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PubMed1991

Hydrochlorothiazide and verapamil in the treatment of hypertension. The Verapamil Versus Diuretic (VERDI) Trial Research Group.

The efficacy and tolerability of hydrochlorothiazide, sustained-release verapamil, and their combination was compared in patients with mild to moderate hypertension. The design was a multicenter, randomized, double-blind clinical trial with a single-blind placebo baseline period of 2 weeks. Three hundred sixty-nine patients with a diastolic blood pressure of 95-120 mm Hg were included. Treatment consisted of 12.5 mg of hydrochlorothiazide once daily, then 25 mg once daily, and finally 25 mg twice daily; the other group received verapamil at a dose of 120 mg once daily, then 240 mg once daily, and finally 240 mg twice daily. Patients not achieving target blood pressure (less than 90 mm Hg diastolic) were given the combination of hydrochlorothiazide and verapamil, that is, 25 and 240 mg once daily and twice daily. During all time points during the study patients receiving verapamil achieved target blood pressure more often than patients receiving hydrochlorothiazide (after 8 weeks, 57.7 and 42.7%; after 24 weeks, 46.8 and 26.4%; and after 48 weeks, 44.8 and 24.7%, respectively). Adding verapamil to hydrochlorothiazide was more effective in lowering blood pressure than adding hydrochlorothiazide to verapamil. The number of treatment withdrawals was essentially the same with the two drugs. Therefore, in the doses currently used in antihypertensive treatment, verapamil was more effective than hydrochlorothiazide as a single agent and in combination in mild to moderate hypertension.

Adult↗
PubMed1981

[Behaviour of serum CPK curves in acute myocardial infarction treated with digitalis, verapamil and combined verapamil-digitalis (author's transl)].

In order to compare the effectiveness of different therapeutic regimens in reducing infarct size serial determinations of CPK activity (at 4 hourly intervals in the first 48 hours from the admission to CCU, at the 72th and at 120th hours) were performed in 100 patients with transmural AMI (53 anterior and 47 inferior) with no obvious evidence of LV failure and basal CPK levels lower than 50 U/L. 20 patients (control group) have been treated with glucose-insulin-potassium (GIK). 20 patients have been treated with GIK plus Verapamil (GIK + V). Verapamil was administered at the dose of 50 mg in continuous drip. 20 patients received GIK plus digoxin at the dose of 0.25 mg b.i.d. (GIK + D). 40 patients received GIK, Verapamil and digoxin at the above doses (GIK + V + D). Different values of CKr and infarct size (IS.) show a statistically significant difference between the various regimens, which is more evident if we consider the whole series. Infarct size was greater in patients treated with digoxin with respect to controls, while it was smaller in patients treated with Verapamil. Combined Verapamil-digoxin therapy is associated to an enzymatic behaviour not different from controls. Authors emphasize that in uncomplicated AMI digoxin causes an increase in infarct size while Verapamil reduces significantly it. Association of Verapamil allows the use of digoxin, if clinically justified, without increase in infarct size.

Adult↗
PubMed1998

Direct interaction between verapamil and doxorubicin causes the lack of reversal effect of verapamil on P-glycoprotein mediated resistance to doxorubicin in vitro using L1210/VCR cells.

Mouse leukemic cell subline L1210/VCR exerts expressive multidrug resistance (MDR) that is mediated by P-glycoprotein. Cells originally adapted to vincristine are also extremely resistant to doxorubicin. Resistance to both vincristine and doxorubicin is connected with depression of drug uptake. While resistance of L1210 cells to vincristine could be reversed by verapamil as chemosensitizer, resistance of cells to doxorubicin was insensitive to verapamil. Action of verapamil (well-known inhibitor of PGP activity) on multidrug resistance was often used as evidence that MDR is mediated by PGP. From this point it may be possible that the resistance of L1210/VCR cells to vincristine is mediated by PGP and the resistance to doxorubicin is mediated by other PGP-independent system. Another and more probable explanation of different effect of verapamil on resistance of L1210/VCR cells to vincristine and doxorubicin may be deduced from the following fact: Using UV spectroscopy we found that doxorubicin dissolved in water buffered medium interacts effectively with verapamil. This interaction may be responsible for the decrease of concentration of both drugs in free effective form and consequently for higher survival of cells. In contrast to doxorubicin vincristine does not give any interaction with verapamil that is measurable by UV spectroscopy and resistance of L1210/VCR cells to vincristine may be fully reversed by verapamil.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1991

Changes in calcium homoeostasis and bone formation in patients recovering from acute myocardial infarction: effect of verapamil treatment. Danish Study Group on Verapamil in Myocardial Infarction.

The effect of the calcium antagonist verapamil on calcium homoeostasis and bone metabolism has been investigated in a double-blind randomized placebo-controlled study. Ten patients randomized to verapamil 120 mg t.i.d. and 9 patients randomized to placebo in The Danish Verapamil Infarction Trial II took part in the study. Bone formation, estimated by 24-h whole body retention of diphosphonate (WBR), osteocalcin, alkaline phosphatase and calcium metabolic indices, was recorded before the start of medication and after 1 and 6 months of treatment. Baseline calcium metabolic variables were not significantly different between the two study groups. There were no significant differences in WBR (0.38 vs 0.37), osteocalcin level (8.2 vs 8.0 micrograms/l) or alkaline phosphatase (218 vs 200 U/l) after treatment for 6 months with verapamil compared to placebo. Serum PTH, calcium and phosphate levels were also not affected by verapamil. The results suggest that prolonged treatment with clinical doses of verapamil does not affect indices of calcium and bone metabolism in humans.

Alkaline Phosphatase↗
PubMed1990

Effect of verapamil on mortality and major events after acute myocardial infarction (the Danish Verapamil Infarction Trial II--DAVIT II)

The effect of verapamil on death and major events (i.e., death or reinfarction) after an acute myocardial infarction was studied in a double-blind, randomized, placebo-controlled multicenter trial. Eight hundred seventy-eight patients started treatment with verapamil, 360 mg/day, and 897 patients with placebo. Treatment started in the second week after admission and continued for up to 18 months (mean 16 months). Ninety-five deaths and 146 major events occurred in the verapamil group and 119 deaths and 180 major events in the placebo group. The 18-month mortality rates were 11.1 and 13.8% (p = 0.11, hazard ratio, 0.80; 95% confidence limits, 0.61 to 1.05), and major event rates 18.0 and 21.6% (p = 0.03, hazard ratio, 0.80; 95% confidence limits, 0.64 to 0.99) in the verapamil and placebo groups, respectively. In patients without heart failure in the coronary care unit the mortality rates were 7.7% in the verapamil group and 11.8% in the placebo group (p = 0.02, hazard ratio, 0.64; 95% confidence limits, 0.44 to 0.94), and major event rates 14.6 and 19.7% (p = 0.01, hazard ratio 0.70; 95% confidence limits (0.52 to 0.93). In patients with heart failure the mortality rates were 17.9 and 17.5% (p = 0.79, hazard ratio, 1.05; 95% confidence limits, 0.72 to 1.54), and major event rates 24.9 and 24.9% (p = 1.0, hazard ratio 0.98; 95% confidence limits 0.72 to 1.39). Long-term treatment with verapamil after an acute myocardial infarction caused a significant reduction in major events, and the positive effect was found in patients without heart failure.

Aged↗
PubMed2000

Rapid and highly sensitive method for the determination of verapamil, [2H7]verapamil and metabolites in biological fluids by liquid chromatography-mass spectrometry.

A rapid and highly sensitive method for the determination of verapamil [2,8-bis-(3,4-dimethoxyphenyl)-6-methyl-2-isopropyl-6-azaoctanitrile+ ++] and [2H7]verapamil and their primary metabolites D-617 [2-(3,4-dimethoxyphenyl)-5-methylamino-2-isopropylvaleronitrile], D-703 [2-(4-hydroxy-3-methoxyphenyl)-8-(3,4-dimethoxy-phenyl)-6-methyl-2-iso-p ropyl-6-azaoctanitrile], D-702 [2-(3,4-dimethoxy-phenyl)-8-(4-hydroxy-3-methoxyphenyl)-6-methyl-2-isopr opyl-6-azaoctanitrile], norverapamil [2,8-bis-(3,4-dimethoxyphenyl)-2-isopropyl-6-azaoctanitrile] and secondary metabolites D-620 [2-(3,4-dimethoxyphenyl)-5-amino-2-isopropylvaleronitrile], D-717 [2-(4-hydroxy-3-methoxyphenyl)-5-amino-2-isopropylvaleronitrile], and D-715 [2-(4-hydroxy-3-methoxyphenyl)-8-(3,4-dimethoxy-phenyl)-2-isopropyl-6-++ +azaoctanitrile] has been developed using high-performance liquid chromatography-electrospray mass spectrometry. D-832, the gallopamil analogue of D-617 and [2H3]norverapamil were used as internal standards. The analytes were extracted automatically from plasma and intestinal perfusate using end-capped CN- and C2 solid-phase extraction cartridges. Separation of the eight analytes was achieved on a LUNA C8 analytical column (150x2 mm I.D., 5 microm particle size) with 5 mM ammonium acetate-acetonitrile as the mobile phase run with a gradient from 70:30 to 40:60 and run times of 15 min. With the mass spectrometer operated in the selected-ion monitoring mode, the limits of quantification in plasma and intestinal perfusate were 1 pmol/ml for D-620, D-617, D-702, D-703, norverapamil, verapamil, and [2H7]verapamil and 2.5 pmol/ml for D-717 and D-715 using a sample size of 1 ml plasma and intestinal perfusate. The method described was successfully applied to the determination of verapamil, [2H7]verapamil and their metabolites in human plasma and intestinal fluid in pharmacokinetic studies.

Body Fluids↗
PubMed1998

Temporal pattern of the effect of verapamil on myocardial reinfarction. DAVIT Study Group. Danish Verapamil Infarction Trial.

The purpose of this study was to compare the effects of verapamil on early versus late reinfarction after an index myocardial infarction. A total of 1775 consecutive patients < 76 years of age, with acute myocardial infarction, included in the Danish Verapamil Infarction Trial II, were followed for 18 months. Reinfarctions during the observation period were retrospectively divided into the 50% earliest occurring and the 50% latest occurring (early and late reinfarction, respectively). Cox regression analysis was applied to assess the significance of clinical baseline variables and treatment group (verapamil vs. placebo) on early, late, and total reinfarction. One hundred and ninety-one reinfarctions were registered during the 18-month observation: 96 in the first 5 months (early) and 95 in the last 13 months (late). On univariate analysis verapamil significantly reduced the rate of total reinfarction (P = 0.04, hazard ratio [HR] = 0.77; 95% confidence Interval [CI] 0.58-1.03) and early reinfarction (P = 0.007, HR 0.56; 95% CI 0.37-0.86), but not late reinfarction (P = 0.99, HR = 1.05; 95% CI 0.70-1.56). In a multivariate model, only the rate of early reinfarction was reduced by verapamil (P = 0.012, HR = 0.59, 95% CI 0.39-0.90). Additionally, predictors of early and late reinfarction were quite different in this model. After an index myocardial infarction verapamil reduces the rate of early but not late reinfarction.

Aged↗
PubMed2000

A steady-state evaluation of the bioavailability of chronotherapeutic oral drug absorption system verapamil PM after nighttime dosing versus immediate-acting verapamil dosed every eight hours.

To compare the steady state pharmacokinetics of the 200 mg verapamil PM CODAS (chronotherapeutic oral drug absorption system) formulation dosed nightly versus immediate-acting verapamil 80 mg tablets dosed three times daily, an open-label, single-dose, two-treatment, two-period, two-sequence, balanced, randomized crossover study was performed with a 7-day washout between two treatment periods. Twenty-four healthy male subjects completed the study. All subjects received CODAS verapamil PM 200 mg under fasting conditions dosed at nighttime or verapamil 80 mg dosed three times daily at 8-hour intervals in a randomized fashion. CODAS verapamil PM 200 mg dosed at night for 5 days results in a plasma profile with a lag time of approximately 4 hours suitable for nighttime dosing. Significantly lower plasma concentrations of both enantiomers of verapamil and norverapamil resulted in lower peak-to-trough fluctuations and should ensure the safety of the product. Both medications tested in this study were well tolerated by the group of healthy volunteers.

Adult↗
PubMed1991

Treatment with verapamil after an acute myocardial infarction. Review of the Danish studies on verapamil in myocardial infarction (DAVIT I and II).

The effect of verapamil on death, reinfarctions, and major events, i.e. death or reinfarction after a myocardial infarction has been investigated in 2 Danish double-blind placebo-controlled verapamil infarction trials (DAVIT I and II). DAVIT I was an early intervention trial that demonstrated a statistically nonsignificant reduction in mortality and reinfarction after 6 months of treatment. DAVIT II was a later intervention trial that demonstrated a nonsignificant reduction in the 18-month mortality rate [p = 0.11, hazard ratio 0.80; 95% confidence limits (CL) 0.61 to 1.05], a significant reduction in the reinfarction rate (p = 0.04, hazard ratio 0.77; CL 0.58 to 1.03), and in the major event rate (p = 0.03, hazard ratio 0.80; CL 0.64 to 0.99) in the verapamil group compared with the placebo group. In patients without heart failure in the coronary care unit, a statistically significant reduction in the 18-month mortality rate (p = 0.02, hazard ratio 0.64; CL 0.44 to 0.94), the reinfarction rate (p = 0.02, hazard ratio 0.67; CL 0.46 to 0.97), and the major event rate (p = 0.01, hazard ratio 0.70; CL 0.52 to 0.93) was observed in the verapamil group compared with the placebo group. No significant differences were found in patients with heart failure. Meta-analyses of DAVIT I (for patients alive at day 8) and DAVIT II showed a statistically significant reduction in the odds ratio of mortality (22%), reinfarctions (27%), and the major event rate (21%) in verapamil-treated patients. It is concluded that long term treatment with verapamil after an acute myocardial infarction is associated with a significant reduction in overall mortality, major events, and reinfarctions, with the greatest effect in patients without heart failure.

Angina Pectoris↗
PubMed1980

Intravenous verapamil for termination of re-entrant supraventricular tachycardias: intracardiac studies correlated with plasma verapamil concentrations.

We evaluated efficacy and mechanisms of the antiarrhythmic action of verapamil in 20 patients with sustained supraventricular tachycardia. Two patients had sinus nodal re-entrant tachycardia, nine atrioventricular (AV) nodal re-entrant tachycardia, and nine AV reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome. The study design comprised a double-blind, randomized, cross-over phase using a 0.075 mg/kg dose of verapamil versus placebo and an open-label phase using a 0.15 mg/kg dose of verapamil. The overall results of both phases showed that 15 of 19 patients converted to sinus rhythm with verapamil while only one of 16 converted to sinus rhythm with placebo. The effective plasma verapamil concentration measured 123 +/- 40 ng/mL (mean +/- SD). Verapamil suppressed sinus nodal and AV nodal re-entry but exerted no selective depression between fast and slow AV nodal pathways. It had no significant effect on accessory AV bypass tract but was effective in terminating AV reciprocating tachycardia by its depressive action on the AV node.

Adult↗
PubMed2000

Verapamil metabolite exposure in older and younger men during steady-state oral verapamil administration.

To determine the effect of age on exposure to the circulating major verapamil metabolites norverapamil, N-dealkylverapamil (D-617), and N-dealkylnorverapamil (D-620), plasma concentrations of verapamil and the three metabolites were determined during the last dose interval of a 14-day administration period of 240 mg of sustained release verapamil once daily in 11 older (aged 65-75 years) and 8 younger (20-28 years) healthy male volunteers. Area under the plasma concentration time curve (AUC) was greater for verapamil (mean +/- S. D.) (2815 +/- 733 older versus 1639 +/- 466 ng/ml.h(-1) young; P <. 0007) and norverapamil (2927 +/- 655 versus 2143 +/- 471 ng/ml. h(-1); P <.007); however, it was not significantly different for D-617 [2386 +/- 772 versus 1894 +/- 418 ng/ml.h(-1); not significantly different (NS)] and N-dealkylnorverapamil (897 +/- 366 versus 757 +/- 104 ng/ml.h(-1); NS) in older as compared with young subjects. These data indicate that impaired verapamil oral clearance previously described in older men does not result in decreased exposure to the formed major metabolites, rather there is increased exposure to norverapamil and the same or a trend toward greater exposure to D-617 as well. This suggests that in addition to the impaired clearance mechanisms for verapamil, which are thought to be primarily mediated by CYP3A, biotransformation processes distal to the formation of norverapamil and D-617 are impaired as well.

Administration, Oral↗
PubMed1991

Effect of verapamil on ischemia and ventricular arrhythmias after an acute myocardial infarction: prognostic implications. The Danish Verapamil Infarction Trial II Study Group.

This article is a review of presented subsets of the Danish Verapamil Infarction Trial II (DAVIT II) regarding the effect of verapamil on postinfarction ischemia, ventricular arrhythmias, and heart rate (HR), and the prognostic implications of these findings. Patients underwent Holter monitoring for 24-48 h at 1 week, i.e., before randomization to long-term treatment with placebo or verapamil, and after 1 month and about 1 year of study treatment. Ischemia: 18% of the patients had transient ST-segment deviation before randomization; 24% of the placebo- and 8% of the verapamil-treated patients (p = 0.04) showed ischemia after 1 month; and after 1 year, the figures were 26 and 4%, respectively (p = 0.02). The 18-month major event rate, i.e., first reinfarction or death, in patients with ischemia before randomization were 40 and 23.8% in patients without ischemia (p = 0.06). Arrhythmias: In the placebo group the prevalence and incidence of many ventricular ectopic beats (VEBs), i.e., more than 10 VEBs/h, increased significantly during the first years after infarction; this was not the case in the verapamil patients group. The mean HR was significantly reduced by verapamil treatment after 1 month and after 16 months of treatment. Multivariate analysis demonstrated the presence of more than 10 VEBs/h only early (i.e., 1 week) but not late (i.e., 1 month) after infarction, to be an independent predictor of major events during 18 months' follow-up observation. A HR above 80 beats/min independently predicted major events when appearing both early and late after infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1987

[Bladder instillation of verapamil as a means of enhancing the efficacy of chemotherapy in superficial bladder carcinoma: influence of bladder instillation of verapamil on the cardiovascular system].

Although it is well known that calcium antagonists in vitro possess enhancing effects on anti-tumor drugs, their clinical use is limited on account of side effects on the cardiovascular system. In the present study, the authors attempted the instillation of Verapamil (calcium antagonist) combined with anti-tumor drugs into the bladder for the treatment of superficial bladder carcinoma. The dosage of Verapamil necessary for maintaining an effective concentration for enhancement of the anti-tumor drug was determined and the influences of bladder instillation of Verapamil on the cardiovascular system and on the bladder were studied. The results obtained were as follows: the use of 5 mg of Verapamil was able to maintain an effective concentration (10(-5) M) for enhancement of anti-tumor drugs for at least 2 h. Absorption of Verapamil from the bladder to the vascular system was minimal. No influence on the cardiovascular system or on the bladder was observed. The results of the present study encourage us to pursue the clinical use of Verapamil combined with anti-tumor drugs for the treatment of superficial bladder carcinoma.

Administration, Intravesical↗
PubMed1984

Verapamil in acute myocardial infarction. Danish Multicenter 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 (CCUs). All patients younger than 75 years admitted to the CCU with suspected acute myocardial infarction (AMI) were evaluated for inclusion. Of 7,415 patients, 3,917 were excluded on admission because of heart failure, heart block, other severely disabling diseases or treatment with beta-blocking drugs or calcium antagonists. Treatment was started in 3,498 patients with 0.1 mg/kg of verapamil intravenously and 120 mg perorally on admission followed by 120 mg 3 times daily, or matched placebo. Treatment was continued for 6 months in patients verified to have had AMI according to all 3 World Health Organization (WHO) criteria. Treatment was stopped in patients in whom AMI was ruled out. Of 1,436 patients with AMI, 717 were treated with verapamil and 719 with placebo. After 6 months, 92 patients (12.8%) in the verapamil group and 100 (13.9%) in the placebo group had died. Fifty patients (7%) in the verapamil group and 60 (8.3%) in the placebo group had had reinfarction. After 12 months, 109 patients (15.2%) in the verapamil group and 118 patients (16.4%) in the placebo group had died.

Administration, Oral↗
PubMed1988

D-verapamil and L-verapamil are equally effective in increasing vincristine accumulation in leukemic cells in vitro.

Leukemic cells isolated from peripheral blood from 6 patients with chronic lymphocytic leukemia, immunocytoma and prolymphocytic leukemia were incubated with vincristine (10 nM) with and without racemic verapamil and its L- and D-isomers (6.6 microM). Verapamil increased vincristine accumulation in all cells, the increase varying between 100 and 700%. Racemic verapamil and the L- and D-isomer increased cellular vincristine accumulation to the same extent. The verapamil effect could not be reversed by increasing the calcium concentration in the incubation medium (final concentration 2.5-5.0 mM). The results indicate that the mechanism behind the effect of verapamil on cellular accumulation of vincristine does not depend upon changes in calcium transport.

Calcium↗
PubMed1994

Role of ischemia in postinfarction heart failure: hypothetical considerations based on use of verapamil in the DAVIT II Study. Danish Study Group on Verapamil in Myocardial Infarction.

Based on a retrospective analysis of the DAVIT II database, we attempted to propose subgroups of post-infarction patients with heart failure, who might benefit or not benefit from antiischemic medical intervention. In DAVIT II, patients were randomized in a double-blind fashion to either verapamil 360 mg/day or placebo in the second week after the infarct and followed up to 18 months. The endpoint was the first major event; that is, death or reinfarction. In patients with heart failure but no ischemia, the event rate was 17.6% in the verapamil-treated patients and 16.5% in the placebo group (hazard verapamil: 1.01; 95% CL: 0.57, 1.79). In patients with both heart failure and residual ischemia, the event rate was 11.3% and 17.8% in the verapamil and placebo groups, respectively (hazard verapamil: 0.60; 95% CL: 0.24, 1.52). Although the latter reduction in major events was not statistically significant, we propose, in accordance with other studies, that in postinfarction patients with both heart failure and residual myocardial ischemia, the harmful negative inotropic effects of antiischemic drugs might be outweighed by their antiischemic effects, by means of which the prognosis might be improved. Patients without ischemia but with heart failure may, however, be at a disadvantage from such treatment.

Angina Pectoris↗
PubMed1995

Effect of verapamil on the prognosis of patients with early postinfarction electrical or mechanical complications. The Danish Verapamil Infarction Trial II (DAVIT II).

The Danish Verapamil Infarction Trial II (DAVIT II) demonstrated from the second postinfarction week, that long term treatment with verapamil significantly improved reinfarction free survival after an acute myocardial infarction (AMI). The present post hoc analysis of DAVIT II was undertaken with the purpose of evaluating the effect of treatment with verapamil in patients with early electrical complications, i.e. ventricular or atrial fibrillation, ventricular tachycardia, or second or third degree atrioventricular block, with or without mechanical complication, i.e. heart failure, during the first post-AMI week. In the placebo group, the 18-month mortality rate was lowest (9.5%) in patients without electrical or mechanical complications, highest (24.6%) in patients with electrical events only, and in-between (17.5%) in patients with mechanical problems regardless of presence of electrical complications. Verapamil significantly reduced the 18-month mortality rate in patients with early electrical without mechanical complications (60% reduction, P = 0.02), and in patients without mechanical complications (35% reduction, P = 0.02). Verapamil did not change the mortality rate in patients with mechanical complications.

Aged↗
PubMed1997

Cardiac event rates after acute myocardial infarction in patients treated with verapamil and trandolapril versus trandolapril alone. Danish Verapamil Infarction Trial (DAVIT) Study Group.

Angiotensin-converting enzyme (ACE) inhibitors improve survival in patients with congestive heart failure (CHF) after an acute myocardial infarction (AMI), but mortality may be as high as 10% to 15% after 1 year. Verapamil prevents cardiac events after an AMI in patients without CHF. We hypothesized that in postinfarct patients with CHF already prescribed diuretics and an ACE inhibitor, additional treatment with verapamil may reduce cardiac event rate. In this multicenter, double-blind study, patients with CHF receiving diuretic treatment were consecutively randomized to treatment with trandolapril 1 mg/day for 1 month and 2 mg/day the following 2 months (n = 49), or to trandolapril as mentioned plus verapamil 240 mg/day for 1 month and 360 mg/day for 2 months (n = 51). Trial medication started 3 to 10 days after AMI. All patients were followed for 3 months. End points in the trandolapril/trandolapril-verapamil groups were death 1/1, reinfarction 7/1, unstable angina 9/3, and readmission for CHF 6/2. The 3-month first cardiac event rate was 35% in trandolapril-treated patients and 14% in trandolapril-verapamil-treated patients (hazard ratio 0.35, 95% confidence interval 0.15 to 0.85, p = 0.015). These data suggest that verapamil reduces cardiac event rates in post-AMI patients with CHF when added to an ACE inhibitor and a diuretic.

Aged↗