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At least 73 records · Page 4Linked to original sources
PubMed1997

Effects of controlled-onset extended-release verapamil on nocturnal blood pressure (dippers versus nondippers). COER-Verapamil Study Group.

Approximately 1 in 4 patients with systemic hypertension have a 24-hour blood pressure (BP) profile characterized by a blunted or absent nocturnal decline in pressure. We evaluated the effects of a chronotherapeutic delivery system of controlled-onset extended-release (COER) verapamil hydrochloride and placebo in 257 hypertensive patients according to their circadian BP pattern in an 8-week prospective, multicenter, randomized, and double-blind clinical trial. Patients were stratified into 193 dippers (>10% decline in BP during the period of 10 P.M. to 5 A.M. compared with the hours of 5 A.M. to 10 P.M.) and 64 nondippers (<10% decline in BP during nighttime). During daytime, placebo-subtracted BP was similarly decreased in dippers and nondippers by COER verapamil. During nighttime, the placebo increased nocturnal BP in dippers (baseline nocturnal BP, 133/78 mm Hg) by 3/3 +/- 2/2 mm Hg and reduced BP by -5/-3 +/- 2/2 mm Hg in nondippers (baseline nocturnal BP, 152/94 mm Hg) (p = NS between groups). After controlling for age, gender, ethnicity, and the regression to the mean observed on placebo for all doses, COER verapamil reduced nocturnal BP more in nondippers than dippers -5.8/-2.4 mm Hg, p <0.0001 for systolic BP and p = 0.09 for diastolic BP). Additionally, a significant dose-related reduction in systolic and diastolic nocturnal BP (r = 0.56, p <0.0001 for systolic BP and r = 0.62, p <0.0001 for diastolic BP) was observed with COER verapamil after controlling for baseline covariates. These data demonstrate that nocturnal BP is decreased by a greater extent in nondipper hypertensives than in dipper hypertensives following treatment with COER verapamil HCL.

Antihypertensive Agents↗
PubMed2001

Effects of verapamil and lidocaine on two components of the re-entry circuit of verapamil-senstitive idiopathic left ventricular tachycardia.

OBJECTIVES: We characterized pharmacologically the slow conduction zone of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) with regard to the late diastolic potential (LDP). BACKGROUND: We showed that the slow conduction zone of ILVT could be divided into two components by LDP; that is, the distal component with a tachycardia-dependent conduction delay property and the proximal one without it. METHODS: Electrophysiologic studies were performed in eight consecutive patients. The LDP was recorded during left ventricular (LV) mapping during ILVT. Entrainment was performed from the right ventricular outflow tract while recording LDP. The effects of lidocaine (1 mg/kg body weight) and verapamil (0.5 or 1.0 mg) were examined during entrainment. RESULTS: The LDPs preceding the Purkinje potential (PP) were serially recorded from the upper third to the middle of the LV septum along the narrow longitudinal line. The ventricular tachycardia (VT) cycle length increased after lidocaine (p < 0.05), and further after verapamil (p < 0.05). The increments in the VT cycle length after administration of the drugs strongly correlated with those in LDP-PP (r > 0.9 for both drugs). The interval from the ventricular potential to LDP was unchanged after administration of the drugs. In one patient, verapamil terminated VT by local conduction block between LDP and PP. The LDP-PP measured during entrainment increased after lidocaine, and further after verapamil, whereas the interval from the stimulus to LDP remained unchanged. CONCLUSIONS: The component distal to LDP is mainly calcium channel-dependent and partly depressed sodium channel-dependent. The proximal component is considered to be sodium channel-dependent (normal).

Adolescent↗
PubMed2001

Myocardial lactate release after intracoronary verapamil application in humans: acute effects of intracoronary verapamil on systemic and coronary hemodynamics, myocardial metabolism, and norepinephrine levels.

Coronary and systemic hemodynamic effects of verapamil have been investigated previously in detail. The acute impact of intracoronary verapamil on coronary hemodynamics has, however, not been correlated to simultaneously changes in myocardial metabolism or norepinephrine levels in humans. After bolus application of 1 mg verapamil into the left coronary artery of 52 patients scheduled for routine coronary angiography, heart rate (HR) remained unchanged, whereas mean arterial blood pressure (MAP) decreased (93.8 +/- 14.9 mmHg to 85.1 +/- 13.7 mmHg, p = 0.001). Coronary blood flow (CBF), calculated from intracoronary Doppler measurements and quantitative coronary angiography, increased after verapamil administration (28.5 +/- 16.7 ml/min to 66.2 +/- 41.8 ml/min, p < 0.001), whereas coronary vascular resistance index (CVRI) decreased (1.43 +/- 0.92 to 0.46 +/- 0.23, p < 0.001). Blood samples, taken simultaneously from the aorta (Ao) and coronary sinus (CS) at baseline and at maximal flow velocity, showed an increase in norepinephrine concentrations in Ao (209 +/- 151 ng/l to 283 +/- 195 ng/l, p < 0.001) and CS (233 +/- 162 ng/l to 323 +/- 248 ng/l, p = 0.004). Myocardial metabolism of pyruvate and free fatty acids were not affected. Glucose release was augmented and initial lactate consumption changed to a net lactate release into the CS (Ao to CS differences: glucose: -1.92 +/- 9.9 mg/dl to -12.8 +/- 22.8 mg/dl, p < 0.001; lactate: 0.07 +/- 0.2 mmol/l to -0.08 +/- 0.3 mmol/l, p = 0.001). Similar results were obtained for the extraction ratios and flux of these metabolites. There was a weak correlation between the increase in CBF and lactate release into the CS. This is the first report of unexpected myocardial lactate release following intracoronary verapamil administration in humans. This lactate release was paralleled by an increased glucose release into the CS at an unchanged metabolism of free fatty acids and pyruvate. One explanation for this unexplained lactate release during increased coronary blood flow might be a wash out phenomenon of lactate from previous ischemic areas, other explanations might be the induction of paradox myocardial ischemia and/or a steal effect. Further studies are necessary to explain these unexpected findings of increased coronary flow and myocardial lactate release. Until reliable explanations are pending, studies using only lactate release as a marker of myocardial ischemia, without taken coronary and systemic hemodynamic parameters into account, should be interpreted with caution.

Adult↗
PubMed1992

The significance of myocardial ischaemia and verapamil treatment on the prevalence of supraventricular tachyarrhythmias in patients recovering from acute myocardial infarction. Danish Study Group on Verapamil in Myocardial Infarction.

Twenty-four hour Holter monitoring and symptom-limited exercise testing were carried out prior to discharge in 157 patients recovering from acute myocardial infarction. Supraventricular arrhythmias (SVT) during Holter monitoring were recorded in 15%, and ST segment depression during exercise in 27%. No association between exercise-provoked ischaemia and SVT was found in the late hospital phase of myocardial infarction. After the tests, patients were double-blindly randomized to treatment with verapamil 120 mg t.i.d. or placebo. One month after randomization 24 h Holter monitoring was repeated in 125 patients (verapamil = 63, placebo = 62). At one month a significantly increased incidence of SVT was found in the placebo group (25%) compared to the verapamil-treated patients (9%) (P = 0.04). The increased prevalence in the placebo group was mainly due to an increased incidence of SVT in patients with exercise-induced ischaemia (P = 0.03). This increment was blurred in the verapamil group. In conclusion, the prevalence of SVT increases during the first month after myocardial infarction. The increase is most pronounced in patients with residual myocardial ischaemia and seemed to be prevented by treatment with verapamil.

Double-Blind Method↗
PubMed1983

The pharmacology of verapamil. V. Tissue distribution of verapamil and norverapamil in rat and dog.

The relative distribution of verapamil and its demethylated metabolite, norverapamil, was studied in rats at intervals after intraperitoneal injection of the parent drug (30 mg/kg). This route of drug administration simulated oral drug dosing, and the highest concentrations of both unchanged drug and metabolite were found in the liver, with lung and kidney containing most of the remainder. The rates of disappearance of verapamil from various organs followed first-order kinetics, and the most rapid elimination occurred from brain and liver. In contrast, verapamil was given intravenously to 3 dogs by a bolus-infusion method to produce sustained steady state plasma concentrations (80, 140, 250 ng/ml) for 1, 2, and 3 h. After systemic administration, the lungs contained almost half the tissue verapamil and, 20% was found in kidney, with the liver accounting for only 17%. Norverapamil was not found in plasma or brain. These studies contrast the pattern of tissue distribution of verapamil after different routes of drug administration. The variable rates of drug elimination from specific tissues may explain the differing durations of the drug's observed effects.

Animals↗
PubMed1992

Internally standardized simultaneous assay of verapamil and N-demethyl-verapamil enantiomers in human plasma by means of high performance liquid chromatography.

A high performance liquid chromatographic method with internal analog standardization for the simultaneous assay of the verapamil and N-demethyl-verapamil enantiomers in human plasma after administration of racemic verapamil is described. The method comprises extraction from alkalinized plasma into an n-hexane/2-propanol phase (95:5), separation of the optical antipodes on a chiral phase (Daicel OJ) and quantification by means of fluorescence detection. A detection limit of about 6 pmol was determined for all four enantiomers. Under routine conditions the limit of quantification (variation coefficient < 10%) was about 8 pmol for the (R)- and (S)-enantiomers. The determination method for verapamil and N-demethyl-verapamil enantiomers is not impaired by their known metabolites. The suitability of the method for clinical pharmacology studies is demonstrated with samples obtained from healthy subjects. First results of comparative kinetics studies in humans and various animal species show marked species-dependency with prevailing (R)-enantiomer levels in humans and dogs, and the opposite in rats.

Chromatography, High Pressure Liquid↗
PubMed1977

Determination of verapamil in human plasma by mass fragmentography using stable isotope-labelled verapamil as internal standard.

In the present investigation a mass fragmentographic procedure for the quantitative determination of verapamil in human plasma was developed which makes use of the principle of mass spectrometry and of isotopic dilution: a known amount of isotopically labelled standard ([13C, 2H2]-verapamil) is added to the plasma sample. After an effective extraction procedure the ratio of the main fragments of verapamil (m/e 303) and the labelled standard (m/e 306) is measured by mass fragmentography. The lower limit of detection is at 1 ng/ml for plasma and at 10 pg/injection for pure verapamil. The precision was found to be between 3.4% and 14.4%, depending on the range (32.7 ng/ml and 2.2 ng/ml, resp.) of the concentration of verapamil in plasma.

Chemical Phenomena↗
PubMed1984

Verapamil in acute myocardial infarction. The Danish Study Group on Verapamil in Myocardial Infarction.

A double-blind study comparing verapamil with placebo was conducted in 16 Danish departments of internal medicine with coronary care units (CCU). All patients under 75 years of age admitted to the CCU with a suspicion of acute myocardial infarction (AMI) were evaluated. Of 7415 patients, 3917 were excluded on admission because of heart failure, heart block, other severely disabling diseases, or treatment with beta-blockers or calcium-antagonists. Treatment was started on 3498 patients with 0.1 mg kg-1 verapamil i.v. and 120 mg perorally on admission followed by 120 mg t.i.d., or matched placebo. Treatment was continued for 6 months for patients ascertained to have had an AMI according to all three WHO criteria. Treatment was stopped in patients in whom these criteria were not fulfilled. Of 1436 patients with AMI, 717 were treated with verapamil and 719 with placebo. After six months, 92 patients (12.8%) in the verapamil group and 100 patients (13.9%) in the placebo group were dead (NS). After 12 months the mortality rates were 15.2% and 16.4%, respectively (NS). By six months after entry a total of 56 reinfarctions were recorded in 50 patients (7%) in the verapamil group and 66 reinfarctions in 60 patients (8.3%) in the placebo group (NS).

Aged↗
PubMed1984

Abrupt withdrawal of verapamil in ischaemic heart disease. The Danish Study Group on Verapamil in Myocardial Infarction.

In order to examine the potential hazards of abrupt withdrawal of verapamil 120 mg t.i.d. after six months treatment, a double blind placebo controlled study was designed as part of the Danish multicenter trial of verapamil in acute myocardial infarction. All patients had had a myocardial infarction six months before withdrawal. At the time of withdrawal, 30% of the verapamil and 28% of the placebo treated patients were experiencing angina pectoris. At follow-up after two to three weeks 15% of 212 patients in the verapamil treated group and 9% of 260 patients in the placebo treated group reported worsening or reappearance of angina pectoris (P less than 0.05). One patient in the placebo group developed a myocardial infarction, and one patient in the verapamil group had episodes of supraventricular tachycardia after withdrawal. A 'withdrawal syndrome' was not found.

Adult↗
PubMed1999

Verapamil and risk of cancer in patients with coronary artery disease. DAVIT Study Group. Danish Verapamil Infarction Trial.

The risk of cancer in users of verapamil was assessed in a long-term follow-up of 1,775 patients who were randomized to verapamil or matching placebo in the Danish Verapamil Infarction Trial-II in the years 1985 to 1987. During 10,474 patient-years, no increased risk of cancer was observed for the verapamil-treated men or women compared with the age- and sex-matched background population.

Aged↗
PubMed1995

Nocturnal dosing of a novel delivery system of verapamil for systemic hypertension. Verapamil Study Group.

To evaluate the efficacy and safety of a novel delivery system of physiologic pattern release (PPR)-verapamil administered nocturnally to patients with stages I and II hypertension using ambulatory blood pressure (BP) monitoring, we performed a multicenter (17 centers), double-blind, randomized, placebo-controlled, parallel-group trial with placebo and 120, 180, 360, and 540 mg of verapamil in 287 randomized patients. The delivery system has a delay in the release of verapamil for 4 to 6 hours, and then delivers the drug from an osmotic pumping system for approximately 12 hours. Patients were dosed at 10 P.M. The primary end point was change from baseline in trough diastolic BP assessed by ambulatory BP monitoring from 6 to 10 P.M. after 8 weeks of therapy, whereas secondary measures included changes from baseline in peak, early morning (6 to 10 A.M.) systolic and diastolic BP, trough clinic BP, and 24-hour average daytime (8 A.M. to 8 P.M.) and nighttime (8 P.M. to 8 A.M.) BP. The 180, 360, and 540 mg verapamil doses achieved statistically significant reductions in trough (6 to 10 P.M.) diastolic BP (-3.9 +/- 1.0, -7.8 +/- 1.2, and -10.6 +/- 1.1 mm Hg, respectively). Reductions in peak early morning (6 to 10 A.M.) diastolic BP were greater (-4.6 +/- 0.9, -13.3 +/- 1.2, and -19.0 +/- 1.2, for 180, 360, and 540 mg, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed2000

Pharmacokinetics of verapamil in lactating rabbits. Prediction of verapamil distribution into rabbit milk.

In this work, we have studied the pharmacokinetics and milk penetration of verapamil following intravenous administration in lactating rabbits. Milk-to-serum drug concentration ratios (M/B(obs)) have been determined using area under the milk and serum concentration-time profiles, and the resulting values have then been compared with those obtained by theoretical classical diffusion milk transfer models that were described by Fleishaker et al. [J. Pharm. Sci. 76 (1987) 189.], Atkinson and Begg [Br. J. Clin. Pharmacol. 25 (1990) 495.], and Stebler and Guentert [Pharm. Res. 9 (1992) 1299.]. The pharmacokinetic profile of verapamil in lactating rabbits following endovenous administration is described in the form of a two-compartment model. Moreover, we detected an important milk transfer after endovenous administration of verapamil in lactating rabbits. M/B(obs) was near 15. The classical diffusional models mentioned were not able to predict this extensive transfer of verapamil into rabbit milk. However, when the classical Fleishaker equation was modified and a stepwise regression was carried out, we found that the M/B(obs) value could be predicted using the plasma and milk protein binding.

Animals↗
PubMed1999

The effect of verapamil on left ventricular remodelling and diastolic function after acute myocardial infarction (the Verapamil Infarction Study on Remodelling and Relaxation--VISOR).

The VISOR is a double blind, randomized, placebo-controlled study aimed to assess the effects of early and prolonged administration of verapamil on the left ventricular geometry and diastolic function in patients with anterior acute myocardial infarction treated with thrombolysis. Patients with heart failure or ejection fraction < 45% were excluded. Within 12 hours from starting thrombolysis, 70 patients were given verapamil (5 mg/hour intravenously for the first 24 hours, followed by 120 mg t.i.d. perorally for 6 months) or equivalent placebo. Echocardiograms were performed on admittance, before discharge, after 3 months and 6 months. The following parameters were calculated: left ventricular volumes, ejection fraction, sphericity index, early (E) and late (A) transmitral peak flow velocities and time-velocity integrals with their ratios, deceleration time and half-time of E, isovolumic relaxation time (IVRT), and non-invasive time constant of ventricular relaxation (tau). The basal and the last available parameters were considered for statistical analysis. The effects of the treatment on the left ventricular volumes, ejection fraction, and sphericity index were not statistically relevant. Conversely, a reduction of E/A ratio (P < .05) and increases of A integral (P < .01), deceleration time and half-time of E, IVRT and tau (P < .05) were found in the placebo group and not in the verapamil group. No significant changes in the blood pressure, heart rate, PQ interval, and biochemical parameters were observed in the two groups. In conclusion, in patients with a thrombolysed anterior acute myocardial infarction and preserved systolic function, verapamil can prevent alterations of the diastolic function in absence of effect on ventricular remodelling, and has a good safety profile.

Calcium Channel Blockers↗
PubMed1983

[Tocolysis with beta sympathomimetics alone or combined with the calcium antagonist verapamil? I. Effect of verapamil on maternal cardiovascular parameters and the course of pregnancy].

In a retrospective study covering 471 cases the influence of the calcium antagonist Verapamil on tocolytic therapy with beta-mimetics was examined. 308 patients received Fenoterol therapy (group A) and 163 were treated with a combination of Fenoterol and Verapamil in a dosage-relation 1/20 (group B). There was no significant difference between group A and B in respect of age, parity, week of gestational age at the beginning of therapy and at delivery, and mode of delivery. The cardiovascular parameters demonstrated alterations as described in literature. The heart frequencies increased significantly in all patients while the systolic and the diastolic blood pressures decreased significantly in hypertonic patients only. These alterations of the cardiovascular parameters were the same in both groups. The efficiency of the tocolytic therapy was tested by comparing the prolongation index (Richter) and the frequency of uterine contractions measured by external cardiotocography. There was no significant difference between groups A and B. Severe complications occurred in 6 patients so that the therapy had to be discontinued (3 women suffered from pulmonary oedemas). These complications were also seen under additional Verapamil application during tocolytic treatment. The side effects as far as reported by the patients were restricted to a significantly lower rate of obstipation in the Fenoterol/Verapamil treated group B. We conclude that administration of the calcium antagonist Verapamil is of no additional value in tocolytic treatment with beta-mimetics.

Adult↗
PubMed1992

Prevalence of transient myocardial ischaemia during the first year after a myocardial infarction. Effect of treatment with verapamil. The Danish Study Group on Verapamil in Myocardial Infarction.

DAVIT-II is a double-blind, randomized, multicentre, placebo-controlled study of long-term treatment with verapamil 360 mg per day administered to patients who have suffered an acute myocardial infarction (AMI). In the present study, comprising a subset of DAVIT-II, 48 h continuous ECG recordings demonstrated transient ST segment deviation indicative of myocardial ischaemia after one week, prior to randomization, in 18% (10 of 57) of the patients. After one month, 24% (11 of 46) of the placebo and 8% (3 of 39) of the verapamil-treated patients (P = 0.04) had myocardial ischaemia; after one year the figures were 26% (9 of 35) and 4% (1 of 27) (P = 0.02), respectively. At 18 months the 'major' event rate in patients who had had ischaemia before randomization was 40% and 23.8% in patients without ischaemia (P = 0.057). In the placebo group, 63% of 91 episodes of ST depression were recorded between 0600 h and 1800 h, and 62% of 26 episodes of ST elevation between 1800 h and 0600 h (P less than 0.001). Nine episodes of ST depression and no episode of ST elevation were recorded in the verapamil-treated patients. In conclusion, 20-25% of post-AMI patients have transient ischaemia; verapamil prevents ischaemia, and a pronounced circadian variation of ST segment deviations can be demonstrated.

Aged↗
PubMed1997

Treatment with verapamil and trandolapril in patients with congestive heart failure and myocardial infarction. The Danish Verapamil Infarction Trial (DAVIT Study Group).

UNLABELLED: EFFECTS OF VERAPAMIL AND TRANDOLAPRIL: Progression of heart failure, sudden death and death from re-infarction are the major cause of the increased mortality in postinfarct patients with congestive heart failure. Angiotensin converting enzyme (ACE) inhibitors such as trandolapril can prevent the progression of heart failure and thus improve survival. The calcium antagonist verapamil has been shown to prevent sudden death and re-infarction in postinfarct patients without congestive heart failure. HYPOTHESIS: The Danish Verapamil Infarction Trial (DAVIT) study group hypothesized the combined treatment with trandolapril and verapamil might prevent cardiac events in postinfarct patients with coronary heart disease. The first double-blind randomized trial included 100 patients and supported this hypothesis, as the cardiac event rate was significantly lower after 3 months in patients treated with the combination than in those treated with trandolapril alone (14 versus 35%, respectively; P = 0.01, hazard ratio 0.35, 95% confidence interval 0.15-0.85).

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1985

An infant fatality following verapamil therapy for supraventricular tachycardia: cardiovascular collapse following intravenous verapamil.

A four-month-old infant with myocarditis and supraventricular tachycardia was given intravenous verapamil (0.1 mg/kg). Immediately following the dosage, the patient developed cardiovascular collapse. Aggressive, appropriate cardiopulmonary resuscitative efforts--including ventricular pacing--failed to reverse verapamil-induced decompensation. Myocarditis may have been responsible for our failure to resuscitate this infant successfully. To our knowledge, this is the first reported pediatric fatality following intravenous verapamil. We suggest that proven or suspected myocarditis should be added to the list of contraindications for intravenous verapamil therapy.

Humans↗
PubMed1980

Pharmacology of verapamil. II. Impairment of glucose tolerance by verapamil in the conscious dog.

The effect of verapamil on glucose tolerance and insulin release in conscious, healthy dogs was studied at plasma drug concentrations which produce therapeutic cardiovascular effects. Plasma glucose and immunoreactive insulin were measured serially in each animal for 90 min after an intravenous glucose challenge (400 mg/kg), both during a control study and again during administration of verapamil. The drug was given by infusion protocols to produce plasma concentrations at low (84 +/- 9 ng/ml), intermediate (161 +/- 30 ng/ml), and high (367 +/- 51 ng/ml) ranges. Insulin release was impaired and glucose levels elevated at both the intermediate and the high verapamil concentrations, and to a similar degree. The reduction in insulin release and subsequent increase in plasma glucose is a pharmacologic effect of verapamil which occurs at drug concentrations likely to be achieved during clinical use.

Animals↗