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1.
目的:证明恶性消化道肿瘤晚期患者血浆肿瘤坏死因子α(TNF-α)与胰岛素抵抗和胰岛素分泌功能相关性,阐明恶性消化道肿瘤晚期患者糖代谢障碍机制.方法:测定40例恶性消化道肿瘤晚期患者和40例正常人员血浆TNF-α和空腹血糖、胰岛素、乳酸含量,并计算稳态模式评估法胰岛素抵抗指数(HOMA-IR)和胰岛素分泌指数(HOMA-β).结果:恶性消化道肿瘤晚期患者血浆TNFα、空腹血糖、空腹胰岛素、空腹乳酸、HOMA-IR和HOMA-β均明显高于正常对照组(3.27±0.92vs1.23±0.36,P<0.01;5.19±0.75vs4.05±0.28,P<0.01;14.24±6.52vs8.27±4.84,P<0.01;7.11±0.69vs3.27±0.41,P<0.01;3.48±0.85vs1.55±0.77,P<0.01;181±39vs326±47,P<0.01),但空腹血糖仍在正常参考范围内.恶性消化道肿瘤晚期患者血TNFα与空腹血糖、空腹胰岛素、空腹乳酸明显正相关(r=0.4352,P<0.05;r=0.3136,P<0.05;r=0.7893,P<0.01),与HOMA-IR明显正相关(r=0.6531,P<0.01),与HOMA-β明显负相关(r=-0.5874,P<0.01).结论:恶性消化道肿瘤晚期患者血浆TNFα在胰岛素抵抗和胰岛素分泌功能下降及糖代谢障碍中发挥重要作用.  相似文献   

2.
目的探讨非糖尿病患者急性心肌梗死时胰岛素抵抗的相关危险因素,并评估胰岛素抵抗对ST段急性心肌梗死患者住院期间预后的影响和意义。方法从2008年10月到2009年9月,连续入选初次发生ST段抬高急性心肌梗死,且在发病24小时内接受急诊经皮冠状介入治疗的患者,在入院第二天清晨测空腹血糖和胰岛素浓度,出院前均进行口服葡萄糖耐量试验,最后纳入非糖尿病患者124例,以稳态模型胰岛素抵抗指数,即HOMA-IR≥2.5认为存在胰岛素抵抗,评价胰岛素抵抗对急性心肌梗死患者预后的影响。结果 124例患者中,存在胰岛素抵抗的患者占49.2%(61/124),病死率占12.1%(15/124)。胰岛素抵抗组较对照组有较高的入院血糖[(7.88±2.83)mmol/L比(6.93±1.60)mmol/L,P=0.025]、空腹血糖[(7.36±2.33)mmol/L比(6.43±1.81)mmol/L,P=0.014]和胰岛素浓度[(16.68±6.98)mU/L比(6.32±2.32)mU/L,P=0.000],组间比较差异具有统计学意义。多元逐步回归方程提示,体重指数[标准化回归系数(β)=0.244,P=0.021]和空腹血糖(β=0.451,P=0.000)是影响HOMA-IR严重程度的主要因素。多因素logistic回归方程提示,在调整其他因素后,胰岛素抵抗[OR=1.506,95%CI(1.062~2.134),P=0.021]、Killip分级≥Ⅱ[OR=3.007,95%CI(1.165~7.779),P=0.023]和心肌肌酸激酶同工酶峰值[OR=1.004,95%CI(1.000~1.008),P=0.036]是急性心肌梗死患者住院期间死亡的独立危险因素。结论心肌梗死急性期胰岛素抵抗现象普遍存在,是急性心肌梗死患者住院期间预后不良的独立危险因素,体重指数和第二天空腹血糖水平是影响胰岛素抵抗的主要因素。  相似文献   

3.
目的 探讨痛风患者从正常糖耐量(NGT)到糖尿病不同糖代谢状态时的胰岛素抵抗与胰岛β细胞功能的演变,分析痛风合并糖代谢紊乱患者的代谢特征.方法 96例痛风患者分为糖耐量正常(NGT)组(n=35)、糖调节受损(IGR)组(n=27)及糖尿病组(n=34).测量身高、体重、血压,测定空腹血糖、空腹胰岛素、HbA1C、血清尿酸、总胆固醇、甘油三酯及C反应蛋白(CRP),计算体重指数(BMI)、稳态模型评估的胰岛素抵抗指数(HOMA-IR)、稳态模型评估的胰岛β细胞功能指数(HOMA-B)和胰岛素敏感指数(ISI).结果 糖尿病组和IGR组的BMI、餐后2h血糖(2hPG)、空腹胰岛素、HbA1C、总胆固醇、甘油三酯、CRP、HOMA-IR均高于NGT组(P<0.05或P<0.01),而糖尿病组及IGR组ISI均低于NGT组(0.023±0.018和0.024±0.017对0.052±0.026,P<0.05).NGT组、IGR组和糖尿病组HOMA-B差异有统计学意义(87.6±25.1、126.46±34.2及173.75±32.1,P<0.05).糖尿病组糖尿病家族史阳性率高于NGT组(41.17%对11.4%,P<0.05).logistic回归分析显示,年龄、BMI、收缩压、甘油三酯、CRP、ISI与糖尿病独立相关,而尿酸与糖尿病无相关性.结论 重度胰岛素抵抗、胰岛β细胞分泌功能障碍、BMI增加、C反应蛋白水平增高、脂代谢异常、遗传易感性是痛风患者合并糖尿病的主要代谢特征.  相似文献   

4.
目的探讨不同糖耐量状态孕妇血清成纤维细胞生长因子21(FGF21)水平与胰岛β细胞功能的关系。方法选取妊娠24~28周于我院接受50 g糖负荷试验(GCT)阳性的孕妇441例,1周后再行75 g OGTT,根据结果分为GDM组228例、妊娠期IGT(GIGT)组122例及妊娠期NGT(GNGT)组91名。ELISA检测血清FGF21水平,胰岛素抵抗指数(HOMA-IR),胰岛素敏感指数(Matsuda指数),胰岛β细胞功能指数(HOMA-β),第1、2时相胰岛素分泌指数及胰岛β细胞代偿胰岛素抵抗的分泌能力(ISSI)评估胰岛β细胞功能。FGF21与胰岛β细胞功能的相关性采用Pearson相关分析。结果 (1)GDM组和GIGT组BMI,0、1、2、3hPG及1、2、3 hIns均高于GNGT组和GIGT组(P0.05或P0.01)。GDM组SBP、DBP、0 hIns和HbA_1c高于GNGT组和GIGT组(P0.05或P0.01);(2)GNGT组、GIGT组及GDM组FGF21水平[(101.74±20.40)vs(137.93±25.52)vs(185.69±31.61)ng/L]和HOMA-IR依次升高[1.74(0.91,2.85)vs2.39(1.31,4.87)vs3.38(2.19,6.75)],Matsuda指数[(58.74±15.68)vs(41.62±15.65)vs(39.73±18.98)]和HOMA-β[(157.69±88.41)vs(144.35±78.98)vs(107.30±87.23)]及ISSI[(72253.55±15167.53)vs(42313.91±7112.47)vs(30032.50±11500.24)]依次降低(P0.05或P0.01)。GDM组第1、2时相胰岛素分泌指数低于GNGT组和GIGT组(P0.01),但GNGT组与GIGT组比较,差异无统计学意义(P0.05);(3)Pearson相关分析显示,FGF21与HOMA-IR呈正相关(r=0.255,P=0.030),与Matsuda指数、HOMA-β、第1、2时相胰岛素分泌指数及ISSI呈负相关(r=0.289、-0.256、-0.224、-0.230、-0.277,P=0.019、0.037、0.045、0.040、0.023)。结论随着糖代谢受损逐渐加重,FGF21水平升高,且与胰岛β细胞功能相关,可能与GDM的发生发展有关。  相似文献   

5.
目的观察新诊断老年糖尿病(DM)患者胰岛β细胞功能特点及其与胰淀素、褪黑素的关系。方法收集初诊DM患者60例,其中老年DM组27例,成年DM组33例,对照组30例。均行口服葡萄糖耐量试验(OGTT),计算胰岛β细胞功能指数(HOMA-β)。采用ELISA法检测患者空腹血清胰淀素、褪黑素水平。同时测定所有受试者的血脂、体重指数(BMI)和腰臀比(WHR),并对结果进行统计分析。结果 (1)老年DM组与成年DM组比较HOMA-β明显降低〔(58.20±24.89)vs(81.20±40.80),P0.01〕,而OGTT2h血糖、胰岛素值及胰岛素抵抗指数(HOMA-IR)明显升高(P均0.05)。(2)与对照组相比,老年DM组血清胰淀素水平显著增高〔(21.57±15.88)vs(17.82±12.15)ng/L,P0.01〕;而褪黑素水平明显降低〔(6.56±1.32)vs(7.65±1.39)pg/ml,P0.01〕。(3)老年糖尿病组HOMA-β与褪黑素呈正相关(r=0.403,P=0.016),与胰淀素(r=-0.461,P=0.003)、HOMA-IR(r=-0.238,P=0.009)呈负相关,与空腹血糖、胰岛素、甘油三酯(TG),WHR则无明显相关性。结论新诊断的老年DM患者存在明显的胰岛素分泌缺陷,胰淀素的增高和褪黑素的降低可能与老年糖尿病的发生有关。  相似文献   

6.
目的探讨非肥胖的高血压病患者的非酒精性脂肪肝(NAFLD)与胰岛素抵抗(IR)的相关性.方法 93例非肥胖的不伴有糖尿病的高血压病患者,根据B超诊断有无脂肪肝分为高血压伴NAFLD 45例,高血压不伴NAFLD 48例.对两组患者的体重指数(BMI)、血压、血糖、血脂、血胰岛素、胰岛素抵抗指数(HOMA-IR)及转氨酶等指标进行比较分析,并对NAFLD与上述指标的关系进行多因素的logistic回归分析.结果高血压伴NAFLD组的BMI(25.2±1.5 vs 24.1±1.9, P=0.002)、甘油三酯(2.3±1.0 vs 1.9±0.8, P=0.034)、空腹胰岛素(15.0±6.0 vs 10.9±5.3, P=0.001)、口服75 g葡萄糖后2 h胰岛素(50.5±22.4 vs 37.9±16.0, P=0.003)、丙氨酸氨基转移酶(ALT) (22.8±8.9 vs 16.7±6.7, P<0.001)、天门冬氨酸氨基转移酶(18.8±6.4 vs 16.2±5.1, P=0.030)及HOMA-IR(1.2±0.5 vs 0.8±0.5, P=0.001)较不伴NAFLD组显著增高,而且NAFLD与HOMA-IR(OR 2.847,95% CI 1.122~7.228;P=0.028)及ALT(OR 1.075, 95% CI 1.013~1.140;P=0.016)呈独立相关.结论高血压病伴NAFLD患者有更显著的IR,而且在非肥胖的高血压病患者中,IR是NAFLD的独立危险因素.  相似文献   

7.
目的观察C-反应蛋白与体重指数、腰围、臀围及糖、脂代谢等指标间的相关性,探讨C-反应蛋白与2型糖尿病的关系.方法将131例受检对象分为肥胖2型糖尿病组、非肥胖2型糖尿病组、单纯肥胖组及对照组,测定体重指数、腰围、臀围、及糖代谢、脂代谢指标、C-反应蛋白等,以HOMA-IR及ISI来评价胰岛素的敏感性.结果①2型糖尿病组CRP及胰岛素抵抗指数均高于对照组(P<0.05);肥胖者的CRP及胰岛素抵抗指数均高于非肥胖者(P<0.05);②BMI、ISI为血CRP水平的影响因素;③Logistic多元回归显示HOMA-IR(OR=106.696)、CRP(OR=6.239)、TG(OR=6.923)是2型糖尿病的危险因素.  相似文献   

8.
目的:通过口服葡萄糖耐量试验研究空腹血糖正常的冠心病患者胰岛素抵抗状态、胰岛β细胞分泌功能及其临床意义。方法:对冠心病组(35例)及对照组(30例)按空腹及服糖后30、60、120和180min进行糖耐量、胰岛素释放实验,测量各时点血糖值及胰岛素值。同时测量其血压、身高、体重、总胆固醇、甘油三酯,并计算出体重指数(BMI)=体重(kg)/身高2(m2)。按照稳态模型胰岛素抵抗指数(HOMA-IR)=空腹胰岛素(FINS)×空腹血糖(FPG)/22.5;胰岛β细胞分泌指数(HBCI)=20×空腹胰岛素/(空腹血糖-3.5);早期胰岛素分泌指数(△I30/△G30)=口服葡萄糖耐量试验30min胰岛素增量与葡萄糖增量的比值;李氏β细胞胰岛素分泌指数(MBCI)=(空腹胰岛素×空腹血糖)/(血糖2h 血糖1h-2×空腹血糖)公式计算稳态模型胰岛素抵抗指数、胰岛β细胞分泌指数、△I30/△G30及李氏β细胞胰岛素分泌指数值。结果:空腹血糖正常的冠心病患者糖代谢异常(120min血糖≥7.8mmol/L)的发生率为43%,明显高于对照组23%,仅用空腹血糖这些患者将不能被诊断;冠心病组空腹及服糖后120min、180min胰岛素水平、稳态模型胰岛素抵抗指数显著高于对照组[(11.4±9.4)vs(5.3±3.1)mU/L,(71.6±48.5)vs(31.2±22.0)mU/L,(42.7±35.4)vs(8.6±6.9)mU/L,(0.62±0.32)vs(0.47±0.21),P<0.01],△I30/△G30、李氏β细胞胰岛素分泌指数低于对照组[(1.13±0.65)vs(1.42±0.57),(1.03±0.35)vs(1.36±0.37),P<0.01],差异有显著性;Logistic回归分析显示稳态模型胰岛素抵抗指数、120min胰岛素水平、总胆固醇与冠心病的发生显著相关(OR值分别为1.432、0.644、1.116,P<0.05)。结论:空腹血糖正常的冠心病患者糖代谢异常发病率明显高于对照组,简易口服葡萄糖耐量试验可揭示血糖代谢状态,应常规用于冠心病患者血糖代谢异常的诊断。冠心病患者存在胰岛素抵抗及胰岛β细胞分泌功能缺陷。  相似文献   

9.
目的 探讨2型糖尿病(T2DM)和非酒精性脂肪肝病(NAFLD)患者胰岛β细胞功能和胰岛素抵抗的特征.方法 206例研究对象根据是否有T2DM和NAFLD分为4组,采用肝脏胰岛素抵抗指数(HIR)、HOMA胰岛素抵抗指数(HOMA-IR)及Matsuda指数(MSI)评估胰岛素抵抗性,采用HOMA-β、早相及晚相胰岛素分泌指数评估胰岛β细胞功能.结果 NAFLD组和T2DM伴NAFLD组的HIR均显著高于对照组和T2DM组(4.13±0.64,4.03±0.69比3.52±0.78,3.53±0.64,P<0.05),T2DM伴NAFLD组的HOMA-IR显著高于T2DM和NAFLD组(3.35±2.69比2.31±1.39,2.40±1.55,P<0.05);NAFLD组的早相胰岛素分泌指标显著低于对照组(2.13±0.17比2.61±0.13,P<0.05),而T2DM组和T2DM伴NAFLD组的HOMA-β、早相及晚相胰岛素分泌指标均明显低于对照组(P<0.05).结论 NAFLD患者主要表现为肝脏胰岛素抵抗,其胰岛β细胞早相胰岛素分泌受损;T2DM患者存在胰岛素抵抗,其胰岛β细胞早、晚相胰岛素分泌功能均受损.当患者既有T2DM又有NAFLD时,胰岛素抵抗将更严重.  相似文献   

10.
目的 观察皮下多次注射胰岛素(MSII)强化降糖治疗对新发及病程1~5年的2型糖尿病患者胰岛β细胞功能的影响.方法 选取2007年6月-2010年6月于本院门诊和住院就诊的血糖控制不佳的2型糖尿病患者128例(新发92例,病程1~5年36例),予MSII强化降糖治疗达标,治疗前、后分别行口服葡萄糖耐量联合胰岛素释放试验.计算早相胰岛素分泌指数(△INS30/△BG30)、稳态模型评估-胰岛素分泌指数(HOMA-IS)、稳态模型评估-胰岛素抵抗指数(HOMA-IR)及胰岛素分泌曲线下面积( AUCINS).结果 所有患者经MSII治疗后胰岛素分泌功能均有不同程度的恢复,治疗后△INS30/△BG30、HOMA-IS、AUCINs明显提高(P<0.05);总组分析治疗前、后HOMA-IR分别为(3.12±2.72)vs.(3.06±1.92),差异无统计学意义(P=0.16).亚组分析显示病程1~5年2型糖尿病患者治疗前、后HOMA-IR分别为(3.83±2.07)vs.(2.70±1.38),P<0.01.新发2型糖尿病治疗后△INS30/△BG30、HOMA-IS、AUCINs明显提高,差异有统计学意义(P<0.05),而HOMA-IR治疗前、后差异无统计学意义(P=0.154).结论 对血糖水平较高的新发及病程1~5年的2型糖尿病患者予MSII强化降糖治疗,可明显改善胰岛β细胞分泌功能及胰岛素抵抗,恢复早相分泌,提高胰岛素敏感性.  相似文献   

11.
目的:探讨急性心肌梗死(AMI)初发高血糖的临床研究即既往无糖尿病病史的AMI患者发病早期血糖变化规律,及高血糖与口服葡萄糖耐量试验(OGTT)的关系,以明确反应性高血糖变化规律并及早发现合并糖尿病和糖调节受损的患者以指导治疗。方法:从2009-02到2009-09,连续入选既往无糖尿病病史,且在发病48 h内接受急诊经皮冠状动脉治疗的ST段抬高型AMI患者,在入院即刻和入院后第2~7天连续6天清晨6点采集患者空腹血液,化验血糖浓度,在出院前进行OGTT,共纳入有效病例158例,按照1999年世界卫生组织OGTT分类标准分为糖代谢正常者、糖调节受损者和新诊断糖尿病者;非糖尿病患者包括糖代谢正常者和糖调节受损者,评价血糖水平在心肌梗死急性期的变化规律。以入院第2天空腹血糖≥7.0 mmol/L为高血糖,评价高血糖与OGTT阳性的关系。结果:158例患者中糖代谢正常者占27.8%(44/158)、糖调节受损者占41.1%(65/158)、新诊断糖尿病者占31.0%(49/158)。所有患者平均血糖在入院后第4天降至正常水平,糖代谢正常者平均血糖在入院后第2天降至正常水平,非糖尿病患者平均血糖在第3天降至正常水平。空腹高血糖与OGTT阳性一致性检验Kappa=0.338,P=0.000,在校正其他变量的情况下,第2天空腹血糖≥7.0 mmol/L都是糖尿病(OGTT阳性)的预测因素(风险比=4.75,95%可信区间2.304~9.79,P=0.000)。结论:既往无糖尿病病史的AMI患者绝大多数合并糖代谢异常,需要进一步通过OGTT及时发现合并糖尿病或糖调节受损的患者以指导临床治疗;AMI患者反应性高血糖一般持续2~3天,如果存在持续高血糖提示患有糖尿病或糖调节受损的可能性大。高血糖是患有糖尿病的一个预测因素。  相似文献   

12.
This study prospectively evaluates the long-term prognosis of patients admitted with chest pain under suspicion of acute myocardial infarction (AMI) with and without confirmed diagnosis. All patients below 76 years of age, free of other severe diseases and alive at discharge, who were admitted to a coronary care unit of a well-defined region during 1 year, constituted the study population. In all, 275 patients with and 257 patients without confirmed AMI (non-AMI) were included. During 7 years of follow-up, 122 cardiac events (96 cardiac deaths and 26 nonfatal AMI) occurred in the AMI patients, and 69 (44 cardiac deaths and 25 nonfatal AMI) were observed in the non-AMI patients. Using univariate analysis, the following risk variables were significantly related to an impaired prognosis of non-AMI patients: age, a history of previous AMI, angina pectoris, clinical heart failure, diabetes and ST or T changes in the electrocardiogram (ECG) on admission. By multivariate analysis, the following risk factors contained independent prognostic information for non-AMI patients: (1) a history of angina pectoris and (2) ST and T changes on the ECG on admission. We conclude that a subset of non-AMI patients at high risk for cardiac events even in the long term can be identified from the medical history and the ECG on admission. These patients should be carefully evaluated prior to discharge, whereas patients without signs of ischemic heart disease have an excellent prognosis.  相似文献   

13.
We examined the prevalence of impaired glucose metabolism and its association with inflammation and insulin resistance (IR) in acute myocardial infarction (AMI) patients without a previous diagnosis of diabetes. This prospective study enrolled 52 AMI patients, and 75-g oral glucose tolerance testing was performed on 30 patients at discharge and again 3 months later. We also measured serum adiponectin, high sensitive C-reactive protein, and IL-6 on both occasions. Data were compared with those of 30 type 2 diabetic patients without a history of AMI. Forty percent and 36.7% of AMI patients had impaired glucose tolerance (IGT) at discharge and at 3 months, respectively. The corresponding proportions for newly diagnosed diabetes are 33.0% and 30.0%. At discharge, AMI patients with IGT or diabetes showed higher high sensitive C-reactive protein and IL-6 levels compared with AMI patients with normal glucose tolerance or control type 2 diabetic patients. Furthermore, AMI patients with IGT or diabetes exhibited higher IR and lower serum adiponectin levels than AMI patients with normal glucose tolerance at 3 months after discharge. Previously undiagnosed diabetes and IGT are common in Korean patients with AMI. These glycometabolic abnormalities are associated with inflammation, IR, and serum adiponectin levels.  相似文献   

14.
15.
In a totally nonselected group of patients with acute myocardial infarction (AMI) (n = 921) admitted from the emergency department to the coronary care unit or other hospital ward, the occurrence of non-Q-wave AMI and the prognosis in these patients was determined and compared with those in whom Q waves were developed. Fifty-two percent had AMI without new Q waves. Patients with a non-Q-wave AMI differed from patients with Q-wave AMI, more frequently having a previous history of AMI (p less than 0.001), angina pectoris (p less than 0.01), diabetes mellitus (p less than 0.05), congestive heart failure (p less than 0.001), and a higher mean age (p less than 0.001), whereas smoking was more common in Q-wave AMI. Patients with non-Q-wave AMI had a 1-year mortality of 31% compared with 26% in Q-wave AMI (p greater than 0.2) and a reinfarction rate of 20% compared with 12% for Q-wave AMI (p less than 0.01). Among patients aged less than 75 years without a previous history of AMI, congestive heart failure, and diabetes mellitus, the 1-year mortality rate was 16% for patients with Q waves versus 15% for those without Q waves (NS). Appearance of Q waves was not independently associated with death. We conclude that in a nonselected group of patients with AMI the occurrence of a non-Q-wave AMI is much higher than previously reported. The prognosis in AMI during one year of follow-up is not associated with development of Q waves.  相似文献   

16.
A circadian variation of symptom onset in acute myocardial infarction (AMI) with an increased frequency in the late morning and possibly also in the evening has been found in several studies. It has been suggested that different circadian rhythms may exist in various subgroups of patients. This possibility was examined in a population of 10,791 patients collected between 1973 and 1987 in a continuously operating register of patients with AMI in Malm?, Sweden. In 6,763 patients (63%) in whom a distinct symptom onset could be established, symptom onset occurred with an increased frequency between 6:01 A.M. and 12:00 noon (30.6%) and between 6:01 P.M. and 12:00 midnight (26.9%). Similar bimodal circadian rhythms were seen in patients aged greater than 70 years (n = 2,923), less than or equal to 70 years (n = 3,840), men (n = 4,528), women (n = 2,235), smokers (n = 2,458), hypertensives (n = 1,999), diabetics (n = 653), patients with (n = 1,872) and without (n = 4,891) a history of previous AMI, and in patients with recent non-Q-wave AMI (n = 333). In 455 patients receiving cardioselective beta blockers the circadian distribution did not differ from a random, whereas in patients taking nonselective beta blockers or calcium antagonists significant bimodal rhythms were found. Statistically significant interactions were found between symptom onset and age dichotomized at 70 years, and between patients with and without a history of previous AMI. In a multivariate analysis only these variables age less than or equal to/greater than 70 years; +/- history of a previous AMI) were found to modify the circadian rhythm of symptom onset in the population.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

17.
BACKGROUND: The outcome of patients with previous coronary artery bypass grafting (CABG) undergoing primary percutaneous coronary intervention (PCI) for the treatment of acute myocardial infarction (AMI) is unclear. We sought to assess the outcome of patients with prior CABG undergoing primary PCI for the treatment of AMI. METHODS AND RESULTS: Between 1991 and 1997, 1072 patients with AMI underwent primary PCI without antecedent thrombolytic therapy at the Mayo Clinic. There were 128 patients with previous CABG and 944 without previous CABG. Patients with previous CABG were further subdivided according to the treated vessel: native vessels (n = 65) and bypass graft (n = 63). Clinical and angiographic characteristics and 30-day and 1-year outcomes were evaluated. Patients with previous CABG were significantly older and had a higher incidence of diabetes, hypertension, and hypercholesterolemia. They had a lower left ventricular ejection fraction and were also more likely to have congestive heart failure. After 1 year of follow-up, adverse cardiac events (death, MI, CABG, or repeat PCI) were significantly greater in patients with prior CABG (49.2% vs 35.9%, P =.04). With use of multivariate logistic regression analysis to adjust for differences in baseline characteristics, the treatment of vein graft was independently associated with adverse cardiac events (relative risk 1.48 [95% confidence interval 1.07-2.03], P =.02), but a history of prior CABG itself was not (relative risk 1.22 [95% confidence interval 0.96-1.56], P =.11). CONCLUSIONS: Primary PCI for AMI in patients with previous CABG is associated with higher adverse events largely attributable to adverse baseline clinical characteristics and the treatment of a vein graft.  相似文献   

18.
A considerable fraction of collaterals has been shown to regress immediately after percutaneous transluminal coronary angioplasty (PTCA), but the fate of these well-developed collaterals is unknown. The authors aimed to show the protective role of these recruitable collaterals in case of an acute myocardial infarction (MI). They identified 22 patients who underwent PTCA and then were rehospitalized owing to acute myocardial infarction. These patients were compared with a group consisting of 48 patients hospitalized owing to acute MI without a history of previous PTCA. Then, the patients with collaterals were compared with the patients without collaterals to define the factors affecting the collateral formation. All the patients with collaterals before PTCA were shown to have collaterals also after AMI, and collateral grades were greater after MI (1.67 +/-0.98) when compared with those before PTCA (0.73 +/-0.7) (p = 0.001). Coronary collaterals were more commonly seen in patients with a history of previous PTCA (p = 0.005), and the grades of collaterals were also higher in these patients when compared with those without PTCA. Left ventricle score indices were lower and left ventricular ejection fractions (LVEF) were higher in patients with a history of PTCA (p = 0.001). Logistic regression analysis revealed that smoking increased the development of collaterals after AMI 3.8 fold, aspirin use 4.1 fold. On the contrary, diabetes mellitus (DM) decreased this 6.67 fold. As a result, well-developed coronary collaterals are preserved even if they have regressed after restoration of flow, and they may become functional and protect the myocardium against acute ischemia.  相似文献   

19.
目的 评价梗死前心绞痛对梗死面积及左室射血分数的影响,初步探讨缺血预适应的临床价值。方法 具有确诊的Q波心肌梗死患者144人,记录其年龄、主要病史及服药史。采用QRS记分(QRSs)法测量梗死面积(MIS),以超声多谱勒测定左室射血分数(LVEF)。将患者按梗死前1月内及48小时内是否曾发作心绞痛分组,对上述指标进行比较。结果 两组患者年龄及高血压史无差别,但梗死前心绞痛组合并糖尿病者较少(P〈)  相似文献   

20.
目的观察新诊断的糖代谢异常对急性心肌梗死后LVEF的影响。方法入选首次急性心肌梗死患者161例(对无糖尿病病史的患者发病7天后行口服葡萄糖耐量试验),根据检查结果及是否有糖尿病病史,分为正常糖耐量组(37例)、糖调节异常组(46例)、新诊断糖尿病组(37例)和既往已确诊糖尿病组(41例)。4组患者分别于发病后72 h内、30天行三维超声心动图检查评价左心室功能。结果糖调节异常组、新诊断糖尿病组和既往已确诊糖尿病组72 h内及30天随访时的LVEF均明显低于正常糖耐量组(72 h:(45.1±7.1)%、(45.0±7.2)%、(45.1±7.2)%vs(48.9±6.8)%,P<0.05;30天:(47.0±7.5)%、(47.8±7.3)%、(48.0±7.4)%vs (53.4±6.4)%,P<0.05]。结论新诊断的糖代谢异常也对急性心肌梗死后左心室功能产生不利的影响。  相似文献   

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