| Objective: This study was explored to the influences on the glucosemetabolism between atorvastatin and pitavastatin in patients with acutecoronary syndrome (ACS).Methods: From July2012to December2012, consecutive patients withACS who was admitted to the Second Hospital of Hebei Medical Universitywere enrolled. Recruiting criteria:(1)Patients complained with ACS accordingto the diagnostic criteria.(2) With or without diabetes, but hemoglobin A1c(HbA1c)<7％.(3) No taking statins before or having ceased at least10days.Exclusion criteria:(1) Statins allergy (2) A long-term regular use of statins (3)severe liver and kidney insufficiency (4) Cardiogenic shock (5) Infectiousdiseases, autoimmune diseases, cancer (6) Over75years old (7) Endocrinediseases such as thyroid diseases, adrenal diseases which can affect plasmaglucose. The patients were divided into two groups randomly: groupA (treatedwith atorvastatin20mg per night orally) and group B (treated with pitavastatin2mg per night orally). All patients were given routine medicine treatmentssuch as aspirin, clopidogrel, low molecular weight heparin, nitrates,angiotensin converting enzyme inhibitor (ACEI) or angiotensin Ⅱ receptorblocker (ARB), beta-blockers and calcium channel bloker (CCB). Standard18-lead ECG was recorded and myocardial enzymes, troponin(cTnI), kidneyfunction and electrolytes were measured at admission immediately. Fastingplasma glucose (FPG), liver function, lipids were recorded in the next daymorning. Patients with acute myocardial infarction (AMI) checked enzymesand cTnI every3hours within the first24hours, every6hours during the next24hours and were monitored for at least3days. FPG, fasting serum insulin(FSI) and HbA1c were rechecked after1week treatment,4weeks treatmentand12weeks treatment. We calculated insulin resistance index respectively according Homeostatic Model Assessment-Insuling Resistance (HOMA-IR)using the equation as follows: HOMA-IR=FPG(mmol/L)×FSI(μU/mL)/22.5,HOMA-IR1=Ln [FPG (mmol/L)×FSI (μU/mL)]. The software of SPSS19.0(SPSS Ins., Chicago, Illinois) was used in the statistic analyses, a two-sided ofP-value <0.05was defined as statistically significant.Results:1A total of109cases were enrolled, with57cases in group A (34malesand23females, average age was56.07±8.97years old) and52cases in groupB (35males,17females, average age was56.21±8.68years old). There wasno significant difference in gender, age, body mass index (BMI), systolicblood pressure (SBP), history of smoking, hypertension, diabetes and previousstatin drug, levels of total cholesterol (TC), triglycerides (TG), low-densitylipoprotein (LDL-C), high density lipoprotein (HDL-C), glutamic-pyruvictransaminase (ALT), and serum creatinine (SCr) between group A and B.2The baseline concentrations of FPG, FSI, HbA1c and HOMA-IR1in thegroup A were7.46±0.56mmol/L,7.97±2.38μU/mL,6.22±0.31%and4.04±0.35respectively. The baseline concentrations of FPG, FSI, HbA1c andHOMA-IR1in the group B were7.54±0.52mmol/L,8.03±2.49μU/mL and6.29±0.29%and4.05±0.35respectively, which indicated no significantdifference between the two groups. After4weeks treatment of statins, FPGand HbA1c between the group A and group B also indicated no significantdifference (7.56±1.11mmol/L vs.7.43±0.90mmol/L, P>0.05;6.36±0.70%vs.6.24±0.56%, P>0.05); but after12weeks treatment of statins, FPG andHbA1c in the group A were higher than group B (8.93±0.81mmol/L vs.7.08±0.71mmol/L, P<0.01;7.11±0.47%vs.6.05±0.43%, P<0.01). As toFSI and HOMA-IR1,both showed significant differences between the twogroups after4weeks treatment and12weeks treatment (8.95±2.68μU/mL vs.7.47±2.28μU/mL, P<0.01;10.32±3.26μU/mL vs.6.56±1.63μU/mL,P<0.01;4.16±0.43vs.3.96±0.41, P<0.05;4.47±0.37vs.3.80±0.32, P<0.01).3No matter FPG, HOMA-IR1or HbA1c, there were significantdifferences at different time(P<0.05). In the group A or the group B, no significant changes of FPG and HbA1c, between4weeks treatment andbaseline(7.56±1.11mmol/L vs.7.46±0.56mmol/L, P>0.05;7.43±0.90mmol/L vs.7.54±0.52mmol/L, P>0.05;6.36±0.70%vs.6.22±0.31%, P>0.05;6.24±0.56%vs.6.29±0.29%, P>0.05). But FPG and HbA1c were higher thanbefore in the group A and lower in the group B after12weekstreatment(8.93±0.81mmol/L vs.7.56±1.11mmol/L,P<0.05;7.08±0.71mmol/L vs.7.43±0.90mmol/L, P<0.01).There were indicated significantdifferences for HOMA-IR1after4weeks treatment and12weeks treatment(4.16±0.43vs.4.04±0.35, P<0.01;4.47±0.37vs.4.16±0.43, P<0.01).As toFSI, there was no significant difference at different time (P>0.05). The levelsof insulin secretion were8.95±2.68μU/mL and10.32±3.26μU/mL after4weeks treatment and12weeks treatment of atorvastatin,7.47±2.28μU/mLand8.03±2.49μU/mL of pitavastatin. As the data aboved, they had theincreasing trend and decreasing trend respectively; however, no significantchanges were shown.Conclusions:1Short-term (within4weeks) treatment of atorvastatin can increase FSIand IR, but doesn’t increase the levels of FPG and HbA1c; while FPG, FSI,HbA1c and IR are all increased after long-term (more than12weeks)treatment of atorvastatin in the patients with ACS.2The indexes of glucose metabolism (FPG, HbA1c, FSI and IR) are notchanged after short-term (within4weeks) treatment of pitavastatin; while theyare all decreased after long-term (more than12weeks) treatment ofpitavastatin in the patients with ACS.3Compared with atorvastatin, long-term treatment of pitavastatin isbeneficial for the improvement of FPG and IR in the patients with ACS. |
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