| Objective: In this paper, we research the prospective clinicalcomparison of anisodamine in the treatment of patients and routine hydrationtherapy in acute coronary syndrome with diabetic nephropathy undergoingelective percutaneous coronary intervention to evaluate the protective effectivesecurity of anisodamine on renal function by analyzing levels of serumcreatinine, cystatin C, creatinine clearance rate, the incidence of contrastinduced nephropathy(CIN), incidence of malignant arrhythmiarate and heartrate.Methods: From February2010to January2012, a total of107ACSpatients with diabetic nephropathy admitted in our hospital underwent electivePCI were enrolled into this randomized study(71male and36female, averageage57.7±10.49years old). Inclusion criteria:(1) The acute coronary syndromediagnostic criteria;(2)The diagnostic criteria of type2diabetes;(3)Thediagnostic criteria of diabetic nephropathy III,IV;(4) Family members ofpatients signed surgical informed consent. Exclusion criteria:(1)The contrastor anesthetic allergy;(2)Aortic dissection, malignant tumors, autoimmunediseases and infectious diseases;(3)Severe hepatic or renalinsufficiency(Ccr<50ml/min), New York Heart Association functional class IV,and hemodynamic instability;(4) Glaucoma;(5)Stenosis of renal artery(unilateral stenosis>70%or bilateral stenosis>50%);(6)Use of contrast agentsor nephrotoxic drugs in one week;(7)Tachycardia arrhythmia;(8) Activeinternal bleeding;(9) Severe anemia or thrombocytopenia;(10) Pregnant orlactating women;(11) Not signed the surgery informed consent. All patientswere randomly divided into the anisodamine group (group A)and the placebogroup(Group B). Before elective PCI, give two groups of patients aspirin, clopidogrel, heparin, statins and nitrates. The two groups both receivedintravenous hydration therapy. The speed of infusion of0.9%sodium chlorideat1ml/kg/h or0.5ml/kg/h(CHF). Patients in the group A received anisodamine50μg/kg bolus injection after randomization within3minutes followed by anadjusted-dose (0.1-0.2μg/kg/min) to24h after PCI, while patients in group Breceived infusion of placebo (0.9%sodium chloride) with the same volume ofA group.The PCI were completed by the radial or ulner path of the forearmand in accordance with success criteria of PCI. Non-ionic low-osmolar CM(Iohexol,350mgI/ml) were used in PCI.The levels of serum creatinine (Scr),cystatin C were detected at24hbefore and24h,48h,72h after PCI. Calculate the creatinine clearance rate(Ccr) and the incidence of CIN according to serum creatinine level. Recordheart rate changes of the patients in the two groups by24-hour Holter. Recordthe result of coronary angiography and PCI. Data were analyzed by SPSS13.0.P<0.05was considered statistically significant.Results:1. There were no significantly difference between baseline clinical documentson age, gender, weight, risk factors, blood glucose, glycated hemoglobin,heart rate, systolic blood pressure, diastolic blood pressure, LVEF, BNP,Scr, Ccr, CysC,UAER,24-hour urine protein, oral drug and so on.(P>0.05)2. There were no significantly difference between the two groups on thedistribution of lesion related artery, stent length, stent diameter, amount ofcontrast agent, hydration liquid volume and so on.(P>0.05) The coronaryblood flow of the two groups achieved TIMI flow grade3.3. The results of renal function3.1Changes of ScrThe SCr concentration at admission was not significantly differentbetween the two groups before PCI(P>0.05). However, the Scr was lower ingroup A than that in group B at48h and72h after PCI (93.2±15.26μmol/Lvs112.51±22.96μmol/L, P<0.05),(84.40±13.47μmol/Lvs94.84±17.65μmol/L, P<0.05). The SCr concentrations in group A was significantly higher at48hafter PCI than that at24h after PCI (93.2±15.26μmol/Lvs84.77±11.95μmol/L,P<0.05), lower at72h after PCI than that at48h after PCI(84.40±13.47μmol/Lvs93.2±15.26μmol/L, P<0.05). SCr concentration at72h returned to baselinelevel(84.40±13.47μmol/Lvs82.22±10.23μmol/L, P>0.05). In group B, the SCrconcentrations was significantly higher at48h after PCI than that at24h afterPCI(112.51±22.96μmol/Lvs86.71±13.63μmol/L, P<0.05), lower at72h afterPCI than that at48h after PCI(94.84±17.65μmol/Lvs112.51±22.96μmol/L, P<0.05). However, SCr concentration at72h after PCI was higher than24hbefore PCI (94.84±17.65μmol/Lvs82.7±10.86μmol/L, P<0.05).3.2Changes of CysCThe CysC level was not significantly different between the two groups at24h before PCI(P>0.05). However, the CysC was significantly lower in groupA than that in group B at24h and48h after PCI (1.17±0.28mg/Lvs1.33±0.33mg/L, P<0.05),(0.97±0.28mg/Lvs1.13±0.29mg/L, P<0.05). TheCysC level in group A was significantly higher at24h after PCI than that at24h before PCI(1.17±0.28mg/Lvs0.91±0.30mg/L, P<0.05). The CysCdecreased at48h after PCI significantly and returned to the level beforePCI(0.97±0.28mg/Lvs0.91±0.30mg/L,P>0.05). The CysC level in group Bwas significantly higher at24h after PCI than that at24h beforePCI(1.33±0.33mg/Lvs0.93±0.31mg/L,P<0.05),The CysC decreased at48hafter PCI significantly than24h after PCI, but it was higher than the levelbefore PCI. The CysC at72h after PCI decreased to the level beforePCI(0.95±0.29mg/Lvs0.93±0.31mg/L,P>0.05).3.3Changes of CcrThe Ccr level was not significantly different between the two groupsbefore PCI(P>0.05). The Ccr level was significantly higher in group A thanthat in group B at24h,48h and72h after PCI (85.62±17.82ml/minvs78.05±18.47ml/min,77.97±17.69ml/minvs71.76±20.36ml/min,85.07±17.73ml/minvs78.41±18.73ml/min, all P<0.05).In group A, The Ccr level was significantlylower at48h after PCI significantly than24h after PCI (77.97±17.69ml/min vs85.62±17.82ml/min, P<0.05). The Ccr level was significantly higher at72hafter PCI than that at48h after PCI and returned to the level beforePCI(85.07±17.73ml/minvs87.27±18.74ml/min,P>0.05). In group B, the Ccrlevel was significantly lower at48h after PCI significantly than24h afterPCI(78.41±18.73ml/minvs71.76±20.36ml/min,P<0.05),it began to rise at72hafter PCI, but, it was lower than24h before PCI (78.41±18.73ml/minvs88.51±17.14ml/min,P<0.05).4. The incidence of CIN between the two groupsThe incidence of CIN was5.6%,7.4%,5.6%at24h,48h,72h after PCIin group A. The incidence of CIN was18.9%,22.6%,20.8%at24h,48h,72hafter PCI in group B. The incidence of CIN in group A was lower than that ingroup B within72hours after primary PCI(P<0.05).There was a significantstatistical difference. Dialysis was not used in the two groups.5.Safety evaluationThere were no palpitation, thirst, blurred vision and retention of urinehappened in the two groups.The average heart rate in group A increasedslightly(76.8±10.6bpmvs72.6±12.8bpm, P<0.05).The heart rate rise fastestafter bolus injection of anisodamine(85.9±16.4bpmvs72.6±12.8bpm, P<0.05).Malignant arrhythmia occurred in one case in group A and the same in groupB(1.85%vs1.89%, P>0.05). No cardiac death happened in the two groups.Conclusion:1Intravenous application of anisodamine on acute coronary syndrome patientswith diabetic nephropathy can alleviate the renal impairment of glomerularand tubular caused by CM effectively and reduce the incidence of CIN.2Intravenous administration of anisodamine in acute coronary syndromepatients with diabetic nephropathy is safe. |
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