| ObjectiveTo investigate influence of single administration of different doses of statins on platelet activation, blood coagulation system and inflammatory reaction and also, to investigate the incidence of main adverse cardiac events(MACE) and adverse drug reactions in patients with acute coronary syndrome(ACS)after percutaneous coronary intervention(PCI). MethodsOne hundred and forty eight patients with acute coronary syndrome(ACS) were randomly enrolled. On the basis of conventional drug therapy, patients were randomized into three groups of different atorvastatin dose at 12 hours before PCI: atorvastatin 20mg(group A), atorvastatin 40mg(group B), atorvastatin 80mg(group C). After PCI, atorvastatin 20mg/day orally were prescribed for all patients in the three groups. The platelet count(PLC), prothrombin time(PT), activated partial thromboplatin time(APTT), Fibrinogen(FIB), thrombin time(TT), d-dimer(DD), fibrinopeptide A(FPA), platelet alpha-granule membrane glycoprotein 140(GMP-140), hypersensitive c-reactive protein(hs-CRP) were measured 12 h before and after PCI, and thrombelastogram(TEG) was performed to compare the reaction time(R), the coagulation time(K), the solidification angle(Angle), the maximum amplitude(MA) 12 h before and after PCI. The incidence of main adverse cardiac events(MACE) and adverse drug reactions during the following 30 days after PCI were also investigatee. Results1.There were no significant differences in the levels of FPA、GMP-140 among the three groups 12 hours before PCI(FPA: group A 98.87±5.65ug/L vs group B 97.39±6.14ug/L vs group C 97.34±5.97ug/L P>0.05; GMP-140: group A 82.88±6.14ug/L vs group B 80.07±9.60ug/L vs group C 80.12±8.04ug/L P>0.05). There were significant differences in the levels of FPA, GMP-140 among the three groups 12 hours after PCI(FPA: group A 96.55±3.58ug/L vs group B 95.36±2.71ug/L vs group C 87.24±3.43ug/L P<0.05; GMP-140: group A 77.28±5.27ug/L vs group B 77.94±5.21ug/L vs group C71.47±7.04ug/L P<.05). Further, for the three groups, FPA, GMP-140 levels was not significantly different between group A and B(P>0.05), while group C was significantly lower than A,B groups(P<0.05).2. There were no significant differences in the levels of R、K、Angle、MA among the three groups 12 hours before PCI.(R: group A 5.66±0.54 min vs group B 5.58±0.54 min vs group C 5.72±0.55 min P>0.05; K: group A 1.47±0.14 min vs group B 1.50±0.13 min vs group C 1.49±0.12 min P>0.05; Angle: group A 67.92±1.66 deg vs group B 68.08±1.72 deg vs group C 68.12±1.64 deg P>0.05; MA: group A 65.19±2.03 mm vs group B 64.72±2.11 mm vs group C 64.84±2.00 mm P>0.05). There were significant differences in the levels of R, Angle, and MA among the three groups 12 hours after PCI.(R: group A 5.79±0.58 min vs group B 5.88±0.58 min vs group C 6.37±0.70 min P<0.05; Angle: group A 67.50±1.50 deg vs group B 67.38±1.66 deg vs group C 63.50±1.50 deg P<0.05; MA: group A 64.39±3.43 mm vs group B 63.73±3.20 mm vs group C 61.8±3.02 mm P<0.05). There were no significant differences in the levels of K among the three groups 12 hours before PCI.(K: group A 1.65±0.16 min vs group B 1.68±0.18 min vs group C 1.71±0.20 min P>0.05). Further, among the three groups, the R, Angle, and MA level was not significantly differene between group A and group B(P>0.05), while the level of Angle and MA level were significantly lower than group A and group B(P<0.05) and the R value in group C was significantly higher than group A and group B(P<0.05).3. There were no significant differences in the levels of hs-CRP among the three groups 12 hours before PCI(hs-CRP: group A 5.02±2.19 mg/L vs group B 5.99±2.05 mg/L vs group C 5.75±2.26 mg/L P>0.05). Among the three groups, the levels of hs-CRP were increased 12 hours after PCI. However, the elevated hs-CRP level showed no significant difference between group A and group B(P>0.05), while in group C it was significantly lower than group A and group B(P<0.05).4. For the incidence of MACE in patients 30 days after PCI, patients in three groups all had angina pectoris, there was no significant difference between group A and group B(P>0.05), while in group C it was significantly lower than group A and group B(P<0.05). No myocardial infarction, target vessel revascularization and cardiac death were found in patients of all the three groups.5. Comparison of adverse drug reactions. There were no myalgia, rhabdomyolysis, and drug-induced liver injury was found in patients of all the three groups. ConclusionFor ACS patients undergoing selective PCI therapy, after comparing effects of different single atorvastatin loading dose of 20 mg, 40 mg and 80 mg 12 hours before PCI, we conclude that:1. Administration of atovastatin(80 mg) loading dose 12 hours before PCI can effectively inhibits the 1evel of GMP-140, MA in patients with acute coronary syndrome(ACS) undergoing percutaneous coronary intervention(PCI). This demonstrate that atovastatin(80 mg) can effectively inhibit platelet activation in patients with acute coronary syndrome(ACS) after percutaneous coronary intervention(PCI).2. Administration of atovastatin(80 mg) loading dose 12 hours before PCI can effectively inhibits the 1evel of FPA, Angle, and also extend R time in patients with acute coronary syndrome(ACS) undergoing percutaneous coronary intervention(PCI). This demonstrate that atovastatin(80 mg) can effectively inhibit coagulation in patients with acute coronary syndrome(ACS) after percutaneous coronary intervention(PCI).3. Administration of atovastatin(80 mg) loading dose 12 hours before PCI can effectively inhibits the 1evel of elevated hs-CRP in patients with acute coronary syndrome(ACS) undergoing percutaneous coronary intervention(PCI). This demonstrate that atovastatin(80 mg) can effectively inhibit inflammatory response in patients with acute coronary syndrome(ACS) after percutaneous coronary intervention(PCI).4. Administration of atovastatin(80 mg) loading dose 12 hours before PCI can effectively reduced MACE 30 days after PCI. No serious adverse reactions of drugs were found. |
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