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PubMed1993

Description of time- and frequency- domain-based measures of heart rate variability in individuals taking antiarrhythmics, beta blockers, calcium channel blockers, and/or antihypertensive drugs after sudden cardiac arrest.

Concomitant drug therapies after sudden cardiac arrest and their potential effect of altering heart rate variability (HRV) represent confounding factors in interpreting the outcome of nonpharmacologic therapies on HRV. The purpose of this study is to describe a broad spectrum of time-domain and frequency-domain measurements of HRV in 50 individuals after sudden cardiac arrest. Some of the individuals were taking antiarrhythmics (n = 9), beta blockers (n = 13), calcium channel blockers (n = 10), nitrates (n = 8), cardiac glycosides (n = 10), and/or antihypertensives (n = 12). Heart rate variability was measured using a Holter recorder for 24 hours and the SpaceLabs FT2000 Monitoring System (Redmond, WA). In those individuals taking antiarrhythmic drugs, the power density within the low-frequency range (.016-.04 Hz) was significantly decreased (P = .001) compared to those not taking antiarrhythmics (n = 41). However, 78% of the people taking antiarrhythmics also had congestive heart failure (New York Heart Association functional classes II and III), which also decreased HRV. Those individuals taking beta blockers tended to have slower heart rates (P < .01). The association between beta blocker use and HRV was positive, but not statistically significant except for the increased power density in the low-frequency range (P < .05). In general, the relationships between HRV and drug therapy--calcium channel blockers, antihypertensives, cardiac glycosides, or nitrates--were not statistically significant.

Adrenergic beta-Antagonists↗
PubMed1995

[Calcium channel blockers (calcium antagonists). Background, effects and use].

The calcium ion plays a decisive role in the effect and regulation of several cellular processes. The heart muscle cells, pacemaker and channel systems and vascular smooth muscle are functionally dependent on Ca2+ influx mainly via potential sensitive L (long lasting)-Ca(2+)-channels, which are blocked by Ca(2+)-channel blockers, a group of organic substances binding to specific sites at the Ca2+ channels. The Ca2+ channel blockers are now well established in the treatment of angina pectoris, arterial hypertension, supraventricular arrhythmia and subarachnoidal haemorrhage. On the basis of chemistry and pharmacodynamics the Ca2+ channel blockers are divided into three groups, with verapamil, nifedipine and diltiazem representing 1. generation derivatives and prototypes for groups I, II and III, respectively. All Ca2+ channel blockers act as vasodilators, while group I (verapamil) and to a lesser degree group III (diltiazem) also have antiarrhythmic effects. All Ca(2+)-channel blockers are contraindicated in hypotension. In cases of pronounced bradycardia, sinoatrial and atriventricular block Ca2+ channel blockers with antiarrhythmic effects are contraindicated and must be used with care in combination with beta-blocker treatment and in heart failure. Headache, flushing, reflex tachycardia, nausea, obstipation and ankle oedema are the most important secondary effects. With respect to pharmacodynamics the newly marketed 2. generation derivatives do not differ essentially from the 1. generation derivatives. The clinical potential of the Ca2+ channel blockers is not fully explored and the possibilities for extending their indications are still to be elucidated.

Calcium↗
PubMed1992

Beta-blockers, calcium channel blockers and the sulfhydryl-ACE inhibitors demonstrate protection against free-radical-mediated injury of cardiovascular cells and membranes.

During reperfusion of previously ischemic cardiac tissue, oxygen-centered free radicals are generated and may result in peroxidative injury of cardiovascular cells and membranes. Since the occurrence of reperfusion injury in patients is unpredictable, particularly in those patients with chronic ischemic coronary artery disease, silent ischemia and those predisposed to significant coronary spasm, it would be advantageous to provide continuing therapy with antioxidant agents.

Adrenergic beta-Antagonists↗
PubMed1999

Effects of calcium channel blockers on calcium release-activated calcium currents in rat hepatocytes.

AIM: To study the influences of calcium channel blockers on calcium release-activated calcium currents (ICRAC) in rat hepatocytes. METHODS: Whole-cell patch-clamp technique was used. RESULTS: The peak amplitude of ICRAC was -0.41 nA +/- 0.09 nA (n = 15), its reversal potential was about 0 mV. Verapamil (Ver), diltiazem (Dil), and nifedipine (Nif) decreased ICRAC strikingly, without affecting its reversal potential. The inhibitory rate of Ver 5 mumol.L-1 was 40% +/- 12% (n = 3), Ver 50 mumol.L-1 reduced the peak amplitude of ICRAC from -0.49 nA +/- 0.12 nA to -0.20 nA +/- 0.09 nA (P < 0.01 vs control, n = 5). The inhibitory rate was 57% +/- 15%. Dil 50 mumol.L-1 and Nif reduced ICRAC from -0.43 nA +/- 0.10 nA to -0.29 nA +/- 0.07 nA (P < 0.01 vs control, n = 5), from -0.32 nA +/- 0.08 nA to -0.27 nA +/- 0.08 nA (P < 0.01 vs control, n = 5). The inhibitory rate was 31% +/- 11%, 19% +/- 7%, respectively. The amplitude of ICRAC was dependent on extracellular Ca2+ concentration. The peak amplitude of ICRAC was -0.21 nA +/- 0.08 nA (n = 3) in Tyrode's solution with Ca2+ 1.8 mmol.L-1 (P < 0.01 vs the peak amplitude of ICRAC in external solution with Ca2+ 10 mmol.L-1). CONCLUSION: The three calcium antagonists inhibited ICRAC effectively and protected hepatocytes from calcium overload via the inhibition of ICRAC.

Animals↗
PubMed1996

Calcium channel blockers.

Calcium ions are essential for the chain of events that leads to myocardial contraction. Its role in the cardiac cycle has been studied extensively for years. Calcium is thought to be effective in the slow channels. Calcium channel blockers were first introduced in this country, more than 20 years ago. The pharmacological effects, usages, side effects, and dosages of some of the most commonly used calcium channel blockers are discussed. In addition, some anesthetic considerations and the latest controversy regarding calcium channel blockers are reviewed.

Anesthesia↗
PubMed1993

Effects of beta-blockers and calcium channel blockers in acute myocardial infarction.

beta-blockers and calcium channel blockers have been evaluated extensively during the acute phase and following myocardial infarction. beta-blockers, when administered early and intravenously, reduce early mortality, reinfarction and cardiac arrests by about 16%. The reduction in mortality is likely to be due to multiple mechanisms including reductions in cardiac rupture, reinfarction and ventricular fibrillation. Recent data also suggest a reduction in intracranial haemorrhage when administered in conjunction with thrombolytic therapy. Prolonged use of beta-blockers for a year or two after myocardial infarction leads to significant reductions in total mortality, sudden deaths and reinfarction. The benefits of beta-blockers are probably mediated through a number of mechanisms, including reduction in heart rate and prevention of plaque rupture, in addition to the mechanisms stated above. Calcium channel blockers do not reduce mortality. It appears that some agents that increase heart rate (e.g. dihydropyridines) may increase the risk of death and reinfarction. On the other hand, agents that reduce heart rate (verapamil and diltiazem) appear to have a neutral effect on mortality but may reduce reinfarction rates. The benefits of beta-blockers appear to be consistent in most subgroups of patients examined, whereas the adverse effects of calcium channel blockers are most marked in those with large infarcts or heart failure. In conclusion, beta-blockers are preferable to calcium channel blockers in the acute phase and long-term after myocardial infarction.

Acute Disease↗
PubMed1986

Mechanisms of action and differences in calcium channel blockers.

Calcium ion (Ca++) serves an important role as an activation messenger; it initiates or regulates key cellular processes including contraction in the heart and vascular smooth muscle. Ca++ acts as both an electrical and a chemical signal. Upon entering the cell, the positively charged Ca++ carries an inward (depolarizing) current that contributes to pacemaker activity in the sinoatrial node and to atrioventricular conduction. Ca++ also binds to anionic surfaces of cell membranes and to anionic groups of both extracellular and intracellular proteins. The intracellular calcium-binding proteins include troponin and calmodulin, which when bound to Ca++ initiate contraction in cardiac and smooth muscles, respectively. Calcium channel blockers inhibit the entry of calcium into the cell, and thus prevent calcium from gaining access to the high-affinity, intracellular calcium-binding proteins. Verapamil and diltiazem decrease myocardial contractility and inhibit smooth muscle tone, while the dihydropyridines are mainly vasodilators. All of these drugs can play an important role in the treatment of hypertension.

Calcium↗
PubMed2003

Glucagon in beta-blocker and calcium channel blocker overdoses: a systematic review.

BACKGROUND: Glucagon is usually accepted as part of the standard treatment in the management of patients with beta-blocker and calcium channel blocker overdoses. METHODS: A systematic review was done in order to evaluate the evidence supporting glucagon use in beta-blocker and calcium channel blocker overdoses. Studies evaluating glucagon for those uses were identified using the Cochrane Database of Systematic Reviews, the Cochrane Controlled Trials Register, MedLine, ToxLine, and EMBASE searches, as well as reviewing medical toxicology textbooks and references of identified articles. Only controlled studies of human or animal studies were included, the latter only when it was an in vivo model of acute poisoning. The quality of the included studies was assessed. RESULTS: The search found no study in humans but identified 30 in animals. In the five studies of animal models of beta-blocker overdose included, glucagon appeared to consistently increase the heart rate at least transiently but appeared to have no effect on mean arterial pressure even though it possibly increased cardiac output. Its effect on the survival rate in animal models of beta-blocker overdose was unclear. In the six studies of animal models of calcium channel blocker overdose included, glucagon appeared to increase heart rate and cardiac output and reverse second and third degree AV blocks, all at least transiently. There appeared to be no effect of glucagon on mean arterial pressure although it did increase in one model. Glucagon appeared to have no effect on survival rate. The included studies for both overdoses were not blinded, had limited numbers of animals, and some had inadequate glucagon regime. CONCLUSION: The evidence supporting the use of glucagon in the management of patients with beta-blocker and calcium channel blocker overdoses is limited to animal studies.

Adrenergic beta-Antagonists↗
PubMed1985

Basic cellular mechanisms of action of the calcium-channel blockers.

Calcium-channel blockers inhibit the entry of calcium ion (Ca++) into excitable cells, including those of coronary and peripheral arterial smooth muscle and the heart. The ability of these drugs to block Ca++ entry into cells inhibits the essential role of this cation as an intracellular messenger. The effects of calcium-channel blockers on the heart include a negative inotropic effect on the working myocardial cells of the atria and ventricles. Because the up-stroke of the action potential in these regions of the heart, and in the rapidly conducting cells of the His-Purkinje system, is due to a fast, sodium-dependent ionic current, calcium-channel blockers do not inhibit conduction in these cells. In the sinoatrial and atrioventricular (AV) nodes, on the other hand, depolarization is due primarily to a Ca++-dependent slow inward current; as a result, the calcium-channel blockers inhibit the sinus pacemaker and AV conduction. Because our knowledge of the molecular structure of the calcium channels in the heart and smooth muscle is rudimentary, little is known of the molecular mechanisms by which calcium-channel blockers inhibit Ca++ entry across the sarcolemmal membranes in these cells. It is apparent, however, that the actions of different members of this class of drugs on the sarcolemma are not the same. Indirect evidence indicates that some members of this class of drugs may interact with hydrophobic regions of the proteins that make up, or regulate, the calcium channels in the plasma membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗
PubMed1998

The safety of calcium-channel blockers.

Calcium-channel blockers are widely used as an effective treatment for hypertension and angina. Several studies have raised questions about their safety, suggesting that calcium-channel blockers can increase the rates of myocardial infarction (MI) and death, particularly in patients with heart disease. Reviews of these studies have uncovered serious methodological shortcomings or have found them restricted to short-acting drugs, frequently at high doses or used inappropriately. One study was based on old data regarding only short-acting nifedipine, which has never been indicated for patients who have suffered an MI or unstable angina. A case-control study of short-acting verapamil, diltiazem, and nifedipine suggested an increased MI rate was confounded by the higher rates of diabetes and preexisting heart disease in the patients treated with calcium-channel blockers. A third study reported significantly decreased survival only in patients taking short-acting nifedipine; in most of the cases reported, blood pressure was not controlled. While these studies alert us to the limitations of short-acting calcium-channel blockers and the necessity of considering side effects such as neurohormonal stimulation, a number of more recent, better-controlled studies have not confirmed increased risk with calcium-channel blockers when appropriately employed. Calcium-channel blockers should still be considered first-line therapy in appropriately selected patients with hypertension or angina.

Angina Pectoris↗
PubMedDate not supplied

Disappearance with ischaemic depolarization of the antifibrillatory activity in a sodium channel blocker and appearance in calcium channel blocker.

Results obtained in the prevention of ventricular fibrillation secondary to myocardial ischaemia are unexpected. Profibrillatory properties might be manifested by Class I antiarrhythmic drugs, normally antifibrillatory. Clear antifibrillatory properties might be manifested by calcium channel blockers, the antifibrillatory effects of which are normally questionable. Therefore, the action of a Class I antiarrhythmic drug, flecainide, and of a calcium channel blocker, verapamil, on the vulnerability to ischaemic ventricular fibrillation was assessed in anaesthetized, open-chest pigs by ventricular fibrillation threshold. Ventricular fibrillation threshold was determined with trains of diastolic stimuli of 100 msec duration, delivered at a rate of 180 beats/min (near that of the ventricular tachycardia), by a subepicardial electrode inserted into the area that could be subjected to ischaemia. Before determining this threshold, ventricles were paced at the same rate, particularly during the ischaemic periods. Ischaemia was produced by complete occlusion of the left anterior descending coronary artery, either at its origin or half-way from it, over increasing periods. The monophasic action potential and conduction time were recorded in the ischaemic area. Before ischaemia, flecainide was adapted to rais the ventricular fibrillation threshold, in spite of a lengthening of the conduction time. Verapamil was devoid of any influence on these parameters. The antifibrillatory effect of flecainide disappeared with ischaemia, which reduced the ventricular fibrillation threshold down to near 0 mA, with triggering of the spontaneous fibrillation at this level: this reduction was no longer counteracted and even hastened by flecainide, becomes finally profibrillatory. Verapamil, on the contrary, delayed the fall in ventricular fibrillation threshold, maintained far from 0 mA, with prevention of fibrillation, unless the occlusion was maintained over a much longer period. Verapamil similarly delayed the shortening of the monophasic action potential duration and the lengthening of the conduction time, preceding fibrillation and leading to it. Consequently, ischaemic depolarization is apparently responsible for the loss of antifibrillatory activity in a sodium blocker, such as flecainide, and the development of antifibrillatory activity in a calcium blocker, since the sodium channel is activated only at high potentials, whereas the calcium channel is activated at lower potentials.

Animals↗
PubMed1994

Beta-blocker and calcium channel blocker toxicity.

Toxicity from beta-blocker and calcium channel blocker drugs is a challenging medical emergency with steadily increasing incidence. Clinical manifestations of intoxication with these drugs are presented in light of known pharmacologic and pharmacokinetic properties, as well as the physiology of the beta-adrenoreceptor and calcium channel. Review of clinical and basic science literature provides the basis for specific management guidelines for beta-blocker and calcium channel blocker toxicity.

Adrenergic beta-Antagonists↗
PubMed2002

Calcium channel blockers for inhibiting preterm labour.

BACKGROUND: Preterm birth is a major contributor to perinatal mortality and morbidity and affects approximately six to seven per cent of births in developed countries. Tocolytics are drugs used to suppress uterine contractions. The most widely tested tocolytics are betamimetics. Although they have been shown to delay delivery, betamimetics have not been shown to improve perinatal outcome, and they have a high frequency of unpleasant and even fatal maternal side effects. There is growing interest in calcium channel blockers as a potentially effective and well tolerated form of tocolysis. OBJECTIVES: To assess the effects on maternal, fetal and neonatal outcomes of calcium channel blockers, administered as a tocolytic agent, to women in preterm labour. SEARCH STRATEGY: We searched the Cochrane Pregnancy and Childbirth Group's specialised register of controlled trials, the Cochrane Controlled Trials Register (February 2002), MEDLINE, EMBASE, and Current Contents. We also contacted recognised experts and cross referenced relevant material. SELECTION CRITERIA: All published and unpublished randomised trials in which calcium channel blockers were used for tocolysis for women in labour between 20 and 36 weeks gestation. DATA COLLECTION AND ANALYSIS: Standard methods of the Cochrane Collaboration and the Cochrane Pregnancy and Childbirth Group were used. Evaluation of methodological quality and trial data extraction were undertaken independently by three authors. Additional information was sought to enable assessment of methodology and conduct of intention-to-treat analyses. Meta-analysis was conducted assessing the effects of calcium channel blockers compared with any other tocolytic agent. Results are presented using relative risk for categorical data and weighted mean difference for continuous data. MAIN RESULTS: Eleven randomised controlled trials involving 870 women were included. When compared with any other tocolytic agent (mainly betamimetics), calcium channel blockers reduced the number of women giving birth within 48 hours (relative risk (RR) 0.73; 95% confidence interval (CI) 0.54, 0.98) and within seven days (RR 0.76; 95% CI 0.59, 0.99). Calcium channel blockers also reduced the requirement for women to have treatment ceased for adverse drug reaction (RR 0.15; 95% CI 0.06, 0.43), the frequency of neonatal respiratory distress syndrome (RR 0.64; 95% CI 0.45, 0.91) and neonatal jaundice (RR 0.73; 95% CI 0.57, 0.93). REVIEWER'S CONCLUSIONS: When tocolysis is indicated for women in preterm labour, calcium channel blockers are preferable to betamimetic agents. Further research should address the effects of different dosage regimens and formulations of nifedipine on maternal and neonatal outcomes.

Calcium Channel Blockers↗
PubMed2001

The risk of limb deficiencies and other congenital abnormalities in children exposed in utero to calcium channel blockers.

AIM: Calcium channel blockers given to pregnant rats have shown an increased prevalence of digital and limb defects and their safety in pregnant women has thus been questioned. We examined the risk of malformations following exposure in utero to calcium channel blockers. METHOD: We conducted a nationwide case-control study based on the Hungarian Case-Control Surveillance of Congenital Abnormalities and identified 22,865 cases with congenital abnormalities and 31,151 population controls during the period 1980-1996. Data on drug exposure were obtained from official questionnaires and obligatory prenatal care logbooks. RESULTS: Among the cases, 586 mothers (2.6%) had been exposed to calcium channel blockers during pregnancy compared with 907 controls (2.4%). The overall prevalence ratios for 17 congenital abnormalities varied between 1.1 and 1.4, and there was no significant increased risk of limb deficiencies or other congenital abnormalities. CONCLUSION: Our data did not indicate an increased prevalence of congenital abnormalities in offspring exposed to calcium channel blockers in utero.

Abnormalities, Drug-Induced↗
PubMed1989

Potentiation of cocaine toxicity with calcium channel blockers.

Three calcium channel blockers were studied for efficacy in preventing seizures and death from cocaine intoxication. Rats were first pretreated with a test drug then subjected to high dose intraperitoneal cocaine. In this model, control animals developed seizures within six minutes, followed by death within ten minutes. Animals that were pretreated with diltiazem, nifedipine, or verapamil developed seizures significantly faster than controls, and at specific doses the death rate was higher than in controls for all three drugs. The potentiation of seizures and death by 2 mg/kg nifedipine pretreatment was further shown by challenge with three different doses of cocaine. This study fails to demonstrate a protective effect and suggests augmentation of cocaine toxicity by pretreatment with the three currently available calcium channel blockers. Several mechanisms by which calcium channel blockers may augment cocaine-induced toxicity are discussed.

Animals↗
PubMed1989

Cutaneous adverse reactions associated with calcium channel blockers.

The calcium channel blockers, nifedipine, verapamil, and diltiazem, are widely used for the treatment of cardiovascular disease. In spite of their widespread use, little data about the frequency and spectrum of cutaneous reactions associated with these agents have been published. Based on reports provided to the FDA's Division of Epidemiology and Drug Surveillance, and the American Academy of Dermatology's Adverse Drug Reaction Reporting System, it appears that the frequency of adverse cutaneous events associated with these drugs is low, but that occasionally severe reactions are associated with the use of these drugs. Among the more serious reactions associated with the calcium channel blockers are toxic epidermal necrolysis with diltiazem, Stevens-Johnson syndrome and erythema multiforme, which have been associated with all three drugs in this class, and exfoliative dermatitis, which has also been reported with all three agents. Most serious reactions associated with these agents occur within two weeks of initiating drug therapy. These findings suggest that calcium channel blockers are occasional causes of a wide spectrum of cutaneous reactions and should be considered as possible causative factors in patients who develop adverse cutaneous reactions while using these drugs.

Adult↗