Amlodipine therapy starting two weeks before PTCA did not reduce luminal loss, but the incidence of repeat PTCA and the composite major adverse clinical events were significantly reduced during the four-month follow-up period after PTCA with amlodipine as compared with placebo.

No abstract

Experiments were performed in order to better define the degradation mechanisms and kinetics for aldicarb and its two metabolites, aldicarb sulfoxide and aldicarb sulfone. The mechanisms studied were oxidation in surface soil and saturated zone soil samples, degradation in saturated zone soil samples and distilled water hydrolysis. The studies showed that soil is an important mechanistic factor, probably because surface catalysis occurs. Temperature and pH are important factors in determining degradation rates. The experiments seem to indicate that microbial oxidation is an important degradation mechanism in the surface soil, but the breakdown of aldicarb residues to noncarbamates is largely the result of chemical hydrolysis. The reduction of aldicarb sulfoxide to aldicarb was observed in the presence of limestone but only after an incubation period of two to six months. No reduction of aldicarb sulfone to aldicarb sulfoxide was observed in these experiments. The complexity of degradation is such that laboratory studies can augment but not replace well‐designed experiments conducted under actual field conditions.

The effect of short-term prostacyclin (PGI2) administration on the incidence of restenosis after coronary angioplasty was studied in a prospective single-blind randomized trial of 286 patients. Of the 270 patients in whom dilation was successful, 134 received prostacyclin and 136 received placebo. Intracoronary prostacyclin was administered before and after dilation and then intravenously for 48 h. The control group received intracoronary placebo infusions before and after dilation. All patients received aspirin and dipyridamole before and after angioplasty, at least until follow-up angiography. Follow-up angiograms were obtained in 93% of patients in whom angioplasty was successful. Restenosis of one or more lesions was present in 34 patients (27%) who were given prostacyclin compared with 40 patients (32%) in the control group (p = NS). Acute vessel closure and ventricular tachyarrhythmias were more common in the control group than in the patients who received prostacyclin (acute vessel closure occurred in 14 [10.3%] of 136 versus 4 [3.0%] of 134, respectively, p less than 0.01; ventricular tachyarrhythmias occurred in 5 [3.4%] of 147 versus 0 of 139 respectively, p less than 0.05). Short-term administration of prostacyclin did not significantly lower the risk of restenosis after coronary angioplasty.