Background Recent studies have revealed that pretreatment with statin is effective in preventing arrhythmia, but its electrophysiological mechanism is unclear. This study was conducted to investigate the cardioprotective effects of simvastatin on reversing electrical remodeling in left ventricular myocytes of rabbit heart undergoing ischemia-reperfusion, so as to explore the ionic mechanism responsible for the anti-arrhythmic effect of statin. Methods Forty-five rabbits were randomly divided into three groups： ischemic-reperfusion group （I-R）, simvastatin intervention group （Statin） and sham-operated control group （CON）. Anesthetized rabbits were subjected to 30-minute ischemia by ligation of the left anterior descending coronary artery and a 60-minute reperfusion after a 3-day administration of oral simvastatin of 5 mg-kg^-1.d^-1 in the Statin group or a placebo in the I-R group. Single ventricular myocytes were isolated enzymatically from the epicardial zone of the infracted region dedved from the hearts in the I-R and Statin group and the same anatomical region in the CON animals. The whole cell patch-clamp technique was used to record membrane ionic currents, including sodium current （IRa）, L-type calcium current （Ica-L） and transient outward potassium current （Ito）. Simultaneously, the level of serum cholesterol was examined. Results There was no significant difference in the serum cholesterol concentration among the three groups. The peak IRa current density （at -30 mV） was significantly decreased in I-R （（22.46±5.32） pA/pF, n=12） compared with CON （（42.78±5.48） pA/pF, n=16, P〈0.01） and Statin （（40.66±5.89） pA/pF, n=15, P〈0.01）, while the peak IRa current density in the Statin group was not different from CON （P〉0.05）. The peak ICa-L current density （at 0 mV） was significantly increased in I-R （（4.34±0.92） pA/pF, n=15） compared with CON （（3.13±1.22） pA/pF, n=13, P〈0.05） and Statin （（3.46±0.85） pNpF, n=16, P〈0
Background Aspirin and clopidogrel can improve myocardial reperfusion and alleviate myocardial injury during percutaneous coronary intervention （PCI）. Whether the addition of intravenous tirofiban during this procedure produces further benefit has not been clarified in ST segment elevation myocardial infarction （STEMI） patients. We evaluated this on STEMI patients who underwent primary PCI （p-PCI） via transradial artery approach. Methods Consecutive patients were randomized into tirofiban group （n=-72） or placebo group （n=-78）. Angiographic analysis included initial and final thrombolysis in myocardial infarction （TIMI） flow grade （TFG）, corrected TIMI frame count （CTFC） and TIMI myocardial perfusion grade （TMPG） of the thrombotic vessel. Platelet aggregation rate （PAR）, creatine phosphokinase （CPK）, CPK isoenzyme MB （CPK-MB） and troponin I levels were measured and TIMI definitions were used to assess bleeding complications. Left ventricular performance parameters were investigated with equilibrium radionuclide ventriculography. Major adverse cardiac events （MACE） were followed up for 6 months. Results The cases of TFG 0 and 1 before PCI, TFG 0 when first crossing of guide wire were less, and the cases of TFG 3 after PCI was more in tirofiban group than those in placebo group. The final CTFC was fewer and the incidence of no reflow phenomenon was lower, as well the percentage of final TFG 3 was higher in tirofiban group than those in placebo group （all P 〈0.05）. Mean peak CPK-MB was significantly lower, while the left ventricular performance parameters 1 week after PCI were much more improved in tirofiban group than those in the placebo group. PAR was significantly decreased shortly after tirofiban infusion. The incidence of 6-month MACE in tirofiban group was obviously lower than that in the placebo group. No statistical difference was noted between the two groups with regard to bleeding complications. Conclusions Intravenous tirofiban infusion, in additi
FU Xiang-hua HAO Qing-qing JIA Xin-wei FAN Wei-ze GU Xin-shun WU Wei-li HAO Guo-zhen LI Shi-qiang JIANG Yun-fa GENG Wei
