Hideki Nagoshi

A better effect of cilostazol for reducing in-stent restenosis after femoropopliteal artery stent placement in comparison with ticlopidine.

Purpose The purpose of this study was to assess the preventive effect of cilostazol on in-stent restenosis in patients after superficial femoral artery (SFA) stent placement. Materials and methods Of 28 patients with peripheral arterial disease, who had successfully undergone stent implantation, 15 received cilostazol and 13 received ticlopidine. Primary patency rates were retrospectively analyzed by means of Kaplan–Meier survival curves, with differences between the two medication groups compared by log-rank test. A multivariate Cox proportional hazards model was applied to assess the effect of cilostazol versus ticlopidine on primary patency. Results The cilostazol group had significantly better primary patency rates than the ticlopidine group. Cumulative primary patency rates at 12 and 24 months after stent placement were, respectively, 100% and 75% in the cilostazol group versus 39% and 30% in the ticlopidine group (P = 0.0073, log-rank test). In a multivariate Cox proportional hazards model with adjustment for potentially confounding factors, including history of diabetes, cumulative stent length, and poor runoff, patients receiving cilostazol had significantly reduced risk of restenosis (hazard ratio 5.4; P = 0.042). Conclusion This retrospective study showed that cilostazol significantly reduces in-stent stenosis after SFA stent placement compared with ticlopidine.

Electropharmacology of Diltiazem in a Chronic Canine Myocardial Infarction, Ventricular Tachyarrhythmia Model

The electropharmacology of diltiazem was evaluated in 11 dogs with chronic myocardial infarction susceptible to the initiation of sustained ventricular tachyarrhythmias (VTs) using programmed pacing. Dogs were studied open chest under pentobarbital anesthesia both before and after either 0.2 (N = 5), 0.4 (N = 5) or 0.8 mg/kg (N = 5) intravenous diltiazem infused over 5 mimutes. Two doses were studied in 4 dogs. The maximal changes in heart rate, AH, HV and QTc intervals, QRS duration and sinus node recovery time were determined. Mean transmyocardial conduction times from endocardium to epicardium, and excitability thresholds and ventricular refractory periods in both normal and infarct tissue were also determined. Although diltiazem had significant doserelated effects on the heart rate, AH interval and sinus node recovery time at these dosages, diltiazem had no significant effect on the transmyocardial conduction times, excitability thresholds or ventricular refractory periods of either normal or chronically infarcted myocardium. Correspondingly, di1tiazem also failed to prevent the initiation of either ventricular tachycardia or fibrillation by programmed pacing in any of these 11 dogs.