Preexisting renal impairment is an all-encompassing risk factor for radiocontrast-associated nephrotoxicity. Renal impairment appears to be associated with the inadequate production of renal prostaglandins at the critical time of radiocontrast administration and for a variable time period afterward. We prospectively studied 130 patients with chronic renal insufficiency (serum creatinine > or =1.5 mg/dL) who were undergoing radiocontrast administration. Using a double-blind, randomized, prospective technique, patients were assigned to either placebo or one of three prostaglandin E1 (PGE1) treatment groups (10, 20, or 40 ng/kg/min). Infusion was started 60 +/- 30 minutes before the administration of radiocontrast and was continued for a total of 6 hours. In the placebo group, radiocontrast administration resulted in a mean increase (+/- SD) in serum creatinine of 0.72 +/- 1.15 mg/dL at 48 hours. This increase was less in each of the PGE1 treatment groups after 48 hours, with a significant difference between placebo and the 20 ng/kg/min PGE1 group (P = 0.01). Using baseline adjusted means, analysis of covariance with baseline serum creatinine as the covariable demonstrated significant differences between the placebo and 20 ng/kg/min PGE1 group (P = 0.03) and between the placebo and 10 ng/kg/min PGE1 group P = 0.047). In a subgroup analysis of the diabetic patients, the increase in serum creatinine was less pronounced in the three PGE1 groups versus the placebo group, and the 20 ng/kg/min PGE1 group had the most favorable outcome. The parenteral administration of PGE1 immediately before radiocontrast exposure and continued for a period of 5 to 5.5 hours significantly reduced the elevation of serum creatinine poststudy. The most effective of the three PGE1 dosing regimens was 20 ng/kg/min.
Objective: To compare the efficacy and tolerability of mibefradil (−11.5 ± 8.2 mm Hg) and 5/10 mg amlodipine (−13.2 ± 7.9 mm Hg). The number of patients with normibefradil and amlodipine in patients with uncomplicated mild-to-moderate essential hypertension. malised SDBP (р90 mm Hg) increased 23.3% in the mibefradil group and 19.5% in the amlodipine group Design: A double-blind, randomised, parallel group multicentre trial.(approximately 74% in both groups). Patients on mibefradil or amlodipine during the withdrawal period had Methods: 239 patients received 50 mg mibefradil or 5 mg amlodipine for 4 weeks, followed by a forced significantly larger decreases in SDBP than those on placebo. Patients on mibefradil had a decrease in heart titration to 100 mg mibefradil or 10 mg amlodipine for an additional 8 weeks. Patients then entered a 4-week rate of 5.5 bpm. Patients on amlodipine had no change in heart rate; however, cessation of amlodipine was withdrawal period either on therapy or switched to placebo.associated with a decrease in heart rate. Conclusions: Mibefradil was as effective as amlodiResults: Statistically equivalent reductions in trough sitting diastolic blood pressure (SDBP) were observed pine in reducing BP; both compounds were effective treatments of hypertension. after 12 weeks of once-daily treatment with 50/100 mg
AimsThe study aimed to compare the addition of felodipine to metoprolol, and of the replacement of metoprolol by felodipine, with continuation of metoprolol, in patients with angina pectoris despite optimal betablockade.
Methods and resultsThe study was double-blind, parallel, randomized and controlled, and comprised 363 patients from 27 outpatient cardiology clinics in the Netherlands. The patients had angina and positive bicycle exercise tests despite optimal beta-blockade (resting heart rate <65 beats . min~ '). Randomization was to three treatment groups: continuation of metoprolol (control), addition of felodipine to metoprolol, and replacement of metoprolol by felodipine. Exercise tests were repeated after 2 and 5 weeks. The main outcome measure was: exercise result after 5 weeks, compared with baseline, betweengroup comparison of changes vs control. There were no significant differences in exercise duration and onset of chest pain vs control. The addition of felodipine increased time until 1 mm ST depression (43 s, 95% confidence interval 20-65 s), and decreased both ST depression at highest comparable work load (0-46 mm, 95% confidence interval 0-19-0-72), and maximal ST depression (0-49 mm, 95% confidence interval 0-23-0-74). Exercise results after replacement of metoprolol by felodipine were not different from control, apart from a significant increase in rate pressure product. Significantly more patients experienced adverse events in the felodipine monotherapy group.
ConclusionCombination of metoprolol and felodipine is to be preferred to felodipine monotherapy in patients who have signs and symptoms of myocardial ischaemia despite optimal beta-blockade.
Our results suggest that intravenously administered PGE1 may be efficient in preventing CM-induced renal dysfunction in patients with renal impairment.
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