Atorvastatin Improved Contrast Media Induced Short Term Renal Function Damage And Effected On Patients With Stable Angina Post Percutaneous Coronary Intervention

PartⅠAtorvastatin Improved Contrast Media Induced Short Term Renal Function DamageObjective To study the effects of atorvastatin on contrast media induced renal function change and plasma hsCRP in patients undergoing coronary angiography. Methods 120 patients who underwent coronary angiography were randomized to receive atorvastatin (20mg/qn,n=60) or no atorvastatin (n=60) treatment 2 to 3 days before coronary angiography. Urinaryα1-MG, TRF and mALB were checked for evidence of tubular or glomerular damage at start, 1 day and 2 days after the administration of a radiocontrast agent. Serum creatinine, BUN, cystatin C and hsCRP levels were also assessed at the same time. Ccr and GFR were calculated ccording to Cockcroft-Gault or GFR(ml/min)=74.835/CysC1.33 formula basing on serum creatinine or cystatin C concentration. Results 1) In control group, comparison with the value before coronary angiography,urinaryα1-MG, TRF and mALB or serum cystatin C and hsCRP significantly increased at day 1 after angiography(P<0.01). In comparison to the day 1 levels taken after angiography, urinaryα1-MG, TRF, mALB, serum cystatin C significantly decreased at day 2 after angiography(P<0.01), butα1-MG, cystatin C remained at a higher level, TRF and mALB levels at day 2 after angiography had no significant change compared to baseline (P>0.05), hsCRP level at days 2 after angiography had no significant change compared to the day 1 levels after angiography (P>0.05)too. 2) In comparison with the value before coronary angiography in atorvastatin-treated group, urinaryα1-MG, TRF and mALB or serum cystatin C levels at day 1 after angiography had no significant change compared to baseline(P>0.05), the same results in day 2 too. HsCRP significantly increased at day 1 after angiography compared to baseline(P<0.01), but it had no significant change compared to day 2 after angiography(P>0.05). 3)Compared to the control group, the values of urinaryα1-MG, TRF and mALB or Cys C and hsCRP significantly decreased at day 1 after angiography in atorvastatin-treated group(P<0.01), urinaryα1-MG, cystatin C and hsCRP significantly decreased at day 2 (P<0.01)too, but TRF and mALB had no significantly change at day 1 or day 2 after angiography in two groups(P>0.05). There was no significant change in BUN, Scr, Ccr levels compared to baseline after angiography in two groups. Conclusion Contrast medium induces light renal function damage. Pretreatment with atorvastatin 20 mg/qn for 2 to 3 days significantly reduced procedural inflammatory reactions, light increasing in urinary protein and the effect of degrading GFR in coronary angiography patients, offering an instruction on prevention of CIN in clinical practice.PartⅡEffect of Different Dose of Atorvastatin on Cardial Protection and Inflammation in Patients with StableAngina after Percutaneous Coronary InterventionObjective To study the effects of atorvastatin for protection of myocardium and inflammatory factors after percutaneous coronary intervention (PCI). Methods 82 patients with chronic stable angina without previous statin treatment at least 2 month before PCI were randomized to receive atorvastatin 10mg/qn (group A n=27), 20mg/qn (group B n=28) or 40mg/ qn (group C n=27) treatment 3 days before PCI. CK-MB, cTnI, hsCRP, IL-6,sICAM-1 were measured at baseline and at 8 and 24 hours after the procedure. One-month clinical follow-up was obtained by office visit in all patients. Results The peak levels of marks of CK-MB and cTnI were increased significantly in all three groups after PCI. There were significant differences among three groups on the two items (P<0.05). Postprocedural peak levels of marks above the upper normal limit in group A, group B and group C were: 40.74%, 22.22% and 11.1% for CK-MB, 55.56%, 28.57% and 18.52% for cTnI. CK-MB elevation >2 time upper normal limit was detected after PCI in 29.62% of patients in group A , 7.41% of those in group B and 3.70% in group C; Similarly, cTnI elevation >3 time upper normal limit was 44.44% in group A , 17.85% in group B and 11.11% in group C. Either above the upper normal limit or elevation >3 time upper normal limit of the mark of cTnI, there was significantly differences in group A and group B (P<0.05)or in group A and group C (P<0.05), however there was no significantly different in group B and group C (P>0.05). Similarly, the result of CK-MB is the same among the three groups. The level of IL-6, sICAM-1 and hsCRP 8 hour after PCI were higher than those before the PCI (P<0.05). There were significant difference of IL-6 and hsCRP among the three groups (P<0.05), but no significant difference about sICAM-1 (P>0.05). The level of hsCRP and sICAM-1 24 hour after PCI were higher than those 8 hour after the PCI (P<0.05) in each group, but IL-6 significantly decreased (P<0.05). There were significant difference of the there items among three groups (P<0.05). Conclusion Even short term pretreatment with atorvastatin before PCI may reduces procedural myocardial injury in chronic stable angina patients, and increase the function as the increase of dose in the study extension, but there is no totally dose-effect relationship. The function of atorvastatin in anti-inflammatory and improving endothelium may play a lot. There is instruction on pharmacological therapy before PCI in clinical practice.