Objectives: To explore the preventive effects of intracoronaryadministration of anisodamine on coronary microcirculation in patients withacute inferior myocardial infarction (AIMI).Methods: From March2011to December2012, a total of92patientsunderwent primary PCI within12hours from the onset of AIMI were enrolled.All subjects were well prepared with oxygen, electrocardiogram (ECG)monitoring as well as adequate anticoagulation and antithrombotic treatment.After Coronary Artery Agiography (CAG), the patients were randomlyassigned to receive anisodamine (group A, n=47) or placebo (group B, n=45).Intracoronary anisodamine was administered immediately when antegradeflow was regained, while patients in control group received intracoronaryadministration of0.9%sodium chloride with the same volume as anisodamingroup in the same way. All patients were placed in drug-eluting stents by thestandard of beyond75%of luminal stenosis. During the procedure, the TIMImyocardial perfusion grade (TMPG) and corrected TIMI frame count (CTFC)of the culprit vessel were recoded, so as to evaluate coronary microcirculationperfusion. The peak of creatinine kinase-MB (CK-MB) and troponin I (cTnI)were compared. Left ventricular ejection fraction (LVEF) and wall motionscore (WMS) were observed at one week and one month. The indicators abovewere used to evaluate the preventive effects of introcoronary injection ofanisodamine on myocardial infarction size and ventricular function. Theincidence of reperfusion bradyarrhythmia and major adverse cardiac events(MACEs) in hospital, including cardiac death, non-fatal reinfarction, severeheart failure and target vessel revascularization, were recorded to asses the effects of anisodamine on reperfusion arrythmias and clinical prognosis.Results: No significant differences were found with regard to baselineclinical characteristics, including age, gender, previous history, time fromsymptom onset to PCI, blood pressure, heart rate, distribution of IRA andbasic medications, etc (P>0.05). Compared with the patients in control group,the proportion of TMPG3was lower than that in anisodamine group (57.8%vs.80.8%, P=0.03). Patients treated with intracoronary anisodamine had abetter post-PCI CTFC (27.3±8.2vs.35.4±10.9, P=0.0001). Afteradministration of anisodamine for ten minutes, the blood pressure and theheart rate were increased (P<0.05). Meanwhile, we found that the incidence ofreperfusion bradyarrhythmia was decreased statistically (P<0.05). The peaklevels of cTnI (13.3±27.2vs.23.9±36.7, P=0.12) and CK-MB (163.8±113.4vs.208.5±126.3, P=0.08) were lower in anisodamine group, but it was notstatistically significant. Obvious changes in both LVEF and WMS wereobserved in the anisodamine group at30days flow-up (P<0.05). During thehospitalization, the incidence of MACEs was not reduced significantly(P>0.05).Conclusions: Preventively intracoronary administration of anisodaminecan improve coronary microcirculatory perfusion, protect cardiac function,meanwhile, maintain hemodynamic stability and effectively prevent thereperfused bradyarrhythmia in the patients with AIMI undergoing primaryPCI. |