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PubMed2002

Blood pressure changes after intrathecal co-administration of calcium channel blockers with morphine or clonidine at the spinal level.

Opioids, alpha(2)-adrenoceptor agonists and blockers of voltage-gated calcium channels have been attributed antinociceptive activity, but only few studies have investigated their influence on the haemodynamic parameters. This study was performed to examine the changes in the mean arterial blood pressure (MAP) after intrathecal (i.t.) co-administration of morphine or clonidine with drugs blocking L- or N-type voltage gated calcium channels (verapamil and omega-conotoxin MVIIA, respectively) in anaesthetized rats. Lower doses of clonidine (0.01-5 microg i.t.) produced dose-dependent decreases in MAP, while the highest dose of clonidine (20 microg i.t.) produced a pressor response. The administration of morphine (0.01-20 microg i.t.) caused only minor decreases of blood pressure and these appeared not to be dose dependent. Both omega-conotoxin MVIIA (1 ng-10 microg i.t.) and verapamil (1-100 microg i.t.) at higher doses decreased blood pressure significantly. Omega-conotoxin MVIIA caused a sustained decrease in MAP, while the effect of verapamil was short-lasting. Co-administration of morphine with verapamil or omega-conotoxin MVIIA led to dose-dependent and sustained decreases in blood pressure. The co-administration of omega-conotoxin MVIIA with clonidine did not influence the effect of clonidine significantly. In contrast, the combination of higher doses of verapamil with clonidine caused far greater blood pressure decreases than saline, verapamil or clonidine treatments alone. These data suggest that the calcium channel blockers differentially influence the cardiovascular effect of the well-known antinociceptive drugs morphine and clonidine after intrathecal co-administration.

Adrenergic alpha-Agonists↗
PubMed2000

Overlapping selectivity of neurotoxin and dihydropyridine calcium channel blockers in cerebellar granule neurones.

Calcium (Ca(2+)) currents have been studied extensively in cerebellar granule neurones, but much of the whole-cell pharmacology is inconsistent. Ca(2+) channel currents were recorded from granule neurones to investigate whether the commonly used Ca(2+) channel blockers show overlapping selectivity. Using combinations of toxin channel blockers, 45% of the total current was shown to be carried by Ca(2+) channels susceptible to block by the combined, or cumulative application of, omega-agatoxin IVA, omega-conotoxin GVIA and omega-conotoxin MVIIC, thus representing P/Q- and N-type channel currents. However, sequential application of these toxins showed that substantial overlap occurred in the proportions of current sensitive to individual toxins. Application of the 1, 4-dihydropyridine nicardipine at 1 microM, a concentration reported to be selective for L-type channels, blocked 16% of the total current, without reducing the current sensitive to the toxins used. However, greater concentrations of nicardipine (>10 microM) blocked a proportion of the total current that could not be accounted for by L-type channels alone. These results demonstrate that a pharmacological approach based on the L, N, P/Q, and R classification does not adequately describe the Ca(2+) channel subtypes found in cerebellar granule neurones due to substantial cross-selectivity to the drugs and toxins used.

Animals↗
PubMedDate not supplied

[Calcium channel blockers in ischemic cardiopathies].

Calcium-entry blockers are the drugs of choice in coronary spasm, unstable angina, and when patients do not have any effort limitation. However, beta-blockers, without sympathomimetic activity, remain the treatment of angina pectoris. When clinical situation is difficult to control, association calcium blockers and bêta-blockers are more efficient than monotherapy. In myocardial infarction, results are controversial: calcium channel blockers should be administered only with beta-blockers.

Angina Pectoris↗
PubMed1997

Calcium-channel blockers and risk of cancer.

BACKGROUND: Previous studies have been interpreted as suggesting an increase in risk of cancer among users of calcium-channel blockers compared with users of beta-blockers. To explore this issue further, we studied a large group of hypertensive patients to investigate the relation of calcium-channel blockers and cancer. METHODS: In cohorts of users of calcium-channel blockers, angiotensin-converting-enzyme (ACE) inhibitors, and beta-blockers, we identified all cases of cancer diagnosed in 1995. We used a nested case-control analysis to estimate the risk of cancer among users of calcium-channel blockers and ACE inhibitors, with users of beta-blockers as a reference group. The study was based on information taken from the General Practice Research Database, and the study population was restricted to patients with at least 4 years of medical history recorded on computer. FINDINGS: The study was based on 446 cases of cancer and 1750 controls. The relative risk estimates for all cancers combined were 1.27 (95% CI 0.98-1.63) and 0.79 (0.58-1.06) for users of calcium-channel blockers and ACE inhibitors, respectively, relative to users of beta-blockers. There was little difference in risk estimates with duration of use of calcium-channel blockers of less than 1.0 year (relative risk 1.46), 1.0-3.9 years (1.26), and 4.0 years or more (1.23). INTERPRETATION: The small positive association between calcium-channel blockers and risk of cancer is unlikely to be causal since there is no increase in risk with increasing duration of calcium-channel blocker use.

Adrenergic beta-Antagonists↗
PubMed1989

In vivo characterization of combination antitumor chemotherapy with calcium channel blockers and cis-diamminedichloroplatinum(II).

We have examined nifedipine, a dihydropyridine class calcium channel blocker, for ability to overcome cis-diamminedichloroplatinum(II) (cisplatin) resistance in a murine tumor line variant, B16a-Pt, which we developed for resistance to cisplatin. Nifedipine significantly enhanced the antitumor actions of cisplatin against primary subcutaneous B16a-Pt tumors and their spontaneous pulmonary metastases. We have characterized, in vivo, the pharmacokinetics and dose-response interactions between nifedipine and cisplatin. We now report our studies designed to compare, in vivo, the efficacy of nifedipine and other calcium active compounds including: (a) structurally similar calcium channel blockers (nimodipine, nicardipine) from the dihydropyridine class, (b) structurally different calcium channel blockers from the benzothiazepine (diltiazem) and the phenylalkylamine (verapamil) classes, and (c) calmodulin antagonists (trifluoperazine and calmidazolium) for ability to enhance the antitumor action of cisplatin. Nifedipine was included as the standard or reference compound. In these studies verapamil and diltiazem failed to enhance the antitumor actions of cisplatin as did both calmodulin antagonists. Our findings suggest that nifedipine has a greater degree of specificity for B16a-Pt cells than structurally different calcium channel blockers from other chemical classes (i.e., diltiazem and verapamil), or the two calmodulin antagonists (i.e., trifluoperazine and calmidazolium). We concluded that nifedipine interacts with specific target site(s) which are not accessible by verapamil, by diltiazem, or by the calmodulin antagonists. Surprisingly, the two dihydropyridine class calcium channel blockers, nimodipine and nicardipine, also failed to enhance cisplatin's antitumor actions despite the fact that their specificity and kinetics for binding to the dihydropyridine receptor component of the calcium channel favors them (nimodipine and nicardipine) over nifedipine. Therefore, we postulate that the synergism between cisplatin and nifedipine is independent of the latter's effect on the voltage sensitive, slow inward calcium channel. We suggest that cisplatin cytotoxicity is enhanced by nifedipine's interaction with an as yet unidentified specific "target site," as opposed to nonspecific interactions with the tumor cell plasma membrane or specific interactions with calmodulin or the P-glycoprotein (which is responsible for pleiotropic resistance).

Animals↗
PubMed2001

Differential efficacy of L- and T-type calcium channel blockers in preventing tachycardia-induced atrial remodeling in dogs.

BACKGROUND: Tachycardia-induced remodeling likely plays an important role in atrial fibrillation (AF) maintenance and recurrence after cardioversion, and Ca(2+) overload may be an important mediator. This study was designed to evaluate the relative efficacies of selective T-type (mibefradil) and L-type (diltiazem) Ca(2+)-channel blockers in preventing tachycardia-induced atrial remodeling. METHODS: Dogs were given daily doses of mibefradil (100 mg), diltiazem (240 mg) or placebo in a blinded fashion, beginning 4 days before and continuing through a 7-day period of atrial pacing at 400 bpm. An electrophysiological study was then performed to assess changes in refractoriness, refractoriness heterogeneity and AF duration. RESULTS: Mean duration of burst-pacing induced AF was similar in placebo (567+/-203 s) and diltiazem-treated (963+/-280 s, P=NS) animals, but was much less in mibefradil-treated dogs (3.6+/-0.9 s, P<0.002) and non-paced controls (6.6+/-2.7 s). In contrast to mibefradil, diltiazem did not alter tachycardia-induced refractoriness abbreviation or heterogeneity. To exclude inadequate dosing as an explanation for diltiazem's inefficacy, we studied an additional group of dogs treated with 720 mg/day of diltiazem, and again noted no protective effect. Acute intravenous administration of diltiazem to control dogs failed to alter atrial refractoriness or AF duration, excluding a masking of remodeling suppression by offsetting profibrillatory effects of the drug. CONCLUSIONS: Whereas the selective T-type Ca(2+)-channel blocker mibefradil protects against atrial remodeling caused by 7-day atrial tachycardia, the selective L-type blocker diltiazem is without effect. These findings are potentially important for understanding the mechanisms and prevention of clinically-relevant atrial-tachycardia-induced remodeling.

Analysis of Variance↗
PubMed1984

Antithrombogenic effects of calcium channel blockers: synergism with prostacyclin and thromboxane synthase inhibitors.

Four calcium channel blockers (nimodipine, nifedipine, verapamil and diltiazem) of three chemical classes were tested in vitro for inhibition of platelet aggregation using heparinized human platelet rich plasma. Both ADP- and thrombin-induced aggregation were inhibited as was the biosynthesis of thromboxane A2 in response to ADP or thrombin. However, the IC50's for the calcium channel blockers were greater than or equal to 110 microM. Nimodipine was also tested in combination with prostacyclin, the potent platelet antiaggregatory agent, or with a thromboxane synthase inhibitor, U63557A. At concentrations at which neither nimodipine or prostacyclin inhibited platelet aggregation greater than or equal to 10%, the two compounds is combination synergistically inhibited both ADP- and thrombin-induced platelet aggregation. U63557A inhibited biosynthesis of thromboxane A2 by platelets in response to ADP or thrombin, but did not inhibit either ADP- or thrombin-induced platelet aggregation. However, U63557A in combination with a threshold inhibitory concentration of nimodipine resulted in a synergistic inhibition of platelet aggregation induced by ADP or thrombin. These results suggest that calcium channel blockers may be of therapeutic value as a new class of antithrombogenic agents when used in combination with agents that inhibit either platelet aggregation or synthesis of platelet thromboxane A2.

Adenosine Diphosphate↗
PubMedDate not supplied

Erythrocyte membrane stabilization by calcium channel blockers, calmodulin antagonists and scavengers of oxygen free radicals.

Calcium channel blockers (nifedipine, verapamil, diltiazem), calmodulin antagonists (trifluoperazine, calmidazolium, compound 48/80) and anti-free radical agents (allopurinol, desferrioxamine, mannitol, L-methionine) were tested for their potency to stabilize human erythrocytes against hypotonic hemolysis. The anti-free radical agents and compound 48/80 did not confer the membrane stabilization. Nifedipine, verapamil, diltiazem, calmidazolium and trifluoperazine at low concentrations, protected the cells from the hypotonic hemolysis while at higher concentrations they caused lysis. Similar biphasic changes were produced by the detergents sodium dodecyl sulphate (SDS) and Triton X-100. The drug concentration-dependency of the biphasic changes in the erythrocytes osmotic fragility produced by calcium channel blockers and calmodulin antagonists was not affected by low concentrations of SDS and Triton X-100. On the other hand, these drugs did not prevent the hemolysis produced by high concentrations of the detergents. The above as well as the observation that the membrane stabilization is conferred only by relatively high concentrations of calcium channel blockers and calmodulin antagonists suggest that membrane stabilization is not responsible for anti-ischemic effects of these agents reported in the literature.

Calcium Channel Blockers↗
PubMed1999

Midazolam alpha-hydroxylation by human liver microsomes in vitro: inhibition by calcium channel blockers, itraconazole and ketoconazole.

The inhibitory effects of five calcium channel blockers (diltiazem, isradipine, mibefradil, nifedipine and verapamil) and three azole antifungal agents (itraconazole, hydroxyitraconazole and ketoconazole) on the alpha-hydroxylation of midazolam, a probe drug for CYP3A4-mediated interactions in humans, were studied in vitro using human liver microsomes. IC50 and Ki values were determined for each inhibitor. The kinetics of the formation of alpha-hydroxymidazolam were best described by simple Michaelis-Menten kinetics. The estimated values of Vmax and Km were 696 pmol min.-(1) mg(-1) and 7.46 micromol l(-1), respectively. All the compounds studied inhibited midazolam alpha-hydroxylation activity in a concentration-dependent manner, but there were marked differences in their relative inhibitory potency. Ketoconazole was the most potent inhibitor of midazolam alpha-hydroxylation (IC50 0.12 micromol l (-1)), being 10 times more potent than itraconazole (IC50 1.2 micromol l(-1)). The inhibitory effect of hydroxyitraconazole (IC50 2.3 micromol l (-1) was almost as large as that of itraconazole. Among the calcium channel blockers, mibefradil was the most potent inhibitor of the alpha-hydroxylation of midazolam, with an IC50 value (1.6 micromol l (-1)) similar to that of itraconazole. The other calcium channel blockers were much weaker inhibitors than mibefradil: verapamil exhibited a modest inhibitory effect with an IC50 of 23 micromol l(-1), while isradipine, nifedipine and diltiazem, with IC50 values ranging from 57 to >100 micromol l (-1), were weak inhibitors. This rank order of potency against the alpha-hydroxylation Qf midazolam was verified by the Ki values. With the exception of diltiazem, these in vitro results conform with the observed interaction potential of these agents with midazolam and many other CYP3A4 substrates in vivo in man.

Antifungal Agents↗
PubMed1987

Do calcium channel blockers protect against renal ischemia?

Data from several studies have indicated that calcium channel blockers may prevent acute renal damage caused by ischemia. If this is true, then the obvious clinical application of this premise would be in surgical cases requiring cross-clamping of the aorta, or in patients experiencing prolonged hypotension. Evidence for the mechanism by which calcium channel blockers mitigate injury include the prevention or amelioration of renal vasoconstriction and/or their ability to inhibit calcium entry into cells, thereby possibly preventing toxic calcium 'overload'. Studies of animal models examining ischemic acute renal failure produced either by infusion of vasoconstrictors or by interrupting renal artery blood flow have provided conflicting results. Certain calcium channel blockers afford some degree of protection only when administered prior to the ischemic episode, while others may protect even if given after the insult. Several investigations have been carried out to determine the mechanism(s) of this protective effect. The results indicate cellular calcium accumulation occurs in cells during the anoxic period; this is most pronounced during reflow. This accumulation of calcium appears to be temporally related to both mitochondrial dysfunction and cell death. The ability of the calcium channel blockers to prevent calcium entry into cells may explain their role in protecting the cell and ameliorating ischemic injury.

Acute Kidney Injury↗
PubMed1987

Differential effects of 1,4-dihydropyridine calcium channel blockers: therapeutic implications.

Increasing recognition of the importance of calcium in the pathogenesis of cardiovascular disease has stimulated research into the use of calcium channel blocking agents for treatment of a variety of cardiovascular diseases. The favorable efficacy and tolerability profiles of these agents make them attractive therapeutic modalities. Clinical applications of calcium channel blockers parallel their tissue selectivity. In contrast to verapamil and diltiazem, which are roughly equipotent in their actions on the heart and vascular smooth muscle, the dihydropyridine calcium channel blockers are a group of potent peripheral vasodilator agents that exert minimal electrophysiologic effects on cardiac nodal or conduction tissue. As the first dihydropyridine available for use in the United States, nifedipine controls angina and hypertension with minimal depression of cardiac function. Additional members of this group of calcium channel blockers have been studied for a variety of indications for which they may offer advantages over current therapy. Once or twice daily dosage possible with nitrendipine and nisoldipine offers a convenient administration schedule, which encourages patient compliance in long-term therapy of hypertension. The coronary vasodilating properties of nisoldipine have led to the investigation of this agent for use in angina. Selectivity for the cerebrovascular bed makes nimodipine potentially useful in the treatment of subarachnoid hemorrhage, migraine headache, dementia, and stroke. In general, the dihydropyridine calcium channel blockers are usually well tolerated, with headache, facial flushing, palpitations, edema, nausea, anorexia, and dizziness being the more common adverse effects.

Angina Pectoris↗
PubMed1992

Effects of antiepileptic drugs, calcium channel blockers and other compounds on seizures induced by activation of voltage-dependent L calcium channel in DBA/2 mice.

1. The convulsant activity of the calcium voltage L-channel agonist Bay k 8644 was studied in genetically epilepsy prone DBA/2 mice. 2. Seizures were induced by intracerebroventricular injection of Bay k 8644. 3. These seizures were reversed by some calcium channel blockers such as dihydropyridines, some excitatory amino acid antagonists such as 2-amino-7-phosphonoeptanoate and CPPene, 2-chloro-adenosine, some anticonvulsant drugs such as magnesium valproate, diazepam and clonazepam and two kappa opioid agonists (U-50488H and U-54494A). 4. The remaining antiepileptic drugs (carbamazepine, phenytoin, phenobarbital and trimethadione) were ineffective in this respect. Other anticonvulsant compounds such as dizocilpine (MK 801), ketamine and drugs enhancing GABAergic transmission did not significantly affect the clonic phase of the seizures induced by Bay k 8644. 5. These results show that Bay k 8644 seizures are relatively resistant to some anticonvulsant compounds. The role of some neurotransmitters on seizures induced by Bay k 8644 is discussed.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMedDate not supplied

[The possible mechanisms of the antioxidant action of calcium channel blockers in the hypoxic syndrome].

The influence of calcium channel blockers on pro-oxidant-antioxidant balance in hypoxic syndrome is studied. Both verapamil and cinnarizine were shown to prevent formation and accumulation of lipid peroxidation products in the tissues and normalize the basic components of the system of antioxidant protection. Probable mechanisms of the antioxidant action of the calcium channel blockers are discussed.

Acute Disease↗
PubMed1989

Effects of calcium channel blockers and hydralazine on epinephrine-induced hyperglycemia in vivo.

Effects of calcium channel blockers from structurally different classes and hydralazine on epinephrine-induced hyperglycemia were studied in vivo. Nifedipine (0.05-0.20 mg/kg, i.p.) and nicardipine (0.40-0.80 mg/kg, i.p.) markedly potentiated the epinephrine-induced hyperglycemia in a dose-dependent manner. In contrast to these dihydropyridine calcium channel blockers, verapamil and diltiazem did not significantly affect the epinephrine-induced hyperglycemia at doses of 0.10-1.0 mg/kg, i.p. At higher doses (10 mg/kg, i.p.), significant potentiation of epinephrine-induced hyperglycemia was observed by these non-dihydropyridine calcium channel blockers. Hydralazine also markedly increased the epinephrine-induced hyperglycemia. These calcium channel blockers and hydralazine had no significant effect on the basal plasma glucose levels at any dose used here. As judged from the rates of glucose disappearance (K values), dihydropyridines significantly impaired the glucose tolerance in much lower doses than those of non-dihydropyridines and hydralazine. Furthermore, epinephrine-induced impairment of glucose tolerance was markedly potentiated by these calcium channel blockers and hydralazine at doses which potentiated the epinephrine-induced hyperglycemia. These results suggest that, at least in part, the potentiation of epinephrine-induced hyperglycemia by dihydropyridines, non-dihydropyridines and hydralazine is related to the inhibition of peripheral glucose utilization produced by insulin.

Animals↗
PubMed1985

Antihypertensive therapy with calcium-channel blockers: comparison with beta blockers.

As a result of concern about the safety and long-term toxicity of diuretics, there is a growing trend toward the use of alternative agents as initial therapy in essential hypertension. Worldwide, beta blockers and vasodilators, especially the calcium-channel blockers, are the most commonly used alternative agents. Several studies comparing these 2 classes of medications are reviewed. These studies indicate that verapamil, nifedipine and diltiazem are all comparable in efficacy to beta blockers. When combined, calcium-channel blockers and beta blockers produce additive responses. These agents may differ in the relation between the magnitude of their antihypertensive effect and patients' pretreatment plasma renin activity and age. Younger persons and those with high plasma renin activity tend to respond better to beta blockers; older subjects and those with low plasma renin activity are more consistently responsive to calcium-channel blockers. The choice of agent should be individualized, based upon accompanying illnesses, adverse-effect profile and demographic factors.

Adrenergic beta-Antagonists↗
PubMed2003

Structure-activity study of L-amino acid-based N-type calcium channel blockers.

Synthesis and structure-activity relationship (SAR) study of L-amino acid-based N-type calcium channel blockers are described. The compounds synthesized were evaluated for inhibitory activity against both N-type and L-type calcium channels focusing on selectivity to reduce cardiovascular side effects due to blocking of L-type calcium channels. In the course of screening of our compound library, N-(t-butoxycarbonyl)-L-aspartic acid derivative 1a was identified as an initial lead compound for a new series of N-type calcium channel blockers, which inhibited calcium influx into IMR-32 human neuroblastoma cells with an IC(50) of 3.4 microM. Compound 1a also exhibited blockade of N-type calcium channel current in electrophysiological experiment using IMR-32 cells (34% inhibition at 10 microM, n=3). As a consequence of conversion of amino acid residue of 1a, compound 12a, that include N-(t-butoxycarbonyl)-L-cysteine, was found to be a potent N-type calcium channel blocker with an IC(50) of 0.61 microM. Thus, L-cysteine was selected as a potential structural motif for further modification. Optimization of C- and N-terminals of L-cysteine using S-cyclohexylmethyl-L-cysteine as a central scaffold led to potent and selective N-type calcium channel blocker 21f, which showed improved inhibitory potency (IC(50) 0.12 microM) and 12-fold selectivity for N-type calcium channels over L-type channels.

Amino Acids↗
PubMed2002

Survival benefit from calcium channel blockers in elderly blacks following acute myocardial infarction.

BACKGROUND: Calcium channel blockers (CCBs) have been used in elderly survivors of acute myocardial infarctions (AMI) and have been found to be safe in this setting. While the elderly have increased mortality following AMI, an ethnic disparity exists, with elderly African Americans having the highest mortality. It is proposed that much of the increased mortality in elderly African Americans may be related to their greater incidence of risk factors at the time of AMI, particularly hypertension. We proposed that elderly African Americans would receive survival benefits from the blood pressure lowering effects of CCBs. METHODS: We analyzed the Cooperative Cardiovascular Project (CCP) database to evaluate the impact of CCBs on survival in elderly patients with AMI. This database comprises patients admitted to US hospitals during 1994-1995 with a diagnosis of acute myocardial infarction. A retrospective chart analysis was performed to identify patients aged 65 years or older admitted with ICD-9 code 410 for acute myocardial infarction. Data were analyzed for trends. RESULTS: Of all elderly AMI admissions, 144,233 were Whites, and 9,906 were Blacks. Hypertension was common in both Whites and Blacks, 60.4% and 79.1%, P<.001, respectively. Calcium channel blockers were used with 27.3% of Whites, and 31.2% of Blacks, P<.001. Blacks had a lower 2-year survival rate, regardless of CCB status, with a 55.7% 2-year survival rate, compared to a 51% 2-year survival rate in Whites. However, in both Blacks and Whites, 2-year survival improved with CCB treatment to a 71.2% 2-year survival rate in Whites and a 68.5% 2-year survival rate in Blacks. Subset analysis by type of CCB demonstrated better survival rates with both dihydropyridine and non-dihydropyridine CCBs, compared to no CCBs, although there was a survival trend favoring non-dihydropyridine CCBs. CONCLUSIONS: Elderly Blacks had a higher mortality rate in the CCP database than elderly Whites, at each time frame. Calcium channel blocker therapy was associated with improved survival in both Whites and Blacks, although Blacks continued to have lower survival rates with CCBs when compared with Whites.

Black or African American↗
PubMed2003

Effect of an educational program on the prevalence of use of antiplatelet drugs, beta blockers, angiotensin-converting enzyme inhibitors, lipid-lowering drugs, and calcium channel blockers prescribed during hospitalization and at hospital discharge in patients with coronary artery disease.

BACKGROUND: There is a marked underutilization of antiplatelet drugs, beta blockers, angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), and lipid-lowering drugs, and an overutilization of calcium channel blockers in elderly patients with coronary artery disease (CAD). METHODS: An ongoing educational program is being given by Dr. Wilbert Aronow on the appropriate utilization of cardiovascular drugs in patients with CAD during hospitalization and at hospital discharge. In a prospective study, charts of 200 unselected patients hospitalized for CAD at least 6 months after the onset of the educational program were analyzed by a medical resident to investigate the appropriate utilization of cardiovascular drugs. The 200 patients included 115 men and 85 women, mean age 70 years, with documented CAD. Of the 200 patients, 127 (64%) had the diagnosis of prior CAD. The use of cardiovascular medications in these 127 patients prior to hospitalization served as a control group. RESULTS: After the educational program, aspirin, clopidogrel, or warfarin was given to 93% of patients compared with 67% in the control group; beta blockers were given to 81% of patients compared with 56% in the control group; ACE inhibitors or ARBs were given to 70% of patients compared with 42% in the control group. Lipid-lowering drugs if dyslipidemia were given to 88% of patients compared with 52% in the control group; calcium channel blockers were given to 18% of patients compared with 24% in the control group. CONCLUSIONS: In patients with CAD, the educational program increased the use of antiplatelet drugs by 26%, beta blockers by 25%, ACE inhibitors or ARBs by 28%, and lipid-lowering drugs by 36%, and decreased the use of calcium channel blockers by 6%.

Adrenergic beta-Antagonists↗