非糖尿病患者急性心肌梗死早期胰岛素抵抗现象研究

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目的:探讨既往无糖尿病病史的急性心肌梗死患者早期胰岛素抵抗情况。方法:2009-02至2009-09,在我院连续入选158例既往无糖尿病病史,且在发病24 h内接受急诊经皮冠状动脉介入治疗的ST段抬高急性心肌梗死患者,出院前均进行口服葡萄糖耐量试验,按照结果分为糖代谢正常组(n=44)、糖调节受损组(n=65)和新诊断糖尿病组(n=49),以稳态模型胰岛素抵抗指数(HOMA-IR)≥2.5认为存在胰岛素抵抗,评价不同糖代谢组患者急性期(入院时)与稳定期(出院时)的胰岛素抵抗情况。结果:158例患者中,胰岛素抵抗者急性期为50.0%(79/158例),稳定期为31.6%(50/158例),胰岛素抵抗比例在急性期明显多于稳定期(P=0.000),差异有统计学意义。急性期HOMA-IR(0.98±0.81)明显高于稳定期HOMA-IR(0.58±0.67),P<0.05,差异有统计学意义。急性期HOMA-IR,新诊断糖尿病组高于糖调节受损组和糖代谢正常组[(1.30±0.84)vs(0.96±0.78)vs(0.57±0.55),P均<0.05],差异均有统计学意义。稳定期HOMA-IR新诊断糖尿病组和糖调节受损组高于糖代谢正常组[(0.78±0.57)vs(0.57±0.80)vs(0.41±0.51),P均<0.05],差异有统计学意义。多元逐步回归方程显示,第2天空腹血糖[标准化回归系数(β)=0.230,P=0.000]、空腹胰岛素(β=0.758,P=0.000)、体重指数(β=0.087,P=0.005)和糖化血红蛋白(β=0.104,P=0.003)是急性期胰岛素抵抗的影响因素;体重指数(β=0.382,P=0.000)是稳定期胰岛素抵抗的影响因素。结论:无论糖代谢情况如何,胰岛素抵抗在急性心肌梗死早期有加重现象;第2天空腹血糖、糖化血红蛋白和体重指数是急性期胰岛素抵抗的影响因素,体重指数是稳定期胰岛素抵抗的影响因素。 Objective: To investigate the early insulin resistance in patients with acute myocardial infarction without previous diabetes mellitus. METHODS: From January 2009 to September 2009, 158 consecutive patients with ST-segment elevation acute myocardial infarction who had no prior history of diabetes mellitus and underwent percutaneous coronary intervention within 24 hours of onset were enrolled in our hospital and were discharged before discharge The oral glucose tolerance test was divided into normal glucose metabolism group (n = 44), impaired glucose regulation group (n = 65) and newly diagnosed diabetes group (n = 49) according to the results. The HOMA- IR) ≥2.5 considered insulin resistance and evaluated the insulin resistance in acute phase (admission) and stable (discharge) patients in different glycometabolism groups. Results: Among the 158 patients, the insulin resistance rate was 50.0% (79/158) in acute phase and 31.6% (50/158) in stable phase. The percentage of insulin resistance in acute phase was significantly higher than that in stable phase (P = 0.000) ,The difference was statistically significant. HOMA-IR (0.98 ± 0.81) in acute stage was significantly higher than that in stable stage HOMA-IR (0.58 ± 0.67), P <0.05, the difference was statistically significant. In the acute phase of HOMA-IR, the newly diagnosed diabetic patients were higher than those in the normal glucose-regulated group and the normal glucose-metabolized group [(1.30 ± 0.84) vs (0.96 ± 0.78) vs (0.57 ± 0.55), P <0.05] Statistical significance. The levels of HOMA-IR in the newly diagnosed diabetes mellitus group and the impaired glucose regulation group were significantly higher than those in the normal glucose metabolism group [(0.78 ± 0.57) vs (0.57 ± 0.80) vs (0.41 ± 0.51), P <0.05] significance. The multiple stepwise regression equation showed that fasting blood glucose (standardized regression coefficient (β) = 0.230, P = 0.000], fasting insulin (β = 0.758, P = 0.000) and body mass index (β = 0.087, P = 0.005) Glycosylated hemoglobin (β = 0.104, P = 0.003) was the influencing factor of acute insulin resistance. Body mass index (β = 0.382, P = 0.000) was the influencing factor of stable insulin resistance. CONCLUSION: Insulin resistance aggravates the early stage of acute myocardial infarction regardless of glucose metabolism. Fasting blood glucose, glycosylated hemoglobin and body mass index are the influencing factors of acute insulin resistance on the second day. BMI is the influencing factor of stable insulin resistance.
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