Protective effects of anisodamine on contrast induced nephropathy in patients with ST segment elevation myocardial infarction undergoing primary percutaneous coronary intervention

Abstract

Introduction: Contrast-induced nephropathy (CIN) is one of most serious complications after percutenous coronary intervention (PCI). Patients with acute myocardial infarction undergoing primary PCI are at high risk for CIN. Anisodamine, an alkaloid extracted from a Chinese herb, is widely used in the treatment of septic shock, acute glomerulonephritis and diabetic nephropathy, and shows protective effective on renal function. Objectives: To investigate anisodamine for the prevention of CIN in patients with ST segment elevation myocardial infarction (STEMI) undergoing primary PCI. Methods: Consecutive patients undergoing primary PCI were randomly assigned to one of two groups: patients in anisodamine group (ANI group) were assigned to receive anisodamine (3- 4ug/kg/min intravenous infusion of anisodamine within 30 minutes before primary PCI), and control group (CON group) to isotonic saline (0.9%) with the same volume. All patients were hydrated with intravenous isotonic saline (0.9%) for 12 hours after PCI. The Serum creatinine (SCr) concentrations were measured at admission, 24 hours, 48 hours and 72 hours after PCI. Results: A total of 126 patients completed the study, while 60 in ANI group and 66 in CON group. The SCr concentrations significantly increased after PCI, with the peak value occurring at 48 hours, and then began to decrease. At 48 hours after PCI, the SCr concentration significantly increased to the maxium in both groups (both P <0.0001). In ANI group, the SCr concentration decreased significantly (P<0.0001) at 72 hours, and retuned to the baseline level (P>0.05). In CON group, however, the SCr concentration decreased significantly (P<0.0001) at 72 hours, but was still higher than baseline level (P<0.0001). The SCr concentrations at 48 and 72 hours after PCI were much lower in ANI group than those in CON group (both P<0.05). The eGFR significantly decreased after PCI, the lowest value occurred at 48 hours, and then it began to increase. In ANI group, the eGFR increased significantly (P<0.0001) at 72 hours, and was similar to the baseline level (P>0.05). In CON group, the eGFR increased significantly (P<0.0001), but failed to retune to baseline at 72 hours (P<0.0001). The eGFR at 24, 48 and 72 hours after PCI were higher in ANI group (all P<0.05). The incidences of CIN in ANI group were lower than those in CON group within 72 hours after PCI (all P<0.05). Conclusion: Intravenous infusion of anisodamine prior to primary PCI may prevent the incidence of CIN in STEMI patients.