnT increases.(2)Elevated cTnT which were related with myocardial injury induced by cardiac microangiopathy in type 2 diabetes patients can predict the patient mortality and the incidence of cardiovascular events.(3)Simply strictly controling blood glucose cannot effectively reduce their big vascular events' risks for elderly diabetic patients with highly cardioascular risk level .
引文
[1] Yang WY, Lu JM, Weng JP,etal. Prevalance of diabetes among men and women in china[J]. N Engl J Med, 2010, 362(12):109021101.
    [2] Krum H,Gilbert RE.Demographics and concomitant disorders in heart failure[J].Lancet,2003,362(9378):147-158.
    [3]李广智.糖尿病性心脏病—陈灏珠院士[J].老年医学与保健,2006,l2(l):64-65.
    [4]刘冬戈,乔旭柏,杜俊,等.糖尿病心肌病的组织病理学观察[J].中华病理学杂志,2007,36(12):801-804.
    [5]李小鹰.冠脉微血管病变的临床特点与防治[J].微循环学杂志,2004,14(3):9-12.
    [6]赵丽君.糖尿病性心脏病76例的心电图分析[J].中华现代内科学杂志; 2006,3(1): 74-75.
    [7]周白丽.心肌肌钙蛋白—心肌损伤的标志物[J].中国综合临床,2003,19(4):298-299。
    [8] Bertrand ME,Simoons ML,Fox KA,et al.Management of acute coronary syndromes in patients presenting without tpersistent ST segment elevation[J]. Eur HeartJ,2003,24(12):1808-1840.
    [9]潘柏申.应重视心脏标志物的临床应用研究[J].中华检验医学杂志,2005,28(9):881-884.
    [10]NACB起草组成员.美国临床生化科学院检验医学实践指南:急性冠状动脉综合征的临床特征和生物标志物的应用[J].临床检验杂志2009,27(5):附4-21.
    [11]金雅丽,张倩辉,郭艺芳.尿微量白蛋白[J].中华高血压杂志,2009,17(3):283-286.
    [12] Deckert T.Nephropathy and death-the fatal twins in diabetes mellitus[J]. Nephrol Dial Transplant, 1994, 9: 1069-1671.
    [13] Lenfnt C.关于高血压新的美国指南JNC7(T)[J].中华全科医师杂志, 2004,3(1): 21.
    [14]胡大一,杨进刚.关注冠心病患者的糖代谢异常[J].中华内科杂志, 2006,45(10):793—795.
    [15]赵霞,邓宏明,刘红.2型糖尿病血管并发症危险因素分析[J].广西医科大学学报,2007,24(5):743-746.
    [16]王生龙.初诊2型糖尿病患者微血管病变与相关危险因素分析[J].慢性病学杂志,2010,12(3):196-198.
    [17]金惠铭,胡仁明.糖尿病性微血管病的临床病理生理[J].中国病理生理杂志,2007,23(2)399-402.
    [18]Jorneskog G,Kuhl J,Katz A,et a1.Early microvascular dysfunction in healthy normal-weight males with heredity for type 2 diabetes[J].Diabetes Care,2005,28(6):1495-1497.
    [19]陈燕,仲肇舒,丁林锋.糖尿病肾病尿白蛋白排泄率对心功能的影响[J].南京医科大学学报.2005,25(l2):908-910.
    [20] Caballero AE,Arora S,Saouaf R,et a1.Microvascular and macrovascular reactivity is reduced in subjects at risk for type 2 diabetes[J].Diabetes,1999,48(9):1856-l862.
    [21] Deed wania PC.Mechanisms of endothelial dysfunction in the metabolic syndrome[J],Current Diabetes Reports,2003,3(4):289-292.
    [22]胡东鹏.糖尿病性心脏病患者的红细胞变形能力及其影响因素[J].山东医药,2004,44(28):36-36.
    [23]苏胜.2型糖尿病患者肺功能改变的研究[J].重庆医学,2010, 39(15):2022-2024.
    [24]林攀,丁小强,袁敏,等.慢性肾脏病患者贫血患病现况调查[J].复旦学报(医学版),2009,36(5):562-565.
    [25]张莹,张史昭.老年慢性肾脏病患者心血管疾病的预后和相关性[J].临床医学,2008,28(10):3-5.
    [26]莫广平.慢性肾脏病患者发生心血管事件危险因素分析[J].临床医学,2010,30(1):18-20.
    [27] Erem C,Hacihasanoglu A,Celik S,et a1.Coagulation and fibrinolysis parameters in type 2 diabetic patients with and without diabetic vascular complications[J].Med Princ Pract,2005,14(1):22-30.
    [28]胡毅,曾敏.糖尿病患者血液流变学与血管并发症的关系[J].临床和实验医学杂志,2007,6(6):122-123.
    [29]丛丽,俞茂华,李益明.chymase与糖尿病心肌病变[J].国外医学:内分泌学分册,2004;24(supp1):31.
    [30]丛丽,俞茂华,李益明,等.心肌胶原代谢变化在糖尿病心肌病变发生中作用的实验研究[J].中国临床康复,2004,8(9):1655.
    [31] Nishikawa N,Yamamoto K,Sakata Y,et al.Differential activation of matrix metalloproteinases in heart failure with and without ventricular dilatation[J]. Cardiovasc Res, 2003, 57 (3):766-774.】
    [32]江时森,程训民,马瑞,等.高血压合并糖尿病对心肌微血管内皮细胞功能的影响[J].上海医学,2007,30(Supply):162.
    [33]赵传艳,崔连群,唐元升,等.冠心病合并2型糖尿病患者临床和冠状动脉病变特点[J].中国老年学杂志,2007,27(9):1792-1794.
    [34]尹浩晔,高雪梅,周馨.冠心病合并2型糖尿病患者的临床特征及冠状动脉病变特点[J].中国慢性病预防与控制,2009,17(2):151-153.
    [35]李小鹰.冠心病合并糖尿病时的心力衰竭[J].中华内科杂志,2004,43(3):231-233.
    [36]高玲,徐标,王涟,等.核素心肌灌注显像对糖尿病微血管病变诊断的临床应用价值[J].中国糖尿病杂志,2009,17(1):49-51.
    [37]张欣,张延军,解静慧,等.冠脉造影正常的II型糖尿病患者核素心肌灌注显像分析[J].中国临床医学影像杂志,2004,15(12):690-691,701.
    [38]毛永辉,王波,吴华,等.血液透析患者血清肌钙蛋白T检测的临床研究[J].中华老年医学杂志,2003,22(11): 649-651.
    [39]吴道爱,王长江,王春,等. 2型糖尿病患者脂代谢异常的临床分析[J].中华全科医学,2009,7(12):1286-1287.
    [40]倪长霖,张亚文,胡筱芸. 2型糖尿病合并冠心病危险因素的临床研究[J].天津医药,2006,34(9):607-609.
    [41]张继惠,李曙远.葡萄糖、胰岛素、甘油三酯对老年糖尿病患者E分泌及微血管病变的影响[J].中国老年学杂志,2008,28(9):889-890.
    [42]魏佳莉,彭佑铭,王建文.139例2型糖尿病肾病患者血脂代谢异常与肾损害[J].中国现代医学杂志,2004,14(15):28-31.
    [43]王平,马芳玲,母义明,等. 2型糖尿病伴高甘油三酯血症患者血清胰岛素样生长因子结合蛋白1水平与胰岛素抵抗的相关性分析[J],中国糖尿病杂志,2007,15(3):140-141.
    [44]陆亚群,苏珂.脂毒性促进胰岛B细胞凋亡在2型糖尿病中的作用[J].上海医药,2009,30(9):399-401.
    [45]王顺,桑晓红.慢性肾脏病3期糖尿病肾病患者左心结构与功能改变的多因素分析[J].实用医学杂志,2009,25(12).
    [46]刘必成.慢性肾脏病新理论与实践[M].第1版.江苏:东大学出版社,2008:66-75.
    [47]陆菊明.糖尿病研究现状及展望[J].解放军医学杂志,2010,35(7):777-780.
    [48] Monnier L, Mas E, Ginet C,et al.Activation of oxidative stress by acute glucose fluctuations compared with sustained chronic hyperglycemia in patients with type 2 diabetes[J].JAMA, 2006, 295(14): 1681-1687.
    [49]方小正,陈敏,李红,等.波动性高血糖状态与糖尿病微血管病变的研究[J].医学临床研究,2008,25(11):1945-1947.
    [50]孙明晓.老年2型糖尿病患者合并心脑血管疾病的危险因素[J].中华心脑血管病杂志,2004,6(6):390-392.
    [51]张斌,向红丁,毛微波,等.北京、上海、天津、重庆四城市住院2型糖尿病患者糖尿病慢性并发症及相关大血管疾病的流行病学分析[J].中国医学科学院学报,2002,24(5):452-456.
    [52]柯琴梅,冯义柏,管思明,等.老年糖尿病患者冠状动脉血流储备的变化[J].中国老年学杂志,2003,23(11):734-736.
    [53]陈翠玲,谢建南.血清肌钙蛋白测定对老年糖尿病性心肌病的临床意义.中国老年学杂志,2005,25(2):202.
    [54]李英华,黄楚枫,林环. 2型糖尿病患者的认知功能与餐后血糖及病程的关系[J].中国临床康复,2005,9(4):40-41.
    [55]郑燕芳,徐应军.血糖对老年糖尿病患者心脑血管病变影响的研究进展[J].中国老年学杂志,2O07,27(10):1012-1014.
    [56]王先令,陆菊明.血糖波动对DM预后及其慢性并发症发生发展的影响[J].国外医学·内分泌学分册,2005,25(3):169-71.
    [57]邢伟,才春华.维持性血液透析患者生存率及死因分析[J].中国误诊学杂志,2009,9(33):8111-8112.
    [58]Cano NJ,Roth H,Aparicio M,et al.Malnutrition in hemodialysis diabetic patients:evaluation and prognostic influence[J]. Kidney Int,2002,62:593-601.
    [59]邢广群,刘丽秋,董晖,等.血清胰岛素样生长因子1和炎症状态与2型糖尿病肾病营养不良[J].临床荟萃2005,20(21):1201-1203.
    [60]夏春英,邵维斌,姚利群,等.血清白蛋白水平对腹膜透析患者残余肾功能的影响[J].国际移植与血液净化杂志,2009,7(5):41-43.
    [61]梁玉凤,江丽萍,傅慧芳.糖尿病患者肾脏损害与心脑血管事件的关系[J].广东医学,2OO4,25(1):64-65
    [62]Hu FB.Stampfer MJ.Is type 2 diabe tes mellitus a vascular condition? Arterioscler Thromb Vasc Bio1.2003,23(10):l 7 15-l7l6.
    [63]谷国强,胡大一,刘坤申,等.心绞痛患者C反应蛋白与冠状动脉病变稳定性和心脏事件关系的探讨[J].中国实用内科杂志,2003,23(11):663-665.
    [64]龙艳,苏珂,于健,等. 2型糖尿病患者C反应蛋白及肿瘤坏死因子α与微血管并发症的关系[J].中国临床康复,2005,9(3):120-122.
    [65]王冬环,赵月霞,尉秀荣.血清心肌肌钙蛋白T和高敏C反应蛋白在糖尿病发心肌病早期诊断中的应用[J].中国医刊,2007,42(7):33-34.
    [66]梁玉凤,江丽萍,傅慧芳.糖尿病患者肾脏损害与心脑血管事件的关系[J].广东医学,2OO4,25(1):64-65.
    [67]郭艺芳,胡大一.从最新循证医学证据思考糖尿病心血管并发症的预防策略[J].中华内科杂志,2009,48(2):97-99.
    [1]边延涛,王国宏,袁申元,等.氯沙坦对实验性糖尿病大鼠心肌的保护作用[J].中华心血管杂志,2000,28(4):293-296.
    [2]刘冬戈,乔旭柏,杜俊,等.糖尿病心肌病的组织病理学观察[J].中华病理学杂志,2007,36(12):801-804.
    [3] Karamitsos TD,KarvounisHI,Dalamanga EG,et al.Early diastolic impairmen of diabetic heart: the significance of right ventricle[J].Int J Cardiol,2007,114(2):218-223.
    [4] Du X L,Edelstein D,Dimmeler S,e1 a1.Hyperg1ycemia inhibits endothelial nitric oxide synthase activity by post-translational modification at the Akt site[J].J Clin Invest,2001,108 (9):1341-1348.
    [5] Du XL,Edelstein D,Rossetti L,et a1.Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing Spl glycosylation[J],Proc Natl Acad Sci USA,2000,97 (22):12222-12226.
    [6] Du XL,Matsumura T,Edelstein D,et a1.Inhibition of GAP.DH activity by poly(ADP-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells[J].J Clin Invest, 2003, 112(7):1049-1057.
    [7] Wang YH,Cai L.Diabetes/obesity-related inflammation,cardiac cell death and cardiomyopathy[J].Zhong Nan Da Xue Xue Bao Yi Xue Ban,2006,31(6):814-818.
    [8] Song Y ,Wang J,Li Y,et a1.Cardiac metallothionein synthesis in strep-tozotocin-induced diabetic mice,and its protection against diabetes-induced cardiac injury[J].Am J Pathol,2005,167(1):17-26.
    [9] Cai L,Wang L,Li Y,et al.Inhibition of superoxide generation and associated nitrosative damage is involed in metallothionein prevention of diabeticcardiomyopathy[J].Diabetes,2005,54(6):1829-1837.
    [10] Pitkanen O P,Nuutila P,Raitakari O T,et al.Coronary flow reserve is reduced in young men with IDDM[J].Diabetes 1998,47(2):248-254.
    [11]金惠铭.加强微血管病发病机制的研究[J].中国微循环,2006,10(2):77-78.
    [12] Thorand B,Baumert J.Chambless L,et a1.Elevated markers of endothelial dysfunction predict type 2 diabetes mellitus in middle-aged men and women from the general population[J].Arterioseler Thromb Vasc Biol,2006,26(2):398-405.
    [13] Deed wania PC.Mechanisms of endothelial dysfunction in the metabolic syndrome[J].Current Diabetes Reports,2003,3(4):289-292.
    [14]胡东鹏.糖尿病性心脏病患者的红细胞变形能力及其影响因素[J].山东医药.2004,44(28):36-36.
    [15] Erem C,Hacihasanoglu A,Celik S,et a1.Coagulation and fibrinolysis parameters in type 2 diabetic patients with and without diabetic vascular complications[J].Med Princ Pract,2005,14(1):22-30.
    [16] Van Bilsen M,Smeets PJ,Gilde AJ,et al.Metabolic remodeling of the failing heart:the cardiac burn out syndrome[J].Cardiovasc Res,2004, 61(2):218-226.
    [17] Fiordaliso F,Bianchi R,Staszewsky L,et a1.Antioxidant treatment attenuates hyperglycemia-induced cardiomyocyte death in rats [J].J Mol Cell Cardiol. 2004,37(5):959-968.
    [18]张晓燕,陈丽红,管又飞.PPAR家族及其与代谢综合征的关系[J].生理科学进展,2005,36(1):6-12.
    [19] Lefebvre P,Chinetti G,Fmchart J C,et a1.Sorting out the roles of PPAR alpha in energy metabolism and vascular homeostasis[J].J Clin Invest, 2006, 116(3): 571-580.
    [20] Matsuzawa Y.The meabolic syndrome and adipocytokines[J].FEBS Lett,2006,580(12):2917-2921.
    [21] How O J,Aasum E,Severson D L,et al.Increased myocardial oxygen consumption reduces cardiac efficiency in diabetic mice [J]. Diabetes, 2006,55(2):466-473.
    [22] Young LH.Diastolic Function and Type 1 Diabetes[J].Diabetes Care,2004,27(8):2081-2083.
    [23] Noda N,Hayashi H,Satoh H,et al.Ca2+transients and cell shortening in diabetic rat ventricular myocytes[J].Jpn Circ J, 1993, 57(5):449-457.
    [24]李勋,杨向军,蒋文平.糖尿病大鼠心室肌细胞钾通道的改变[J].中华高血压杂,2006,14(8):647-650.
    [25] Swynghedauw B.Molecular mechanisms of myocardial remodeling [J].Physiol Rev,1999,79(1):215-262.
    [26] Fiordaliso F,Leri A,Cesselli D,et a1.Hyperglycemia activates p53 and p53-regulated genes leading to myocyte cell death[J].Diabetes, 2001, 50(10): 2363-2375.
    [27] Messina E,Giacomello A.Diabetic cardiomyopathy:a“cardiac stem cell disease”involving p66Shc,an attractive novel molecular target for heartfailure therapy[J].Circ Res,2006,99(1):1-2.
    [28] Esposito K,Nappo F,Marfella R,et a1.Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans,role of oxidative stress[J].Circulation,2002,106(16),2067-2072.
    [29] Backlund T,Palojoki E,Saraste A,Eriksson A,et al.Sustained cardiomyocyte apoptosis and left ventricular remodelling after myocardial infarction in experimental diabetes[J].Diabetologia,2004, 47(2):325-330.
    [30]丛丽,俞茂华,李益明.chymase与糖尿病心肌病变[J].国外医学,内分泌学分册,2004,24(supp1):31.
    [31]丛丽,俞茂华,李益明,等.心肌胶原代谢变化在糖尿病心肌病变发生中作用的实验研究[J].中国临床康复,2004,8(9):1655.
    [32] Lee S,Kramer CM,Mankad S,et a1.Combined angiotensin converting enzyme inhibition and angiotensin AT(1) receptor blockade up-regulates myocardial AT(2) receptors in remodeled myocardium post-infarction [J].Cardiovasc Res,2001,51(1):131.
    [33] Stewart JA Jr,Wei CC,Brower GL,et al.Cardiac mast cell and chymase mediated matrix metalloproteinase activity and left ventricular remoldeing in mitral regurgitation in the dog[J].J Mol Cell Cardiol, 2003,35(3):311-319.
    [34] Nishikawa N,Yamamoto K,Sakata Y,et al.Differential activation of matrix metalloproteinases in heart failure with and without ventricular dilatation[J].Cardiovasc Res,2003,57(3):766-774.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700