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PubMedDate not supplied

A comparison of the effects of two modified release preparations of nifedipine-nifedipine retard 10 mg twice daily and nifedipine GITS 20 mg once daily--in the treatment of mild to moderate hypertension.

A multicentre, randomised, double-blind, cross-over comparison of nifedipine GITS 20 mg once daily and nifedipine retard 10 mg twice daily in 49 patients with mild to moderate hypertension was conducted. Both treatments resulted in clinically significant trough blood pressure reductions (nifedipine GITS -10.1/-8.9 mmHg, nifedipine retard -7.5/-8.2 mmHg). The study demonstrated that nifedipine GITS was 'at least equivalent' to nifedipine retard in the reduction of trough diastolic blood pressure (one-sided lower 95% confidence limit, -1.2 mmHg). The overall incidence of adverse events (nifedipine GITS 25.5%, nifedipine retard 34.0%), as well as the incidences of headache (nifedipine GITS 8.5%, nifedipine retard 12.8%) and peripheral oedema (nifedipine GITS 2.1%, nifedipine retard 8.5%), was higher with nifedipine retard compared to nifedipine GITS. Nifedipine GITS 20 mg once daily is 'at least equivalent' to nifedipine retard 10 mg twice daily in patients with mild to moderate hypertension, as well as being better tolerated.

Adult↗
PubMed1988

Comparative dosing and efficacy of continuous-release nifedipine versus standard nifedipine for angina pectoris: clinical response, exercise performance, and plasma nifedipine levels.

To assess the dosing equivalency and the early and late antianginal efficacy of a gastrointestinal therapeutic system for once-daily, continuous-release nifedipine (N-GITS), 10 patients with stable angina pectoris, who were previously receiving chronic treatment with nifedipine, completed a 12-week trial comparing N-GITS with standard nifedipine. All patients (nine men and one woman; mean age 54 +/- 2 [SEM] years) who were receiving standard nifedipine (mean dose 40 +/- 5 mg/24 hr) for more than 2 weeks (mean 8 +/- 2 months, range 2 to 36 months) were switched to an equivalent once-daily dose (39 +/- 5 mg/24 hr) of N-GITS. Standard nifedipine and N-GITS were compared by symptom-limited exercise treadmill tests with a baseline test (A) performed 3 hours after a standard dose of nifedipine. Exercise tests were also performed after 2 weeks of treatment with N-GITS 3 hours (B) and 24 hours (C) after the drug was given, and after 12 weeks of treatment with N-GITS, 24 hours after dosing (D). Results of exercise tests showed no significant difference in mean exercise time--(A) 422 +/- 25 vs (B) 426 +/- 36 vs (C) 438 +/- 35 vs (D) 487 +/- 37 seconds. Likewise, there was no significant mean difference in peak double product, resting heart rate, peak exercise heart rate, or resting or maximal systolic blood pressure for any of the exercise test points. Furthermore, five patients (50%) reported side effects with standard nifedipine (all vasodilator-flushing, dizziness, or both), which resolved after treatment with N-GITS (p +/- 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1987

Treatment of angina pectoris with nifedipine: a double blind comparison of nifedipine and slow-release nifedipine alone and in combination with atenolol.

The relative efficacy of nifedipine and slow-release nifedipine (Adalat Retard) in the treatment of stable exertional angina pectoris was evaluated in a double blind randomised crossover study in eight patients on no concomitant antianginal treatment and in 10 patients who were additionally on atenolol. Patients were assessed by angina diaries and exercise testing. Slow-release nifedipine was as effective as nifedipine in the treatment of these patients, both alone and in combination with atenolol.

Angina Pectoris↗
PubMed1987

Nifedipine gastrointestinal therapeutic system in stable angina pectoris. Results of a multicenter open-label crossover comparison with standard nifedipine.

To compare the clinical efficacy and dose equivalency of standard nifedipine versus a new gastrointestinal therapeutic system (GITS) formulation of nifedipine, 98 patients with chronic stable angina pectoris participated in a 14-week, multicenter, open-label, crossover trial. All patients were administered nifedipine capsules for one month prior to study entry and continued receiving other antianginal, non-calcium blocker medications. Ninety-one patients (93 percent), 80 men and 11 women, mean age 62 +/- 1 years, completed the trial, which included two weeks receiving standard nifedipine followed by 12 weeks receiving nifedipine GITS starting at a dosage equal to the 24-hour total dose of nifedipine capsules and titrated upward as necessary. However, throughout the trial, mean nifedipine dosage was similar on nifedipine GITS compared with standard nifedipine. Angina frequency was significantly less with nifedipine GITS at Weeks 6, 10, and 14 (0.8 episodes/week) compared with baseline with standard nifedipine (1.3 episodes/week, p less than 0.05). Likewise, nitroglycerin consumption was also less at Weeks 6, 10, and 14, but only significantly less at Week 6 (nifedipine 1.2/week versus nifedipine GITS at six weeks, 0.7/week; p less than 0.05). Resting hemodynamic parameters, including systolic and diastolic blood pressure and heart rate, were not significantly different with standard nifedipine versus nifedipine GITS during the 12-week study. Total incidences of side effects were similar for both treatments (standard nifedipine, 16; nifedipine GITS, 17). However, incidence of vasodilator side effects (flushing, dizziness, and light-headedness) was significantly less frequent with nifedipine GITS (standard nifedipine, 12; nifedipine GITS, six; p less than 0.05). Thus, results from this open-label, crossover trial suggest that nifedipine GITS dosing is similar to multidose standard nifedipine with equivalent 24-hour efficacy for nifedipine GITS.

Aged↗
PubMed2004

Comparison of once-daily nifedipine controlled-release with twice-daily nifedipine retard in the treatment of essential hypertension.

AIMS: Nifedipine is a short-acting calcium antagonist formulated into several different oral preparations, each of which may have different effects on haemodynamics and autonomic nervous function. We compared the effects of nifedipine controlled-release (CR) and nifedipine retard on 24-h blood pressure, heart rate, rate-pressure product, and power spectral measures of heart rate variability in patients with essential hypertension. METHODS: After 4 weeks of a drug-free period, 25 patients were randomized to receive either once-daily treatment with nifedipine CR (20-40 mg daily; 12 patients) or twice-daily treatment with nifedipine retard (20-40 mg daily; 13 patients) for 12 weeks. The ambulatory blood pressure, heart rate, and ECG R-R intervals were measured during a 24-h period using a portable recorder (TM-2425) at the end of the drug-free and the treatment periods. A power-spectral analysis of R-R intervals was performed to obtain the low-frequency (LF) and high-frequency (HF) components. RESULTS: Nifedipine CR and nifedipine retard reduced 24-h blood pressure significantly by 15.9 +/- 3.2 (SE)/8.7 +/- 1.4 mmHg and by 10.9 +/- 2.8/9.4 +/- 1.7 mmHg, respectively, after the 12-week treatment. Nifedipine CR did not change the 24-h heart rate significantly, while nifedipine retard increased it significantly by 3.9 +/- 2.1 beats min(-1). Nifedipine CR produced a significant reduction in rate-pressure product throughout a 24-h period, while nifedipine retard did not change the rate-pressure product significantly. In addition, nifedipine retard significantly decreased the 24-h and daytime average values of the LF and HF components, while nifedipine CR affected the nighttime LF component alone and did not change the HF component throughout a 24-h period. CONCLUSIONS: These results demonstrate that both nifedipine CR and nifedipine retard are effective as antihypertensive agents, but nifedipine CR has less influence on the autonomic nervous system and heart rate than nifedipine retard.

Adult↗
PubMed1998

Nifedipine-retard versus nifedipine-capsules for the therapy of hypertensive crisis in black patients.

In a randomized parallel-group placebo-controlled study, we compared the short-term hypotensive efficacy and the safety of a single administration of nifedipine-retard (20-mg tablets) with that of two administrations 6 h apart of nifedipine capsules (10 mg) in 10 and 11 black patients, respectively, with acute severe hypertension. Both groups had similar pretreatment blood-pressure (BP) values. Blood pressure was recorded at 10-min intervals for 12 h by using an automated device. In the first 3 h of treatment, nifedipine capsules induced a faster and greater hypotensive effect than nifedipine retard, which was associated with an increase in heart rate. At 2 h after treatment, nifedipine capsules decreased BP to levels (159 +/- 5/105 +/- 3 mm Hg) that were significantly lower than those reached by nifedipine-retard (175 +/- 4/118 +/- 4 mm Hg; p < 0.05). Both preparations induced a similar maximal BP decrease of approximately 30% of the placebo values, but the peak decrease of BP occurred significantly later with nifedipine-retard (283 +/- 31 min after administration) than with nifedipine capsules (100 +/- 14 min; p < 0.01). Four hours after administration, the hypotensive effect of nifedipine capsules was blunted, and a second administration was necessary, whereas nifedipine-retard reduced BP slowly and continuously for < or =12 h and more smoothly. Flush and headache were more frequently found with nifedipine capsules. We conclude that in black patients with hypertensive crisis, nifedipine capsules produce an abrupt decrease in BP that may be potentially harmful. Thus for patients suitable for treatment with nifedipine, nifedipine-retard is preferable because it effectively reduces BP for > or =12 h while achieving a rapid enough effect without critical short-term decreases in BP.

Administration, Oral↗
PubMed1994

The 24-hour efficacy of a new once-daily formulation of nifedipine. Italian Nifedipine GITS Study Group.

Nifedipine GITS (Gastro-Intestinal Therapeutic System) is a recently launched long-acting formulation of nifedipine. The aim of the Italian Nifedipine GITS Study was to determine the duration of the antihypertensive effect of once-daily nifedipine GITS in outpatients with essential hypertension. After a 2-week placebo run-in period, 126 patients with mild to moderate essential hypertension (diastolic BP95 to 114mm Hg) were randomised to receive nifedipine GITS 30mg (n = 42), nifedipine GITS 60mg (n = 42) or placebo (n = 42), once daily in a double-blind fashion for 4 weeks. At the end of the run-in and treatment periods, ambulatory BP monitoring was performed (Spacelabs 90202 or 90207 device) to provide regular 15-minute BP readings for 24 to 36 hours. In the 81 patients with at least 24 hours of valid ambulatory BP data, the average systolic and diastolic BP changes after treatment with nifedipine GITS 30mg (n = 25), nifedipine GITS 60mg (n = 28) and placebo (n = 28) were -16.5/-10.8, -16.3/-10.0 and +0.4/+0.9mm Hg, respectively. BP changes with nifedipine GITS differed significantly (p < 0.01) from those with placebo. Heart rate was not significantly altered by nifedipine GITS. The effects of nifedipine GITS and placebo on ambulatory BP 24 hours and 36 hours after the last dose were evaluated in 56 patients with complete 36-hour ambulatory BP profiles. After 24 hours, both doses of nifedipine GITS caused significant (p < 0.01) reductions in systolic and diastolic BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Combination of nifedipine and carteolol compared to nifedipine alone in diurnal blood pressure variation and exercise blood pressure in patients with essential hypertension.

A combination of nifedipine (40 mg twice daily) plus carteolol (10 mg twice daily) was compared with nifedipine monotherapy in ten patients with essential hypertension. Ambulatory blood pressure (BP) monitoring over 24 hours and treadmill exercise testing were performed before treatment with nifedipine (but after the placebo period), after four weeks of nifedipine treatment, and after four weeks of nifedipine+carteolol combination therapy. At the end of nifedipine monotherapy, 24-hour average ambulatory BP, minimum ambulatory BP during sleep, maximum ambulatory BP, and casual BP all decreased significantly (P less than 0.01). However, the standard deviation (SD) of the ambulatory BP was not affected. The change in systolic BP response to treadmill exercise increased. After a four-week period of nifedipine+carteolol combination therapy, average ambulatory BP and maximum ambulatory BP were further decreased (P less than 0.01). The SD of the ambulatory BP and the change in BP response to exercise were significantly decreased (P less than 0.01), but the minimum ambulatory BP was not affected. These findings suggest that nifedipine and carteolol differ in their influence on diurnal BP variation and on exercise-induced BP elevation. Carteolol may mainly attenuate stress-induced BP elevation and have little influence on nocturnal BP decline. In contrast, nifedipine may affect the BP profile uniformly over the entire day. Nifedipine+carteolol combination therapy may be superior to nifedipine monotherapy because carteolol has a minimal effect on nocturnal BP and decreases stress-induced BP elevation.

Blood Pressure↗
PubMed2005

[Effects of nifedipine controlled release on blood pressure and heart rate of spontaneously hypertensive rats. Comparison with nifedipine standard and with amlodipine].

BACKGROUND: Antihypertensive therapy aims to reduce long-term morbidity and mortality. Drugs characterized by controlled release show a better pharmacokinetic and pharmacodynamic profile compared to standard formulations. METHODS: The present study evaluated the effects of nifedipine controlled release (0.33, 0.66 and 1.32 mg/kg per os), nifedipine standard (0.08, 0.165 and 0.33 mg/kg per os) and amlodipine (0.08, 0.165 and 0.33 mg/kg per os) on mean arterial blood pressure, heart rate and pressure rate index of spontaneously hypertensive rats (SHR). These were treated by gastric gavage, and analyzed after 30 min, 1, 3, 6, 12, and 24 hours. Moreover, plasma levels of nifedipine and amlodipine were also assayed by high-performance liquid chromatography. RESULTS: Nifedipine controlled release showed a longer antihypertensive effect when compared with standard formulation and with amlodipine. The highest dose of nifedipine controlled release decreased blood pressure soon after 1 hour with a maximum decrease (-20 mmHg) at 3 hours. The effect was still significant 24 hours later (p < 0.05). Amlodipine antihypertensive effect lasted 12 hours with a maximum decrease of 18 mmHg at 6 hours. The treatment of SHR rats with nifedipine controlled release, at each of the tested doses, did not cause any significant alterations in heart rate recorded at the beginning of the experiments. Nifedipine standard (0.165 and 0.33 mg/kg) and amlodipine (0.33 mg/kg) increased heart rate in SHR rats. Interestingly enough, pressure rate index was slightly affected by nifedipine standard release and amlodipine whereas it was remarkably reduced by nifedipine controlled release (p < 0.01 vs vehicle until 9 hours). All the compounds showed maximum plasma concentrations paralleled by maximum antihypertensive effects, as evidenced at high-performance liquid chromatography method. CONCLUSIONS: Nifedipine controlled release showed more pronounced antihypertensive effects and longer pharmacokinetic properties with respect to nifedipine standard release and amlodipine.

Administration, Oral↗
PubMed1984

Effects of nifedipine on esophageal motor function in humans: correlation with plasma nifedipine concentration.

We studied the effects of the calcium-channel blocker nifedipine on esophageal smooth muscle function in 10 normal volunteers. Lower esophageal sphincter pressure and relaxation and esophageal contraction amplitude, peristalsis, velocity, and duration after wet swallows were determined before and for 120 min after the sublingual/buccal administration of placebo and of nifedipine in doses of 10, 20, 30, and 40 mg. Blood samples for measurement of plasma nifedipine concentration were obtained at baseline and every 30 min during this 120-min period. Nifedipine led to decreases in sphincter pressure of 13.3%, 29.9%, 34.3%, and 35.1% as the dose was increased from 10 mg to 40 mg. These changes were significantly (p less than 0.05) different from baseline and placebo for the 20-, 30-, and 40-mg doses and were more sustained with the higher doses, lasting as long as 90 min. Contraction amplitude fell 5.3%, 5.9%, 13.5%, and 19.6% at the corresponding doses. These changes were significantly (p less than 0.05) different from baseline and placebo only for the 30- and 40-mg doses, with the effect lasting up to 60 min. Peak plasma nifedipine concentration ranged from 28.7 +/- 3.7 ng/ml (mean +/- SEM) after 10 mg to 138.7 +/- 43.7 ng/ml after 40 mg of the drug, and occurred at either the 30- or 60-min measurement. The mean percent of decrease in sphincter pressure and contraction amplitude in the esophageal body correlated (p less than 0.001) with plasma nifedipine levels. There were no changes in sphincter relaxation or in peristalsis, velocity, or duration of contraction with any dose of nifedipine. It is concluded that (a) nifedipine significantly decreases lower esophageal sphincter pressure and contraction amplitude in the body of the esophagus, (b) the effect on sphincter pressure requires a lower dose of nifedipine and is more marked than that on contraction amplitude, and (c) the effects on both sphincter pressure and contraction amplitude correlate with plasma nifedipine levels. Calcium-channel blockers such as nifedipine may have a role in the treatment of motility disorders of the lower esophageal sphincter or esophageal body, and further controlled clinical studies are indicated.

Adult↗
PubMed1993

Early administration of nifedipine in suspected acute myocardial infarction. The Secondary Prevention Reinfarction Israel Nifedipine Trial 2 Study.

BACKGROUND: The administration of nifedipine, 30 mg/d, between 7 and 22 days after hospitalization for an acute myocardial infarction (Secondary Prevention Reinfarction Israel Nifedipine Trial study) showed no effect on subsequent mortality and morbidity. Since a possible indication of benefit was observed in patients with a second- or higher-order infarction, a second trial was conducted with a higher dose (60 mg/d), early administration (usually within 3 hours of hospital admission), and in high-risk patients only. METHODS: A total of 1358 men and women with suspected acute myocardial infarction (MI), judged not to require calcium antagonist therapy, were randomized to receive nifedipine, 60 mg/d, or placebo between November 1985 and July 1986. Study medication was discontinued in 352 patients because they did not exhibit study criteria for MI or lacked high-risk criteria, or because they decided to discontinue the study. Thus, the treated high-risk group included 1006 patients, of whom 826 were successfully titrated to the target dose of 60 mg/d and were treated for up to 6 months. RESULTS: In the 1006 patients, mortality was 18.7% among those randomized to nifedipine and 15.6% in the patients randomized to placebo. This reflected an increased mortality of 7.8% as compared with 5.5% during the first 6 days in the nifedipine and placebo groups, respectively (adjusted mortality odds ratio by logistic regression, 1.60; 95% confidence interval, 0.86 to 3.00). Among the 826 patients who continued treatment, mortality was equal in the nifedipine (9.3%) and placebo (9.5%) groups. No differences in the rates of nonfatal MI (5.1% and 4.2% in the nifedipine and placebo groups, respectively), hospitalization due to unstable angina, and frequency of chest pain reported during follow-up were observed. An increased rate of sudden death (4.9%) in the placebo group in comparison with the nifedipine group (2.3%) was not statistically significant on post hoc testing, nor was an effect of nifedipine demonstrable in post hoc analyses by congestive heart failure status of randomized patients. CONCLUSION: Nifedipine as a prophylactic treatment in patients immediately after acute MI or in survivors recovering 1 week or longer after acute MI appears ineffective. Early routine administration of nifedipine in acute MI, other than to patients in whom it may be specifically indicated (eg, those with Prinzmetal's variant angina or severe hypertension) may be hazardous and seems to be contraindicated.

Aged↗
PubMed1995

Comparison of perioperative myocardial protection with nifedipine versus nifedipine and metoprolol in patients undergoing elective coronary artery bypass grafting.

A randomized study was performed on 70 patients undergoing elective coronary bypass grafting to examine whether the combined infusion of the calcium channel blocker nifedipine (10 micrograms/kg per hour) and the beta 1-blocker metopropol (12 micrograms/kg per hour, n = 34) reduces the prevalence of perioperative myocardial ischemia and arrhythmias. The control group received nifedipine alone (n = 36). In both groups the infusion was started from the onset of extracorporal circulation and maintained over a period of 24 hours. Repeated 12-lead electrocardiographic and 3-channel Holter monitor recordings for 48 hours were used to define perioperative myocardial ischemia (transient ischemic event, myocardial infarction) and arrhythmias (sinus tachycardia, supraventricular tachycardia, atrial flutter/fibrillation, ventricular tachycardia). Hemodynamic parameters were repeatedly assessed for 24 hours and serum enzyme levels (creatine kinase, MB isoenzyme of creatine kinase) for up to 36 hours after the operation. The two groups did not differ significantly with respect to preoperative anamnestic and surgical data. No signs of perioperative myocardial infarction were detected in either group. However, a significantly lower incidence of transient ischemic episodes was observed in the nifedipine-metoprolol group than in the nifedipine group (3% vs 11%; p < 0.05). In addition, there was a tendency toward lower creatine kinase MB levels and peak values of creatine kinase and creatine kinase MB in the nifedipine-metoprolol group. With regard to perioperative arrhythmias, there was a significantly lower incidence of sinus tachycardia and atrial flutter/fibrillation in the nifedipine-metoprolol group (9% and 6%) than in the nifedipine group (33% and 27%, p < 0.05). In addition, postoperative heart rate was lower in the nifedipine-metoprolol group starting from the sixth hour after release of the aortic crossclamp (p < 0.05 and p < 0.01, respectively). No other hemodynamic parameters showed significant differences between the two groups and all returned to preoperative levels within 24 hours. In conclusion, perioperative application of nifedipine and metoprolol in patients undergoing elective coronary bypass grafting reduces the prevalence of perioperative myocardial ischemia and arrhythmias without significant negative inotropic effects. The combined infusion of the two drugs appears superior to nifedipine alone in preventing perioperative myocardial ischemia and reducing reperfusion-induced arrhythmias.

Adrenergic beta-Antagonists↗
PubMed2001

Blood pressure control in patients with mild to moderate essential hypertension switched from nifedipine gastrointestinal therapeutic system (GITS) 30 mg to nifedipine GITS 20 mg.

BACKGROUND: Nifedipine gastrointestinal therapeutic system (GITS) is a once-daily formulation of nifedipine that provides sustained plasma nifedipine concentrations throughout the 24-hour dosing interval. OBJECTIVE: This study was undertaken to determine if adult patients with mild to moderate essential hypertension whose blood pressure had been controlled for > or = 3 months with nifedipine GITS 30 mg could be successfully switched to a 20-mg daily dose with continued antihypertensive efficacy. METHODS: This was a randomized, double-blind, parallel-group study. Patients entered a 1-week run-in period during which they continued to receive their usual antihypertensive medication, including nifedipine GITS 30 mg. After baseline assessment, patients entered a 6-week treatment period during which they were randomly assigned to receive nifedipine GITS 30 or 20 mg. Men and women were eligible to participate if they were > or = 55 years of age, had received a diagnosis of mild to moderate essential hypertension (sitting diastolic blood pressure [DBP] 95-114 mm Hg), and had exhibited good blood pressure control (sitting DBP < or = 90 mm Hg) while taking nifedipine GITS 30 mg once daily for > or = 3 months. Systolic blood pressure (SBP), DBP, and heart rate were recorded at baseline and after 1, 3, and 6 weeks of treatment. Adverse events were reported by patients. The responder rate was defined as the percentage of patients whose sitting DBP was < 95 mm Hg at the final study assessment. Results were based on the intent-to-treat analyses, which included data for all patients who received > or = 1 dose and had 1 postbaseline blood pressure assessment. Statistical significance was set at P < 0.05. RESULTS: Seventy-five patients entered the 1-week run-in period; 71 patients (94.7%) were randomized to treatment. Twenty-four patients received nifedipine GITS 30 mg for 43.0 +/- 3.3 days, and 47 patients received nifedipine GITS 20 mg for 42.5 +/- 6.7 days. Both groups exhibited a sustained decrease in blood pressure throughout the study; minor variations were not statistically significant. End-point SBP and DBP for the 30- and 20-mg groups were 135.5 +/- 9.8/81.7 +/- 5.4 mm Hg and 138.6 +/- 11.8/82.9 +/- 7.6 mm Hg, respectively. Changes from baseline in end-point SBP and DBP did not differ significantly between groups. At the end of treatment, goal DBP (< 95 mm Hg) was achieved by 24 of 24 patients (100%) receiving the 30-mg dose and 45 of 47 patients (95.7%) receiving the 20-mg dose. Blood pressure control (sitting DBP < 90 mm Hg) was achieved by 21 of 24 (87.5%) patients in the 30-mg group and 35 of 47 (74.5%) patients in the 20-mg group. The most commonly reported adverse event was headache; 2 patients discontinued the study because of adverse events. Overall, 9 of 24 patients (37.5%) in the 30-mg group and 14 of 47 patients (29.8%) in the 20-mg group experienced > or = 1 treatment-related adverse event. CONCLUSIONS: Patients whose mild to moderate essential hypertension is controlled with nifedipine GITS 30 mg once daily may be able to switch to 20 mg once daily with continued antihypertensive efficacy. In addition to safety and economic advantages, such a switch may be a reasonable alternative in patients with lower body weight or as an adjunct to existing antihypertensive therapy.

Aged↗
PubMed2001

Enteral suspension of nifedipine for neonates. Part 2. Stability of an extemporaneously compounded nifedipine suspension.

OBJECTIVE: To investigate the chemical, microbiological and physical stability of an extemporaneously prepared nifedipine oral suspension, packaged in disposable syringes and prepared in a hospital pharmacy for paediatric use. METHODS: Two different suspensions were prepared, from nifedipine tablets and drug powder, by using an autoclaved 1.0% solution of hypromellose as the vehicle. The final theoretical drug concentration was 1 mg/mL. Doses of 1.0 ml were packaged into a 2 ml syringe with a cap. Nifedipine suspensions were stored under three conditions: at room temperature (22 degrees C), in a refrigerator (6 degrees C) protected from light, and at room temperature (22 degrees C) exposed to artificial daylight (400 lux) under controlled circumstances. The nifedipine concentration was measured in suspensions protected from light on days 0, 1, 3, 5, 7, 14, 21 and 28, and in suspensions exposed to light at 0, 3, 6, 18 and 24 h, and on days 2, 3, 5 and 7 after preparation. Nifedipine was analysed by a reproducible and validated stability-indicating HPLC-method. Microbiological and physical stability of the nifedipine suspension samples protected from light were examined for 28 days. RESULTS: Mean nifedipine concentration remained over 90% of the initial concentration throughout the 4-week study period in light-protected unit-dose suspensions, prepared from either crushed tablets or drug powder with hypromellose 1.0%. When exposed to light, however, nifedipine decomposed rapidly. Photodegradation of nifedipine exceeded 25% within 3 h and was essentially complete within 7 days. CONCLUSION: In the University Hospital of Kuopio, newborns have been treated with nifedipine suspension prepared from tablets, and preliminary experiences with administration of suspension have been encouraging. It may also be possible to apply this methodology to other medicines used in paediatrics.

Calcium Channel Blockers↗
PubMed1996

Trough:peak ratio of nifedipine gastrointestinal therapeutic system and nifedipine retard in essential hypertensive patients: an Italian multicentre study.

OBJECTIVE: To evaluate the antihypertensive effect of nifedipine gastrointestinal therapeutic system and retard in terms of trough:peak ratio efficacy. METHODS: According to a double-blind, randomized, crossover design, 58 patients with mild-to-moderate essential hypertension, after 1 month placebo washout, received 30 mg/day nifedipine gastrointestinal therapeutic system, 20 mg nifedipine retard twice a day and the corresponding placebos for 1 month. At the end of each treatment period, blood pressure was measured by using a mercury sphygmomanometer at trough and 1, 2, 3 and 4 h after the last dosing. The peak effect was identified as the maximum decrement induced by the three randomized treatments with respect to the value at the end of the placebo washout period during the 4 h interval. The trough:peak ratios of systolic and diastolic blood pressure were calculated as group ratios and individual ratios from decrements induced by nifedipine gastrointestinal therapeutic system and retard, corrected for those induced by randomized placebo. Patients were defined as responders to each randomized treatment if their diastolic blood pressure at trough time was reduced by at least 10 mmHg relative to that at the corresponding time at the end of placebo washout. RESULTS: Nifedipine gastrointestinal therapeutic system and retard significantly reduced blood pressure to a similar extent both at trough and at peak. Systolic and diastolic group trough:peak ratios in responders to nifedipine gastrointestinal therapeutic system (n = 41) were 0.80 and 0.88, respectively, and those in responders to nifedipine retard (n = 30) 0.84 and 0.93, respectively. The percentage of patients with trough:peak ratios > 0.50 was > 80% (systolic trough:peak ratios) and above 90% (diastolic trough: peak ratios) for both nifedipine formulations. CONCLUSIONS: Our data show that 30 mg/day nifedipine gastrointestinal therapeutic system and 20 mg nifedipine retard twice a day have a favourable trough:peak ratios efficacy when given as monotherapy to essential hypertensive patients.

Adult↗
PubMed1990

[Efficacy of prophylactic nifedipine therapy during aortocoronary vein bypass interventions. Drug concentration with oral or intravenous nifedipine administration; hemodynamics and plasma catecholamines].

To assess the usefulness of prophylactic nifedipine in coronary artery surgery, in this study nifedipine plasma concentrations were determined in patients, who had been given 10 mg nifedipine orally before operation. Furthermore, plasma and tissue concentrations of nifedipine were measured in patients receiving a nifedipine infusion. In this group of patients the efficacy of nifedipine, based on changes in hemodynamics and plasma catecholamines was also investigated. Patients with normal global left ventricular function (LVEDP less than 15 mm Hg, EF greater than 0.5) undergoing coronary artery bypass grafting (CABG) operations were included in this study. The preoperative antianginal therapy was continued until the time of surgery, the last beta-adrenoceptor blocker was given on the day of surgery. A standardized premedication and anesthesia (fentanyl-flunitrazepan infusion) was given to all patients. Hemodynamic parameters were obtained using indwelling arterial, venous and pulmonary artery thermodilution catheters. The high-pressure-liquid-chromatography (HPLC) method was used to measure plasma catecholamines as well as plasma and tissue nifedipine concentrations. Eight patients received 10 mg nifedipine orally one hour prior to anesthetic induction. Plasma nifedipine concentration (Figure 1) showed a wide interindividual scattering at anesthetic induction (25 +/- 38 ng/ml) in this group and they decreased to low, noneffective levels during surgical stimulation (12 +/- 12 ng/ml) and aortic cannulation (8 +/- 8 ng/ml). 24 patients with a nifedipine infusion of 0.30 micron/kg/min prior to extracorporeal circulation (start: following intubation, termination: at aortic cannulation) were compared to a control group of 24 patients with respect to hemodynamics, plasma catecholamines, anesthetic requirements and need for additional vasodilator and vasopressor therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

Sustained-release nifedipine (nifedipine-L) suppresses plasma thromboxane B2 and 6-keto prostaglandin F1 alpha in both young male smokers and nonsmokers.

Sustained-release nifedipine (nifedipine-L) (40 mg twice a day) was administered orally to healthy young adult male smokers and nonsmokers for 10 days, and its effects on platelet aggregation, beta-thromboglobulin and platelet factor 4 levels, and plasma thromboxane B2 (TxB2) and 6-ketoprostaglandin F1 alpha (6-Keto-PGF1 alpha) concentrations were studied. The plasma nifedipine-L concentration in smokers (46.0 +/- 7.4 ng/ml) was significantly lower than that in nonsmokers (88.2 +/- 1.2 ng/ml). Nifedipine-L did not affect platelet aggregation induced by adenosine diphosphate, collagen, or epinephrine in either smokers or nonsmokers. The plasma beta-thromboglobulin level on the tenth day of nifedipine-L administration in nonsmokers was lower than that in smokers, but there were no significant differences either with or without nifedipine-L or between nonsmokers and smokers. Nifedipine-L had no effect on the concentration of platelet factor 4 in either smokers or nonsmokers. On the other hand, nifedipine-L significantly decreased the plasma TxB2 and 6-keto-PGF1 alpha concentrations in both smokers and nonsmokers. Thus we concluded that nifedipine-L suppressed the production of plasma TxB2 from platelets and also subsequently suppressed the production of 6-keto-PGF1 alpha and that this action was not affected by cigarette smoking.

6-Ketoprostaglandin F1 alpha↗