Topic
Diltiazem
About: Diltiazem is a research topic. Over the lifetime, 4581 publications have been published within this topic receiving 96719 citations. The topic is also known as: (+)-cis-diltiazem & Cardizem®.
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TL;DR: Diltiazem was as effective as treatment based on diuretics, beta-blockers, or both in preventing the combined primary endpoint of all stroke, myocardial infarction, and other cardiovascular death.
923 citations
TL;DR: Nifedipine is a potent, long-acting vasodilator that has proved highly efficacious in relieving anginal symptoms caused by coronary vasospasm, and its value as an antiarrhythmic agent remains to be delineated.
Abstract: Calcium antagonists (slow channel blocking agents) are a very heterogeneous group of agents with dissimilar structural, electrophysiologic and pharmacologic properties. Nifedipine is a potent, long-acting vasodilator that has proved highly efficacious in relieving anginal symptoms caused by coronary vasospasm. In vivo, it exerts no myocardial depressant effects and has no antiarrhythmic properties. Treatment with nifedipine can safely be combined with administration of a beta receptor blocking agent. VErapamil prolongs atrioventricular (A-V) conduction (A-H interval) in a dose-dependent manner. It is the drug of choice for the treatment of reentrant supraventricular arrhythmias, irrespective of whether reentry occurs within the A-V node or through an accessory pathway (the Wolff-Parkinson-White syndrome). Verapamil is only moderately effective as an antianginal agent. Diltiazem is efficacious for the treatment of angiospastic angina, but its value as an antiarrhythmic agent remains to be delineated.
860 citations
TL;DR: Organic inhibitors of calcium influx prevent outward as well as inward current through cardiac calcium channels but do not slow current activation, and organic drugs show varying degrees of use-dependent block.
Abstract: Organic inhibitors of calcium influx prevent outward as well as inward current through cardiac calcium channels but do not slow current activation. Although block is antagonized by raising external calcium or barium concentrations, the competitive effect of permeant cations does not occur at the same cation binding site at which inorganic blockers act. Organic drugs show varying degrees of use-dependent block, due in part to blockade of open channels. Nitrendipine blockade of calcium currents requires doses >100-fold higher than expected from radioligand binding to isolated membranes.
848 citations
TL;DR: Twice-daily doses of ranolazine increased exercise capacity and provided additional antianginal relief to symptomatic patients with severe chronic angina taking standard doses of atenolol, amlodipine, or diltiazem, without evident adverse, long-term survival consequences.
Abstract: ContextMany patients with chronic angina experience anginal episodes despite
revascularization and antianginal medications. In a previous trial, antianginal
monotherapy with ranolazine, a drug believed to partially inhibit fatty acid
oxidation, increased treadmill exercise performance; however, its long-term
efficacy and safety have not been studied in combination with β-blockers
or calcium antagonists in a large patient population with severe chronic angina.ObjectivesTo determine whether, at trough levels, ranolazine improves the total
exercise time of patients who have symptoms of chronic angina and who experience
angina and ischemia at low workloads despite taking standard doses of atenolol,
amlodipine, or diltiazem and to determine times to angina onset and to electrocardiographic
evidence of myocardial ischemia, effect on angina attacks and nitroglycerin
use, and effect on long-term survival in an open-label observational study
extension.Design, Setting, and PatientsA randomized, 3-group parallel, double-blind, placebo-controlled trial
of 823 eligible adults with symptomatic chronic angina who were randomly assigned
to receive placebo or 1 of 2 doses of ranolazine. Patients treated at the
118 participating ambulatory outpatient settings in several countries were
enrolled in the Combination Assessment of Ranolazine In Stable Angina (CARISA)
trial from July 1999 to August 2001 and followed up through October 31, 2002.InterventionPatients received twice-daily placebo or 750 mg or 1000 mg of ranolazine.
Treadmill exercise 12 hours (trough) and 4 hours (peak) after dosing was assessed
after 2, 6 (trough only), and 12 weeks of treatment.Main Outcome MeasuresChange in exercise duration, time to onset of angina, time to onset
of ischemia, nitroglycerin use, and number of angina attacks.ResultsTrough exercise duration increased by 115.6 seconds from baseline in
both ranolazine groups (pooled) vs 91.7 seconds in the placebo group (P = .01). The times to angina and to electrocardiographic
ischemia also increased in the ranolazine groups, at peak more than at trough.
The increases did not depend on changes in blood pressure, heart rate, or
background antianginal therapy and persisted throughout 12 weeks. Ranolazine
reduced angina attacks and nitroglycerin use by about 1 per week vs placebo
(P<.02). Survival of 750 patients taking ranolazine
during the CARISA trial or its associated long-term open-label study was 98.4%
in the first year and 95.9% in the second year.ConclusionTwice-daily doses of ranolazine increased exercise capacity and provided
additional antianginal relief to symptomatic patients with severe chronic
angina taking standard doses of atenolol, amlodipine, or diltiazem, without
evident adverse, long-term survival consequences over 1 to 2 years of therapy.
647 citations
TL;DR: Diltiazem exerted no overall effect on mortality or cardiac events in this population of patients with previous infarction, and this neutral effect reflected a diltsiazem-related reduction in cardiac events on x-ray examination in the majority of patients without left ventricular dysfunction and an increase in such events in the minority of Patients with left Ventricular dysfunction.
Abstract: We studied the effect of diltiazem on mortality and reinfarction in 2466 patients with previous infarction from 38 hospitals in the United States and Canada. The patients were randomly assigned to receive diltiazem (240 mg per day, n = 1234) or placebo (n = 1232) and followed for 12 to 52 months (mean, 25). Total mortality rates were nearly identical among the two treatment groups (167 and 166, respectively), as were cumulative mortality rates. There were 11 percent fewer first recurrent cardiac events (death from cardiac causes or nonfatal reinfarction) in the diltiazem group than in the placebo group (202 vs. 226; Cox hazard ratio, 0.90; 95 percent confidence limits, 0.74 and 1.08). A significant (P = 0.0042) bidirectional interaction between diltiazem and pulmonary congestion was observed on x-ray examination. In 1909 patients without pulmonary congestion, diltiazem was associated with a reduced number of cardiac events (hazard ratio, 0.77; 95 percent confidence limits, 0.61 and 0.98); in 490 patients with pulmonary congestion, diltiazem was associated with an increased number of cardiac events (hazard ratio, 1.41; 95 percent confidence limits, 1.01 and 1.96). A similar pattern was observed with respect to the ejection fraction, which was dichotomized at 0.40. Thus, diltiazem exerted no overall effect on mortality or cardiac events in this population of patients with previous infarction. This neutral effect reflected a diltiazem-related reduction in cardiac events in the majority of patients without left ventricular dysfunction and an increase in such events in the minority of patients with left ventricular dysfunction.
609 citations