Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Calcium Channel Blockers”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 523 records · Page 29Linked to original sources
PubMed2002

Association of calcium channel blockers and mortality in haemodialysis patients.

Patients with end-stage renal disease show disturbances of calcium metabolism, including calcification of arterial walls. Such patients show increased mortality, in particular due to increased cardiovascular-associated deaths. The association of calcium channel blockers and mortality in patients undergoing haemodialysis was investigated. A total of 188 patients who were receiving haemodialysis as of July 1998 were followed up for 30 months. Baseline characteristics, including age, sex, laboratory and clinical data, medication and dialysis prescription, were obtained. As of December 2000, 51 of the patients (27%) had died. In the deceased group, age was significantly higher, body mass index was significantly lower, and smoking was significantly more frequent compared with the survival group (each P <0.001). The percentage of patients taking calcium channel blockers was significantly higher in the survival group. Cox proportional hazard regression analysis showed that haemodialysis patients assigned calcium channel blocker therapy had a significantly lower risk of mortality [relative risk 0.33 (95% confidence interval 0.17-0.67); P <0.001]. Thus, in haemodialysis patients who were at high risk of cardiovascular events, administration of calcium channel blockers was associated with lower mortality.

Aged↗
PubMed1998

Calcium channel blocker use and the risk of prostate cancer.

A recent study suggested that the risk of all cancers, including prostate cancer, is increased by the use of calcium channel blockers. The objective of this study was to determine whether prostate cancer is associated with calcium channel blocker use. A case-control study was conducted in Massachusetts using cases diagnosed from December 1992 through February 1995. Cases were men identified by tumor registrars who were less than 70 years old with newly diagnosed prostate cancer. Controls were men with no history of prostate cancer or symptoms of undiagnosed prostate cancer, and were matched to the cases on precinct of residence and half-decade of age. A total of 1217 cases of prostate cancer and 1400 community controls are included in this analysis. Data were collected by telephone interview. Multiple logistic regression was used to estimate relative risks for calcium channel blockers use while controlling for confounding. The relative risk for prostate cancer for any use of calcium channel blockers relative to nonuse was 1.2 (95% confidence interval [CI], 0.9-1.5). There was no evidence of a trend according to duration of use. When the analysis was confined to symptomatic men, the relative risk estimate was 1.1 (0.8-1.4) overall and 1.2 (0.8-1.7) among those aged 65 to 69 years. Relative risk estimates for the use of other classes of antihypertensive drugs among symptomatic men were close to 1.0; the corresponding estimates among asymptomatic men were generally further from 1.0. These findings suggest that calcium channel blockers do not increase the risk of prostate cancer. The differences in the relative risk estimates between symptomatic and asymptomatic men are compatible with detection bias. Because of the widespread use of Prostate-Specific Antigen testing for early detection of prostate cancer, potential detection bias needs to be considered in future studies of prostate cancer.

Adult↗
PubMed1990

Effects of calcium channel blockers and hydralazine on plasma glucose levels in streptozotocin-induced diabetic rats in vivo.

Effects of calcium channel blockers from structurally different classes and hydralazine on plasma glucose levels were examined in streptozotocin-induced diabetic rats in vivo. Non-dihydropyridine calcium channel blockers (verapamil, diltiazem, 1.0-10 mg/kg, i.p.) did not significantly affect the basal plasma glucose level, and dihydropyridine calcium channel blockers (nifedipine, 0.1-0.3 mg/kg, i.p,; nicardipine, 0.35-0.70 mg/kg, i.p.) caused mild hyperglycemia, which was blocked by the administration of the beta-adrenoceptor antagonist propranolol. In contrast, hydralazine markedly produced hyperglycemia, which was also inhibited by the combined administration of propranolol. The selective alpha 1-adrenoceptor antagonist prazosin greatly potentiated the hydralazine-induced hyperglycemia. Isoproterenol alone showed hyperglycemia similar to that of hydralazine. Hexamethonium (40 mg/kg, i.p.), a ganglionic blocker, blocked the hydralazine-induced hyperglycemia. There was a negative correlation between the hyperglycemic effect and the blood pressure lowering effect by different doses of hydralazine in streptozotocin-diabetic rats, but not in normal rats. These results suggest that endogenous catecholamines are involved in the hydralazine-induced hyperglycemia through the interaction with beta-adrenoceptors in streptozotocin-diabetic rats in vivo.

Animals↗
PubMedDate not supplied

Dual calcium-channel blocker therapy in the treatment of hypertension.

OBJECTIVE: To review the in vitro receptor binding data of calcium-channel blockers (CCBs) and in vivo studies in humans regarding the use of dual calcium-channel blocker therapy, with a focus on the use of this therapy for hypertension. DATA SOURCE: A MEDLINE search was conducted to identify literature pertaining to CCBs. STUDY SELECTION: In vitro studies and investigations that evaluated CCB receptor binding and the interactions between subclasses of CCBs were chosen. All studies in humans and clinical trials that evaluated the use of dual CCB therapy in the treatment of cardiovascular diseases were selected for review. Also, case reports describing the use of dual CCB therapy were included in this article. DATA EXTRACTION: The methodology, results, and conclusions of the selected data were evaluated. Data regarding the in vitro receptor binding kinetics of CCBs, as well as interactions, were reported. Because there is limited information on dual CCB therapy for hypertension, clinical studies using this treatment for ischemic heart disease were also reviewed. They were summarized and compared on the basis of the degree of disease control (e.g., blood pressure, exercise tolerance), adverse effects, and other clinical endpoints of pharmacologic therapy. DATA SYNTHESIS: In vitro studies have identified binding sites for the dihydropyridine (nifedipine), diphenylalkylamine (verapamil), and benzothiazepine (diltiazem) subclasses of CCBs, and indicate that they are allosterically related to each other within the voltage-sensitive calcium-channel receptor. Dihydropyridine binding affinity is decreased with concomitant verapamil binding, but is enhanced by concomitant diltiazem binding. Dual CCB therapy has been shown to be efficacious in patients with ischemic heart disease. Although this therapy is limited by dose-related adverse effects, it appears to have an important role in patients with ischemia that is refractory to conventional therapy, or for those whose therapeutic options are limited by contraindications. Theoretically, many patients with hypertension may benefit similarly from dual CCB therapy. Because data evaluating this treatment option are sparse, recommendations regarding safety, efficacy, and the role of dual CCB therapy for hypertension would be premature. CONCLUSIONS: Controlled data evaluating dual CCB therapy for the treatment of hypertension are lacking. This treatment modality may be beneficial in the future, but requires further investigation to determine safety and efficacy.

Calcium Channel Blockers↗
PubMed2004

The influence of the calcium channel blocker verapamil on experimental glaucoma.

PURPOSE: To study the influence of the calcium channel blocker verapamil on the development of glaucoma in the adrenalin-induced experimental model of glaucoma. METHODS: In the experimental model, glaucoma was induced in albino rabbits by repeated injections of small doses of adrenalin. The criteria for experimental glaucoma were (1) increased IOP, (2) decreased outflow and (3) decreased blood supply to the eye. One group with advanced glaucoma served as a control. In the other 3 groups, instillations of 0.25% verapamil were applied at different stages of the glaucomatous process. RESULTS: Verapamil blocked the development of experimental glaucoma when applied concurrently with the adrenalin injections, and instillations at the initial or advanced stages of the disease stabilized the progression of glaucoma. CONCLUSION: We demonstrate that mechanisms involving adrenalin and calcium are involved in glaucoma and that the use of calcium channel blockers is most effective in the early stages of the glaucomatous process.

Animals↗
PubMed2000

Retrospective evaluation of the conversion of amlodipine to alternative calcium channel blockers.

STUDY OBJECTIVE: To evaluate the effectiveness, safety, and costs associated with a formulary conversion from amlodipine to alternative calcium channel blockers. DESIGN: Retrospective study. SETTING: Veterans Affairs Medical Center. PATIENTS: One hundred patients with hypertension who were receiving amlodipine. INTERVENTION: Data from a random sample of 100 patients who were taking amlodipine and converted to a formulary calcium channel blocker from February 1, 1999-October 30, 1999, were entered into an Excel database for evaluation of the conversion. MEASUREMENTS AND MAIN RESULTS: Patients were required to have a diagnosis of hypertension and have had two consecutive clinic visits with blood pressure measurements (and no changes in antihypertensive therapy) before conversion. End points were changes in average systolic blood pressure, diastolic blood pressure, and mean arterial pressure (MAP) from the two clinic visits before and after conversion. In addition, data were collected and analyzed with regard to adverse drug reactions, average dosage of the alternative calcium channel blocker, number of additional antihypertensives begun or discontinued, and number of dosage changes in antihypertensives within the two visits after conversion, and the overall cost impact of conversion. Average systolic blood pressure was reduced from 141.6 +/- 15.1 to 139.2 +/- 15.3 mm Hg after the conversion (NS). Average diastolic blood pressure was significantly reduced from 74 +/- 9.5 to 72.6 +/- 10.1 mm Hg after conversion (p=0.032), as was MAP (97.0 +/-q 9.3 to 94.8 +/- 10.0 mm Hg, p=0.026). Five patients had other changes in therapy made concurrently at the time of conversion, and 19 had changes after conversion. When these patients were excluded from analysis, the reduction in systolic blood pressure after conversion was significant (141.4 +/- 14.5 to 137.7 +/- 14.3 mm Hg, p=0.022), as were reductions in diastolic blood pressure (74.4 +/- 9.4 to 71.7 +/- 9.8 mm Hg, p=0.014) and MAP (96.7 +/- 9.1 to 93.7 +/- 9.3 mm Hg, p=0.007). Of patients who had postconversion changes in therapy, 8 (42%) were converted to diltiazem ER, nifedipine CC, or doses of felodipine that were 50% of the original dose of amlodipine. The overall cost impact of the conversion was a net savings of $14,858/year for each 100 patients converted. CONCLUSION: Conversion from amlodipine to other calcium channel blockers resulted in statistically significant reductions in diastolic blood pressure and MAP, and was safe as well as cost-effective. Conversion to calcium channel antagonists other than felodipine or less than equal dosages of felodipine may require dosage titration. When converting patients from amlodipine, dosages usually should be equal to those of felodipine; if converting to other calcium channel antagonists, the need for adjustments should be anticipated.

Amlodipine↗
PubMed1998

Inhaled nitric oxide as a screening agent for safely identifying responders to oral calcium-channel blockers in primary pulmonary hypertension.

In a subset of patients with primary pulmonary hypertension (PPH), high doses of oral calcium-channel blockers (CCB) produce a sustained clinical and haemodynamic improvement. However, significant side-effects have been reported during acute testing with CCB. Therefore, to identify accurately patients who may benefit from long-term CCB therapy, there is a need for a safe, potent and short-acting vasodilator. The aim of this study was to compare the acute response to inhaled nitric oxide (NO) and oral high doses of CCB in 33 consecutive patients with PPH. A significant acute vasodilator response was defined by a fall in both mean pulmonary artery pressure and total pulmonary resistance by >20%. Ten patients responded acutely to NO, nine of whom responded acutely to CCB, without any complications. The 23 other patients failed to respond to NO and CCB. In these nonresponders, nine serious adverse events were observed with CCB (38%). There was no clinical or baseline haemodynamic feature predicting acute vasodilator response. Long-term oral treatment with CCB was restricted to the nine acute responders and a sustained clinical and haemodynamic improvement was observed in only six patients. In primary pulmonary hypertension, the acute response rate to high doses of calcium-channel blockers is low (27%). Serious adverse reactions to high doses of calcium-channel blockers during acute testing are frequently observed in nonresponders. It is concluded that nitric oxide may be used as a screening agent for safely identifying patients with primary pulmonary hypertension who respond acutely to calcium-channel blockers and may benefit from long-term treatment with these agents.

Administration, Inhalation↗
PubMed1988

Gynecomastia associated with calcium channel blocker therapy.

Gynecomastia is a reaction that is not usually associated with calcium channel blocker therapy. The Division of Epidemiology and Surveillance, within the US Food and Drug Administration (Rockville, Md), has received 31 reports of gynecomastia occurring after the use of these drugs. The underlying mechanism of this reaction is unknown, although two patients did report elevated prolactin levels. Gynecomastia developed in two patients, resulting in the surgical removal of the breast and/or nodules before discontinuation of drug therapy. The possibility of an association between calcium channel blockers and gynecomastia should be considered before an extensive workup or surgical procedure is undertaken.

Aged↗
PubMed2006

3D pharmacophore based virtual screening of T-type calcium channel blockers.

Virtual screening of the commercial databases was done by using a three dimensional pharmacophore previously developed for T-type calcium channel blockers using CATALYSTtrade mark program. Biological evaluation of 25 selected virtual hits resulted in the discovery of a highly potent compound VH04 with IC(50) value of 0.10 microM, eight times as potent as the known selective T-type calcium channel blocker, mibefradil. Search for similar compounds yielded several hits with micro-molar IC(50) values and high T-type calcium channel selectivity. Based on the structure of the virtual hits, small molecule libraries with novel scaffolds were designed, synthesis and biological evaluation of which are currently in progress. This result shows a successful example of ligand based drug discovery of potent T-type calcium channel blockers.

Animals↗
PubMed1998

Calcium channel blockers shorten the periodicity of ultradian variation in blood pressure in patients with essential hypertension.

We studied ultradian and circadian variations in blood pressure (BP) in patients with essential hypertension who were receiving antihypertensive agents. No patient had previously received antihypertensive agents before this study began. After a 2-wk control period, we performed ambulatory blood pressure monitoring (ABPM) in 86 patients with essential hypertension (WHO stages I or II). The patients were then given a long-acting angiotensin converting enzyme inhibitor (ACEI) (captopril or imidapril), a beta-receptor blocker (arotinolol or bisoprolol), or a calcium channel blocker (nisoldipine or benidipine) twice daily to control BP. We evaluated the patients' BP once every 2 wk to ensure optimal control. After 12 wk, ultradian and circadian variations in BP were analyzed by the maximum entropy method (MEM). All antihypertensive agents decreased office systolic BP (SBP), office diastolic BP (DBP), 24-h SBP, and 24-h DBP. ACEI did not change office, 24-h, daytime, or nighttime pulse rate (PR). Arotinolol and bisoprolol decreased 24-h PR. All antihypertensive agents decreased 24-h, daytime, and nighttime pressure rate product. MEM showed that no antihypertensive agent affected the circadian variation in the 1st peak (24-h periodicity) of SBP, DBP, or PR. However, calcium channel blockers shortened the periodicity of circadian variations in the 2nd peak (12-h periodicity) of SBP and the 3rd peak (8 to 6 h periodicity) of SBP. Therefore, ultradian variations in BP should be carefully monitored in hypertensive patients treated with calcium channel blockers.

Activity Cycles↗
PubMed1999

Calcium channel blocker enhances lung preservation.

BACKGROUND: The standard program for lung transplantation employs PGE1 pretreatment for donor lungs, but its efficacy remains controversial. Calcium channel blocker has been reported more effective for reducing potassium-induced vasoconstriction. We investigate the efficacy of calcium channel blocker in the initial lung flush using rat lung transplant model. METHODS: The excised rat lungs (n = 30) were flushed with either University of Wisconsin solution (UWS) with a prior injection of 50 microg/kg PGE1 into the pulmonary artery (UWS + PGE1; n = 7), UWS only (UWS; n = 7), or UWS containing 10(-6) M nifedipine (UWS + Nif; n = 8). After storage (4 degrees C) for 24 hours, all lungs were reperfused for 2 hours using an isolated, pulsatile blood perfused lung model. Control lungs (n = 8) were reperfused immediately after harvest. Blood gas analysis and shunt fraction, lung airway resistance, dynamic lung compliance, and pulmonary vascular resistance were assessed. RESULTS: The pO2 at 30 minutes after reperfusion in the control, UWS, UWS + PGE1, and UWS + Nif group were 88.0 +/- 3.2, 49.6 +/- 2.2, 52.0 +/- 2.4, 85.1 +/- 2.1 (mmHg), respectively. Until 30 minutes after reperfusion, the pO2 in UWS and UWS + PGE1 group were significantly lower than those in UWS + Nif group (p < .001). Shunt fraction, lung airway resistance, and dynamic lung compliance also demonstrated the superiority of UWS + Nif group. CONCLUSIONS: The early graft function after storage was significantly enhanced in lungs flushed with UWS containing nifedipine. Calcium channel blocker is more effective than PGE1 in reducing the potassium-induced vasoconstriction. Optimal composition of the flush may require both calcium channel blocker for pulmonary vasodilation and PGE1 for pulmonary protection by non-vasodilatory mechanisms.

Adenosine↗
PubMedDate not supplied

Calcium channel blockers in cardiac failure.

Congestive cardiac failure is an increasingly prevalent syndrome associated with a high morbidity and mortality. The role of calcium channel blockers in the treatment of heart failure is unclear. The potential benefits of these agents derive not only from their vasodilator properties, but also from anti-ischemic effects, beneficial effects on endothelial function and the development of atherosclerosis, and favorable effects on calcium cycling at a molecular level. Pitted against this array of potential benefits are direct negative inotropic effects and the potential for neuroendocrine activation. Treatment with short-acting dihydropyridine agents has not resulted in long-term clinical benefits in patients with cardiac failure. Diltiazem may be beneficial in patients with nonischemic heart failure, and verapamil has a neutral effect in cardiac failure, although it may have a role in combination with ace inhibition. To date, amlodipine has been associated with the most promising results, with evidence of a mortality benefit in nonischemic heart failure. Mibefradil is of no benefit in the management of heart failure, although the trend toward increased mortality in the treatment arm of the Mortality Assessment in Congestive Heart Failure (MACH)-1 trial may have been due to drug interactions. The potential role of calcium blockers in diastolic dysfunction and in combination with ace-inhibition requires further study.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

[The effect of an alpha-adrenoblocker and a calcium-channel blocker on the spontaneous tonus of an isolated blood-perfused artery].

The existence of spontaneous myogenic tone was shown on an experimental model of an isolated artery perfused "ex vivo" with blood from the rat donor. Administration of the alpha-adrenoblockers prasosine and yohimbine into the perfusion medium in the bath was followed by a 60% decrease in the myogenic tone. The nonspecific blocker of calcium channels CaCl2 decreased the rest of the tone by 15%. The remaining 20-25% of the initial myogenic tone was inhibited by sodium nitroprusside. Urethane (300 mg/kg) or nembutal (20 mg/kg) injected intravenously into the rat donor may lead to an increase or a decrease in the myogenic tone, respectively. The conclusion is made that the advantage of the experimental model proposed lies in the existence of the spontaneous myogenic tone of an arterial vessel depending on humoral catecholamines and some other vasoconstrictor factors.

Adrenergic alpha-Antagonists↗
PubMed2001

Structure-activity study and analgesic efficacy of amino acid derivatives as N-type calcium channel blockers.

The synthesis and structure-activity relationship (SAR) study of a novel series of N-type calcium channel blockers are described. L-Cysteine derivative 2a was found to be a potent and selective N-type calcium channel blocker with IC(50) 0.63 microM on IMR-32 assay. Compound 2a showed analgesic efficacy in the rat formalin-induced pain model by intrathecal and oral administration.

Amino Acids↗
PubMed1996

Suppressive effects of Bay K 8644 on toxicity of calcium channel blockers in cultured rat embryos.

Previous study revealed that calcium channel blockers (CCBs) reduced embryonic heart rates (HRs) and produced morphological abnormalities when Gestational Day (GD) 11.5 rat embryos were cultured for 20 hr. The present study was to investigate whether a calcium channel agonist, Bay K 8644 (BAY), prevented CCB-induced embryotoxicity in vitro. GD 11.5 embryos were exposed to nifedipine (NIF), diltiazem (DIL), and verapamil (VER) either alone or in combination with BAY at 0.1, 1.0, and 10 micrograms/ml. These doses of BAY alone had no effect on gross morphology. Embryonic HRs were increased at 10 micrograms/ml of BAY, but were within control levels at 0.1 and 1.0 microgram/ml. The doses of NIF, DIL, and VER were 40, 6.0, and 2.0 micrograms/ml, respectively, and were the minimum concentrations to produce a 100% effect on morphological abnormalities. Embryonic HRs were reduced to 22, 31, and 34% below control levels in the NIF, DIL, and VER groups, respectively. The negative chronotropic effects of CCBs were inhibited by coadministration with BAY, depending on its concentration. When embryos exposed to each CCB were supplemented with BAY at 1.0 or 10 micrograms/ml, embryonic HRs were comparable to those of controls. Combined exposures of each CCB and 10 micrograms/ml BAY did not cause any morphological abnormalities. These results suggested that mechanisms of CCB embryotoxicity were directly related to pharmacological consequences of calcium channel blockage in developing rats.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1999

Mibefradil, a T-type and L-type calcium channel blocker, limits infarct size through a glibenclamide-sensitive mechanism.

Mibefradil is a novel calcium channel blocker with activity at both L-type and T-type calcium channels. There are data suggesting that this compound can protect the ischemic/reperfused myocardium in spite of the fact that there is a very low abundance of T-type calcium channels within ventricular tissue. The aims of this study were two-fold. First, we wished to study the protective effect of mibefradil on ischemia/reperfusion injury in the isolated rat heart using infarct size as the endpoint of injury. In this respect, we compared mibefradil with amlodipine, a well-known and potent L-type calcium channel blocker, and with ischemic preconditioning, an intervention known to reduce infarct size consistently. Secondly, we investigated the possible mechanisms through which protection was achieved. For this second purpose, we examined the effects on protection of glibenclamide (an ATP-dependent K+ channel blocker) and chelerythrine (a protein kinase C inhibitor). Isolated rat hearts were perfused in the Langendorff mode at constant pressure. Control, mibefradil-treated (0.3 microM), mibefradil plus glibenclamide (50 microM), and mibefradil plus chelerythrine (10 microM) treated hearts underwent 35 minutes regional ischemia followed by 120 minutes reperfusion. At the end of the experiments, infarct size was determined with triphenyltetrazolium chloride and was expressed as a percentage of the ischemic risk zone (I/R%). A significant reduction in infarct size with mibefradil treatment was observed (I/R 11.1 +/- 2.1% vs. 35.5 +/- 3.1% in controls). This was comparable with the infarct reduction seen with two 5-minute cycles of ischemic preconditioning (17.7 +/- 2.5%). Amlodipine 0.1 microM, a concentration that caused equivalent coronary vasodilatation as that produced by mibefradil treatment, had no significant effect on infarct size (I/R 29.7 +/- 3.5%). The protective effect of mibefradil was not significantly modified by the presence of the PKC inhibitor chelerythrine 10 microM (I/R 19.1 +/- 4.9%) but was abolished when glibenclamide 50 microM was coadministered with mibefradil prior to ischemia (I/R 28.1 +/- 4.7%). Neither chlelerythrine nor glibenclamide alone had any influence on infarct size. We conclude from these data that mibefradil, unlike amlodipine, markedly reduces infarct size in the rat isolated heart. This protection is sensitive to inhibition by glibenclamide, suggesting that KATP channel opening may be an important additional and novel mechanism of mibefradil's action.

Animals↗
PubMed1993

Calcium channel blockers in the treatment of hypertension.

Physicians need to weigh the efficacy, adverse effects and cost of first-line antihypertensive agents. Calcium channel blockers lower blood pressure, improve coronary blood flow and depress cardiac contractility by relaxing smooth muscle and cardiac muscle. They have beneficial or neutral effects in hypertensive patients with angina, asthma, chronic obstructive pulmonary disease, postural hypotension, peripheral vascular disease, depression, sexual dysfunction, diabetes and hyperlipidemia. The major adverse effect of some calcium channel blockers is that they may worsen congestive heart failure in some patients. Because calcium channel blockers are metabolized in the liver, the dosage must be lowered in the elderly and in patients with hepatic disease. Diltiazem, verapamil and nifedipine represent prototypes of the three classes of calcium channel blockers, each with slightly different effects.

Calcium Channel Blockers↗
PubMed2001

Is there a role for calcium channel blockers in congestive heart failure?

Over the past several decades, we have made great strides in understanding the pathophysiology of heart failure and have developed new therapeutic targets based on utilizing several different models in clinical trials. Currently, standard therapy involves angiotensin-converting enzyme inhibitors and beta-blockers. In an effort to further reduce mortality, investigators focused on other vasodilators (calcium channel blockers) that might prove to be advantageous when added to standard therapy. Large- scale trials showed that the calcium channel blockers did not have a specific role in mortality reduction, but the third-generation dihydropyridine calcium channel blockers were safe to use in patients with heart failure.

Calcium Channel Blockers↗