Nifedipine Therapy Research Articles

Comparison of the cardiovascular effects of nifedipine and nicardipine in the presence of atenolol

A placebo controlled double blind crossover study was performed in 12 healthy volunteers to compare the cardiovascular effects of single oral doses of nifedipine (5, 10 and 15 mg) and nicardipine (20 and 30 mg) in the presence of atenolol 100 mg. Haemodynamic measurements were made by transthoracic electrical bioimpedance cardiography (TEBC) 2 h following drug administration during passive tilting, graded bicycle exercise (30-150 W) and recovery from exercise. In the absence of calcium channel blockade, atenolol reduced mean blood pressure, heart rate, and cardiac index, and increased stroke volume, peripheral resistance, pre-ejection period, and ventricular ejection time, particularly during and after exercise. In comparison with atenolol alone, addition of nifedipine or nicardipine reduced peripheral resistance but did not produce significant changes in stroke volume, cardiac output, dZ/dt [max], pre-ejection period (PEP). Ventricular ejection time (VET), PEP/VET, or Heather index at any point in the experiment. Similar reductions in peripheral resistance were produced by nifedipine 10 mg and nicardipine 20 and 30 mg. These apparently equivalent doses of nifedipine and nicardipine had similar effects on stroke volume, cardiac index, PEP/VET and Heather index. Thus the increases in ventricular performance previously demonstrated in association with nifedipine and nicardipine therapy were not observed in the presence of beta-adrenoceptor blockade. Under these conditions no important differences have been observed in the cardiovascular effects of these two calcium channel blockers.

Prevalence of Persistent Cough During Long-term Enalapril Treatment: Controlled Study Versus Nifedipine

The prevalence and severity of cough during long-term enalapril treatment were examined by comparing a cohort of 136 hypertensive patients who started treatment with enalapril with consecutive age and sex-matched patients who commenced nifedipine therapy during the same period. Cough and other symptoms were assessed by a questionnaire designed to avoid bias towards reporting cough. After a mean of 27 months' treatment patients on enalapril had an excess of persistent cough (16 per cent, 95 per cent CI 7-25, p less than 0.01), voice change (14 per cent, 95 per cent CI 2-27, p less than 0.05) and sore throat (10 per cent, 95 per cent CI -0.1 to 20.3 per cent, p less than 0.01) when compared to nifedipine-treated patients. The cough was usually dry, moderate or severe, paroxysmal, and troublesome at night. Cough tended to be more common in women (23 per cent vs. 7.2 per cent), non-smokers, and at higher doses of enalapril, but was not related to age, duration of treatment, or chronic respiratory disease. Dry cough commonly persists as a troublesome side-effect during long-term enalapril treatment, and is often associated with voice change and sore throat.

Normalization of left ventricular mass and associated changes in neurohormones and atrial natriuretic peptide after 1 year of sustained nifedipine therapy for severe hypertension

Sixteen patients with severe hypertension were treated for 1 year with extended release nifedipine, during which time serial changes in left ventricular mass index and associated alterations in left ventricular systolic function, left ventricular filling, plasma renin activity, atrial natriuretic peptide and catecholamines were evaluated. Mean seated blood pressure (± SE) was significantly reduced from 200 ± 8/122 ± 3 to 144 ± 5/89 ± 2 mm Hg (p < 0.0001) at 1 year. After 6 months, left ventricular mass index was significantly reduced by 19% from 121 ± 8 to 96 ± 7 g/m2and this reduction was sustained at 1 year. Septal and posterior wall thickness were reduced from 13.4 ± 0.1 to 11.2 ± 0.04 mm and from 12.8 ± 0.1 to 10.0 ± 0.03 mm (p < 0.001), respectively.The prevalence of left ventricular hypertrophy decreased from 63% to 25%. Left ventricular fractional shortening increased from 34 ± 2% to 41 ± 3% (p < 0.05) and the relation between fractional shortening and end-systolic stress did not change. Over the year of sustained blood pressure reduction, the peak velocity of early filling increased from 57 ± 3 to 63 ± 4 cm/s (p = 0.07), peak velocity of late filling did not change and the ratio of late to early peak left ventricular filling velocity significantly decreased (p < 0.05). Plasma atrial natriuretic peptide levels, markedly elevated at entry, decreased from 70 ± 15 to 41 ± 8 pg/ml at 1 year (p < 0.05). Plasma renin activity and catecholamine levels were not altered.It is concluded that treatment of severe hypertension with extended release nifedipine for 1 year is accompanied by left ventricular mass regression, maintenance of left ventricular systolic function, reduction in atrial natriuretic peptide level and no detectable activation of either the sympathetic or the renin system.

Comparison of Sublingual Captopril and Nifedipine in Immediate Treatment of Hypertensive Emergencies

Sublingual captopril (25 mg) was compared with sublingual nifedipine (10 mg) to determine their effectiveness and safety in the treatment of hypertensive emergencies. In nine of 10 patients who received sublingual captopril, mean (+/- SD) systolic blood pressure and diastolic blood pressure dropped from 245 +/- 39 to 190 +/- 25 mm Hg (P less than .0025) and from 144 +/- 8 to 115 +/- 8 mm Hg (P less than .001) at 50 minutes, respectively. The hypotensive effect of the drug was maintained for a mean of 4 hours. In six of nine responders to sublingual captopril, blood pressure-lowering effect was associated with a clear improvement of end-organ failure within 60 minutes. There were no side effects, including a dangerous fall in blood pressure or reflex tachycardia. Sublingual nifedipine lowered diastolic blood pressure and systolic blood pressure in eight of 10 patients. The hypotensive effect of nifedipine was more rapid than that of captopril (10 vs 20 minutes for diastolic blood pressure and 20 vs 30 minutes for systolic blood pressure, respectively), but no difference was observed in the time or in the magnitude of peak hypotensive effect between the two treatments, nor was a difference observed in the duration of hypotensive effect. In six of eight responders to nifedipine therapy, a clear improvement of symptoms and signs of end-organ failure was observed within 60 minutes. In three patients, minor side effects were observed. We conclude that sublingual captopril effectively and safely lowers arterial blood pressure in patients with hypertensive emergencies.

Impaired venoarteriolar reflex as a possible cause for nifedipine-induced ankle oedema

Ankle oedema is not an uncommon side effect of treatment with nifedipine. To evaluate the possible effect of nifedipine on the microcirculation of the skin, 18 patients with systemic hypertension who were known to develop ankle oedema after nifedipine and 19 patients with systemic hypertension who did not develop ankle oedema after nifedipine were studied. Following four weeks of nifedipine therapy (10 mg, three times daily), the microcirculation on the dorsum of the foot was measured using laser-Doppler flowmetry. Estimation of the microcapillary flow was made both after supine resting and on standing upright. The venoarteriolar reflex was expressed as the standing flow in percentage of the resting flow. There was no significant difference between the two groups of patients in the resting flow, supine flow, or the venoarteriolar reflex before nifedipine therapy ( P > 0.4). Before nifedipine, the blood blow in the skin of both groups of patients was reduced from the supine level upon standing, thus indicating a normal response to dependency. After nifedipine administration, no significant difference was observed between the two groups of patients in the resting flow ( P > 0.5). The flow on standing, however, was 96.2% of that measured during resting supine in patients who developed ankle oedema and 79.8% of the resting flow in the patients who did not develop ankle oedema, suggesting a weaker venoarteriolar reflex in patients who developed ankle oedema following administration of nifedipine ( P < 0.0001). Thus, the microcapillary flow did not decrease upon standing in patients who developed ankle oedema following nifedipine therapy, indicating an abnormal venoarteriolar reflex. This may explain why ankle oedema develops in such patients following nifedipine.

Effect of Nifedipine on the Progression of Coronary Atherosclerosis in Humans. Analysis of Coronary Angiogram by Videodensitometry.

This study was conducted retrospectively to elucidate whether the long-term use of nifedipine is effective against the progression of coronary atherosclerosis in humans. Twenty-nine subjects with ischemic heart disease, on whom repeated coronary angiographic examinations (CAG) were performed, were randomly selected. Sixteen subjects were on nifedipine therapy (40 mg/day; NIF group, age 53 +/- 2) and 13 subjects not on nifedipine therapy served as the control group (C group, age 58 +/- 3). No significant differences were observed in clinical backgrounds, including the interval between CAG, between the 2 groups. The lesions with 25 to 75% stenosis on the first CAG were defined as the regions of interest (ROI), and the magnitude of stenosis was quantitatively measured by videodensitometry for each ROI on the first and the second CAG. The magnitude of stenosis showed a small increase (54.1 +/- 2.6 to 58.6 +/- 3.3%: N.S.) for 37 ROIs in the C group. In contrast, it showed a significant decrease (52.5 +/- 3.8 to 46.2 +/- 4.3%: p less than 0.05) for 33 ROIs in the NIF group. The trend was more apparent in the left coronary artery. The change in the mean value for ROIs in each subject produced similar results. These results suggest that the long-term use of nifedipine might be effective in retarding the progression of coronary atherosclerosis in humans. However, a prospective study should be performed to confirm this.

A prospective, randomized, double-blind, crossover study to compare the efficacy and safety of chronic nifedipine therapy with that of isosorbide dinitrate and their combination in the treatment of chronic congestive heart failure.

We performed a prospective, randomized, double-blind, crossover study to compare the efficacy and safety of vasodilation with the calcium entry blocker nifedipine with that of isosorbide dinitrate (ISDN) and their combination as treatment for heart failure. Twenty-eight patients with New York Heart Association Functional class II or III chronic heart failure due to left ventricular systolic dysfunction were studied. All patients were maintained on a constant dose of digitalis and diuretics throughout the study. Eight weeks of therapy with nifedipine alone or in combination with ISDN resulted in a significantly higher incidence of heart failure deterioration necessitating hospitalizations and/or additional diuretics. Twenty-four percent of patients required hospitalization during nifedipine therapy and 26% required hospitalization during nifedipine-ISDN combination therapy in comparison to 0% requiring hospitalization during ISDN therapy alone. The total number of heart failure-worsening episodes was nine among patients on nifedipine, three among patients on ISDN (p less than 0.09 versus nifedipine), and 21 among patients on nifedipine-ISDN combination (p less than 0.001 versus nifedipine, p less than 0.0001 versus ISDN). Premature discontinuation of drug administration due to clinical deterioration or other side effects occurred in 29% of patients during nifedipine therapy, 5% of patients during ISDN therapy (p = 0.05 versus nifedipine), and 19% of patients during the combination therapy. A comparison of eight patients who demonstrated clinical deterioration on nifedipine with the remainder of the patients demonstrated no significant difference in left ventricular ejection fraction (0.24 +/- 0.06 versus 0.23 +/- 0.07) or maximal oxygen uptake during exercise (13 +/- 3 versus 14 +/- 2 ml/kg/min).(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of nifedipine therapy on fetal and placental Doppler waveforms in preeclampsia remote from term

Twenty patients with preeclampsia at a gestational age of 26 to 35 weeks were treated with oral nifedipine until delivery. The mean oral daily dose was 45.1 ± 11 mg/day (range, 40 to 80 mg/day). Fetal aorta, internal carotid artery, umbilical artery, and uteroplacental Doppler flow velocity waveforms were recorded before treatment and then serially. The mean nifedipine concentration at the time of the Doppler studies was 60.3 ng/ml (range, 10 to 90 ng/ml). The use of nifedipine therapy was associated with a significant decrease in both maternal systolic blood pressure (baseline, 154 to 135 mm Hg, p<0.001) and diastolic blood pressure (baseline, 100 to 88 mm Hg, p<0.001). However, there was no significant difference in the resistance index between baseline and postnifedipine Doppler studies in either the fetal or uteroplacental vessels. The use of oral nifedipine to control blood pressure in preeclampsia does not affect the resistance indices in fetal or uteroplacental vessels as measured by the Doppler technique.

Doppler assessment of the fetal and uteroplacental circulation during nifedipine therapy for preterm labor

Doppler assessment of the fetal and uteroplacental circulation during nifedipine therapy for preterm labor

Doppler assessment of the fetal and uteroplacental circulation during nifedipine therapy for preterm labor

International Journal of Gynecology & ObstetricsVolume 33, Issue 2 p. 187-187 Citations from the literature perinatology Doppler assessment of the fetal and uteroplacental circulation during nifedipine therapy for preterm labor G Mari, G MariSearch for more papers by this authorKJ Moise Jr., KJ Moise Jr.Search for more papers by this authorW Lee, W LeeSearch for more papers by this authorDB Cotton, DB CottonSearch for more papers by this author G Mari, G MariSearch for more papers by this authorKJ Moise Jr., KJ Moise Jr.Search for more papers by this authorW Lee, W LeeSearch for more papers by this authorDB Cotton, DB CottonSearch for more papers by this author First published: October 1990 https://doi.org/10.1016/0020-7292(90)90622-RAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume33, Issue2October 1990Pages 187-187 RelatedInformation

Doppler assessment of the fetal and uteroplacental circulation during nifedipine therapy for preterm labor

Doppler assessment of the fetal and uteroplacental circulation during nifedipine therapy for preterm labor

Prehospital use of nifedipine for severe hypertension

The prehospital management of severe hypertension is limited by a paucity of pharmacologic agents suitable for field use. This prospective study was designed to test the safety and efficacy of intraoral nifedipine therapy in 50 patients with severe hypertension being transported by an urban emergency medical service system. Ten milligrams of nifedipine were administered. Serial blood pressure determinations were obtained at 3, 5, 10, and 15 minutes and patients were observed for possible side effects. A marked effect on systolic blood pressure (SP), diastolic blood pressure (DP), and mean arterial pressure (MAP) was evident and was statistically significant in all three categories by 3 minutes. MAP decreased from 169 to 129 mm Hg (ΔMAP of 40 mm Hg) at 15 minutes with parallel changes in the SP (55 mm Hg) and ΔDP (32 mm Hg). These changes were highly significant ( P < .01) when compared with those of 50 historical controls. No evidence of severe adverse effects were noted. Nifedipine appears to be a promising agent for the prehospital treatment of severe hypertension, but its proper role is not yet defined.

The role of nifedipine therapy in achalasia: Results of a randomized, double-blind, placebo-controlled study: M. Traube, S. Dubovik, R.C. Lange, et al. Am J Gastroenterol 84:1259–1262, (October), 1989

The role of nifedipine therapy in achalasia: Results of a randomized, double-blind, placebo-controlled study: M. Traube, S. Dubovik, R.C. Lange, et al. Am J Gastroenterol 84:1259–1262, (October), 1989

Defective venoarteriolar reflex as a possible cause for ankle oedema following nifedipine therapy

Defective venoarteriolar reflex as a possible cause for ankle oedema following nifedipine therapy

Health Implications of Drug Interactions

The awareness of the digoxin-quinidine interaction in the mid-70s led to increased interest in drug interactions. Much has been published on the subject in the form of interaction reports, handbooks, lists, cards, discs etc. However, only a few interactions in the literature have clinical significance and can be remembered by thinking in terms of groups, pharmacokinetics and probabilities. It is important to realise that drugs in a given class will have similar properties. Thus, phenylbutazone, like any other nonsteroidal anti-inflammatory drug (NSAID), is likely to potentiate the effects of warfarin. A knowledge of drug pharmacokinetics is also essential; a highly protein-bound drug may displace another when they are administered together. Remembering those drugs which induce liver enzyme formation will prevent their co-administration with drugs which have a critical dose-range. If a general practitioner can remember the few drugs in clinical practice with a narrow therapeutic index, he can consult a handbook before anything else is prescribed. Some interactions will rarely be encountered in daily general practice, i.e. those associated with tuberculosis treatment or anesthetic agents. Other interactions, e.g. the interaction between antihypertensive treatment and over-the-counter medication containing phenylpropanolamine, are more common. While most drug interactions can be avoided by thinking in terms of groups, pharmacokinetics and probabilities, some learning by rote is required, e.g. the potential for heart failure with concomitant beta-blocker and nifedipine therapy. In general, a schematic approach using thinking in terms of groups, pharmacokinetics and probabilities will prevent most clinically significant drug interactions; the rest can be avoided by consulting appropriate handbooks and specialists.

ニフェジピン療法を受けている患者の歯肉増殖有病状況についての予備的研究

ニフェジピン療法を受けている患者の歯肉増殖有病状況についての予備的研究

The Effect of Calcium Channel Blockers on the Cyclosporine Dose Requirement in Renal Transplant Recipients

Thirteen patients found to be hypertensive following renal transplantation were treated with either a calcium channel blocker or other antihypertensive therapy for control of blood pressure. Immunosuppression was either with cyclosporine and prednisone alone or with cyclosporine, azathioprine, and prednisone. Patients had weekly or biweekly cyclosporine whole-blood levels measured by radioimmunoassay drawn approximately 12 h after their last dose. Patients treated with cyclosporine and prednisone alone had their cyclosporine dosage adjusted to maintain their cyclosporine level between 400 and 900 ng/mL between 1 and 6 months following transplantation. Patients treated with cyclosporine, azathioprine, and prednisone had their cyclosporine level adjusted to be between 100 and 400 ng/mL during this same time period. Cyclosporine levels were significantly higher in verapamil-treated patients and significantly lower in nifedipine-treated patients as compared to controls. The dose of cyclosporine administered was significantly lower in the verapamil-treated patients and higher in the nifedipine-treated patients than controls. Normalizing the whole-blood cyclosporine level for the dose of cyclosporine, and verapamil-treated patients had a significantly greater, and the nifedipine-treated patients a significantly lower value than control patients. These data suggest the verapamil treatment results in significantly higher levels of cyclosporine whereas nifedipine therapy may actually result in lower cyclosporine levels for a given dose of cyclosporine than seen in patients not exposed to these drugs.

Comparison of Sublingual Captopril and Sublingual Nifedipine in Hypertensive Emergencies

AbstractHypertensive crises require immediate therapy, usually by parenteral drug administration. Sublingual nifedipine has been shown to be highly effective. However, the blood pressure fall following nifedipine is frequently associated with side-effects. The use of sublingual captopril has recently been indicated in hypertensive crisis, assuming that by this route, there would be a faster absorption and thus a more rapid effect on blood pressure than with the oral route. To verify this hypothesis, we have compared the hypotensive effects of sublingual nifedipine and sublingual captopril in 52 patients with hypertensive emergencies: 25-mg captopril and 10-mg nifedipine were administered sublingually to 28 and 24 patients, respectively. Blood pressures and heart rates were continuously measured up to 240 min postdose. A significant (P<0.001) hypotensive effect of both sublingual captopril and nifedipine therapy occured at 5 min and persisted for 240 min. Heart rates increased with nifedipine, but decreased with captopril. We observed no side-effects in the captopril group, but flushing, tachycardia and headache were observed in 6 patients in the nifedipine group. We conclude that sublingual captopril is effective in patients with hypertensive emergencies and that captopril may be an excellent alternative to sublingual nifedipine in the urgent treatment of hypertensive crisis.

Comparison of sublingual captopril and sublingual nifedipine in hypertensive emergencies.

Hypertensive crises require immediate therapy, usually by parenteral drug administration. Sublingual nifedipine has been shown to be highly effective. However, the blood pressure fall following nifedipine is frequently associated with side-effects. The use of sublingual captopril has recently been indicated in hypertensive crisis, assuming that by this route, there would be a faster absorption and thus a more rapid effect on blood pressure than with the oral route. To verify this hypothesis, we have compared the hypotensive effects of sublingual nifedipine and sublingual captopril in 52 patients with hypertensive emergencies: 25-mg captopril and 10-mg nifedipine were administered sublingually to 28 and 24 patients, respectively. Blood pressures and heart rates were continuously measured up to 240 min postdose. A significant (P less than 0.001) hypotensive effect of both sublingual captopril and nifedipine therapy occurred at 5 min and persisted for 240 min. Heart rates increased with nifedipine, but decreased with captopril. We observed no side-effects in the captopril group, but flushing, tachycardia and headache were observed in 6 patients in the nifedipine group. We conclude that sublingual captopril is effective in patients with hypertensive emergencies and that captopril may be an excellent alternative to sublingual nifedipine in the urgent treatment of hypertensive crisis.

Doppler assessment of the fetal and uteroplacental circulation during nifedipine therapy for preterm labor

To investigate the effects of nifedipine on the human fetal circulation, 11 fetuses whose mothers were treated with nifedipine for treatment of preterm labor were studied. Maximum velocity waveforms were obtained in the middle cerebral artery (n = 8), renal artery (n = 6), ductus arteriosus (n = 8), and umbilical artery (n = 10). Transvalvular maximal velocity waveforms were obtained across the aortic (n = 11) and pulmonary (n = 7) valves. Maternal uterine arteries also were studied (n = 7). Doppler data were collected before and 5 hours after nifedipine therapy. Patients received an oral loading dose of 30 mg of nifedipine followed by a second oral dose of 20 mg 4 hours later. No significant difference in the flow velocity waveforms was found in the vessels studied 5 hours after the initial dose. These results suggest that short-term nifedipine therapy does not influence either fetal or uteroplacental circulation as evaluated with the Doppler technique.