| Objective: To explore the preventive effect of intensive atorvastatintherapy in patients with acute ST-segment elevation myocardial infarctionundergoing emergency percutaneous coronary invention and Possiblemechanisms.Methods: From October2009to October2011, patients with STEMIwithin12hours of symptom onset who underwent Primary percutaneouscoronary intervention(N=161),admitted in Second Affiliated Hospital ofHebei medical university,were enrolled in this study. Inclusion criteria: acuteST-segment elevation myocardial infarction within12hours undergoingemergency PCI.exclude criteria:(1) Cardiogenic shock(2)Infectious diseases,autoimmune diseases, cancer (3)Any history of using statin medicine (4)Anybaseline increase in liver enzymes aspartate aminotransferases(ALT)；Renalfailure with a creatinine level>3mg/dl (5)Any contraindication of usinganticoagulant drugs (6)History of renal artery stenosis (7)Aftercardiopulmonary resuscitation (8)The contrast agent allergy.The patients wererandomized into two groups: Intensive atorvastatin therapy group (GroupA,N=78);The normal-does group (Group B,N=83) with the random figures.All the patients of group A immediately chew atorvastatin80mg before theemergency PCI and40mg/d after the PCI. The patients of group B chew noloading atorvastatin before the emergency PCI and20mg/d after the PCI.Allthe patients accepted routine medicine treatment as Aspirin, clopidogrel,nitrates, low molecular weight heparin, ACEI class drugs, β receptor blockersand other drugs before and after PCI.All the patients accepted PCI via the radial artery and got hydration treatment after PCI.All observed in patients undergoing emergency PCI were routinelycubital vein blood for biochemical tests to check liver function, LDL-C,kidney function ct. The serum creatinine levels were monitored at the24hours,48hours,72hours after PCI. Cystatin C was measured24h afterPCI.LDL-C was rechecked at the3rdday, ALT and CK were rechecked at theSecond week, angiography results were recorded, the amount of contrast agentand stent using in the PCI.Application of SPSS13.0software for statisticalanalysis, P <0.05was considered statistically different.Result:1,161patients were enrolled in the the study,group A (N=78),groupB(N=83),Clinical baseline data of group A and group B(age, gender, bodymass index, smoking,Hyperlipidemia,pressures,diabetes,killip classes,AnteriorMI,total cholesterol, low density lipoprotein cholesterol, serum creatinine,Peak CK-MB, ejection fraction,Blood glucose,Hydration and drug use)between the two groups were no significant different (P>0.05).(Tablet1)2,Group A and group B, the two groups at the onset to surgery time, time ofopening IRA(infarction related artery), the IRA type, lesion type, using ofhydrochloric acid tirofiban, number of stenting, situation of no-reflow inemergency PCI, using thrombus aspiration devices were no significantdifferent3, Group A compared with group B, preoperative serum creatinine, nosignificant statistical difference (82.3±11.2μmol/L vs.82.6±11.3μmol/L, P>0.05).In group A,serum creatinine level at the24thhour after PCI comparedwith that in group B has no significant statistical difference(84.5±12.9μmol/Lvs.86.8±14.2μmol/L, P>0.05), serum creatinine level of the two groupswere elevated compared with the preoperative levels (group A,82.3±11.2μmol/L vs.84.5±12.9μmol/L, P <0.05; group B82.6±11.3μmol/Lvs.86.8±14.2μmol/L, P <0.05), In group A,serum creatinine level at the48thhour after PCI compared with that in group B has statistically significantdifferences (93.4±17.1μmol/L vs.112.6±23.3μmol/L, P <0.0001). The48thhour serum creatinine level compared with the24thh level were elevated (group A93.4±17.1μmol/L vs.84.5±12.9μmol/L, P <0.05; group B112.6±23.3μmol/L vs.86.8±14.2μmol/L, P <0.05),,serum creatinine level at the72thhour after PCI compared with that in group B had statistically significantdifferences (84.2±14.2μmol/L vs.95.3±17.7μmol/L, P <0.0001), The72thhour serum creatinine level compared with the48hh level were dropped(group A84.2±14.2μmol/L vs.93.4±17.1μmol/L, P <0.05; group B95.3±17.7μmol/L vs.112.6±23.3μmol/L, P<0.05). The incident of CIN(ContrastInduced Nephropathy)in the two groups (2cases in group A,13cases in GroupB) had statistically significant differences (2.6%vs.15.7%, P=0.01, P <0.05).4, Preoperative Ccr in the two groups had no significant statistical difference(93.2±5.3ml/min vs.93.1±5.1ml/min, P>0.05), The24thhour level of Ccrhad no significant difference compared with group B (91.8±6.1ml/min vs.91.4±6.9ml/min, P>0.05), the levels of the24thhour in the two groups wereelevated compared with the preoperative levels(group A,91.8±6.1ml/minvs.93.2±5.3ml/min, P <0.05; group B91.4±6.9ml/min vs.93.1±5.1ml/min, P <0.05).The48thhour level of Ccr in group A had significant differencewith group B(89.3±8.2ml/min vs.79.2±10.2ml/min, P <0.0001). the levelsof the48thhour in the two groups were dropped compared with the24thhourlevels (group A89.3±8.2ml/min vs.91.8±6.1ml/min, P <0.05; group B79.2±10.2ml/min vs.91.4±6.9ml/min, P <0.05). The72thhour level of Ccrin group A had significant difference with group B (92.2±7.2ml/min vs.87.4±8.3ml/min, P <0.0001). the levels of the72thhour in the two groups wereelevated compared with the48thhour levels (group A92.2±7.2ml/minvs.89.3±8.2ml/min, P<0.05; Group B87.4±8.3ml/min vs.79.2±10.2ml/min,P <0.05). preoperative Cystatin C level in two groups have no significantdifference (0.42±0.09mg/L vs.0.42±0.10mg/L, P>0.05), The24thhourCystatin C levels were statistically significant differences compared withgroup B (0.51±0.14mg/L vs.0.61±0.13mg/L, P <0.0001).The24thhourCystatin C levels compared with preoperative were elevated in the two groups(group A0.42±0.09mg/L vs.0.51±0.14mg/L, P <0.0001; group B,0.42±0.10mg/L vs.0.61±0.13mg/L, P<0.0001). Levels of two groups of CRP had no significant difference compared with preoperative (7.7±8.9mg/L vs.8.0±9.2mg/L, P>0.05),CRP Peak of group A were significantly lower than groupB(11.5±10.3mg/L vs.15.4±11.4mg/L, P <0.05).In the CIN patients of groupA, CRP Peak were significantly lower than that in group B (22.7±22.3mg/Lvs.26.7±25.3mg/L, P <0.05), Non-CIN patients CRP peak in group A weresignificantly lower than that in group B (9.8±9.2mg/L vs.12.4±8.9mg/L, P<0.05).5, Through the liver function monitoring at the second week after PCI,thecases abnormal liver function in two groups: one case in group A,one case ingroup B,two groups had no significant difference (1.2%vs.1.2%, P>0.05).NoRhabdomyolysis happened in two groups.Conclusion:1,Intensive atorvastatin therapy can significant prevent the incidence of CINcompared with routine dose and the prevention mechanism maybe related tothe decrease of the inflammatory response.2,Intensive atorvastatin therapy is safe and feasibility with low incidences ofside effects such as liver function damage ct. |
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