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Diltiazem has electrophysiologic effects similar to those of verapamil. Its efficacy and safety in 4 doses for treatment of induced supraventricular tachycardia (SVT) were examined and compared with those of placebo in 87 patients (25 with atrioventricular [AV] nodal reentry tachycardia, 60 with AV reentry associated with an accessory AV connection, and 2 with atrial tachycardia). Conversion to sinus rhythm occurred in 4 of 14 patients (29%) with 0.5 mg/kg of diltiazem, 16 of 19 (84%) with 0.15 mg/kg, 13 of 13 (100%) with 0.25 mg/kg, and 14 of 17 (82%) with 0.45 mg/kg compared with 6 of 24 (25%) treated with placebo. Conversion rates in groups receiving doses of 0.15 to 0.45 mg/kg of diltiazem were superior to that in the placebo group (p

Silent myocardial ischemia is associated with adverse outcome in several subsets of coronary artery disease patients. This article presents results of a placebo-controlled, randomized, double-blind study of the effects of sustained-release diltiazem (180 mg twice daily) on ischemic episodes in 60 patients with documented coronary artery disease. The mean age of the study population was 60 years and 93% were male. The mean number of episodes of silent ischemia per patient was 5.6 (placebo) and 2.8 (diltiazem), a 50% reduction (p

The use of calcium antagonists for the treatment of patients with unstable angina and acute myocardial infarction has been a promising area of both basic and clinical research. Despite consistently beneficial effects experimentally, the clinical extrapolation of these results has been less than ideal, especially in patients with evolving myocardial infarction. Calcium antagonists have in some instances failed to manifest benefit and at times have been shown to have negative effects. One reason for this could be the use of oral or sublingual preparations, which result in variable absorption, variable volumes of distribution, and variable clearance. For this reason, an intravenous preparation of one of the calcium antagonists, diltiazem, may be more beneficial. Such a preparation has been developed and its safety confirmed in patients without cardiovascular disease and in patients with acute infarction. Substantial benefit has been documented in patients with stable angina and during noncardiac surgery. Preliminary data in patients with unstable angina suggest that the drug is effective, although studies comparing intravenous diltiazem with other agents or with the oral preparation of diltiazem have not yet been reported. Experimental data in animals with acute infarction have demonstrated that administration of intravenous diltiazem after occlusion, but prior to reperfusion, elicits a marked increase in the degree of myocardial salvage induced by thrombolysis. This appears to be due to the inhibition of lipid peroxidation rather than alterations in coronary perfusion. Thus, it appears that the intravenous preparation may permit the more effective use of diltiazem in patients with acute coronary artery disease.

For 18 patients consecutively admitted to the coronary care unit for unstable angina, 48-hour electrocardiographic Holter monitoring was performed after they were randomly assigned in a single-blind fashion to 1 of 2 treatment groups. The first group was treated with acetylsalicylic acid (ASA) and intravenous nitroglycerin, the second with ASA and intravenous diltiazem. All of the patients treated with nitroglycerin still had ischemic episodes after 48 hours (33% were symptomatic), in contrast with 11% of the diltiazem group (11% asymptomatic). Maximal ST-segment depressions of symptomatic and asymptomatic episodes were significantly different; and no significant increases in heart rate were observed either during the 15 seconds before ischemia began or during the ischemic episode. During the 48 hours, the diltiazem group had significantly fewer ischemic episodes (17) than did the nitroglycerin group (145). We concluded that 'on-line' ST-segment observation is of prime importance for monitoring unstable angina; that the majority of the ischemic episodes associated with unstable angina are silent; and that intravenous diltiazem could be an effective pretreatment for patients who must undergo mechanical or surgical therapy., Angina is chest pain caused by a reduction in the blood supply to the heart; unstable angina is a condition of worsening angina in which episodes of chest pain occur more frequently and are more severe, and may occur at rest. Patients with this condition are at risk for serious complications, including heart attack and sudden death. Silent myocardial ischemia, or asymptomatic episodes of inadequate blood supply to the heart, is also associated with serious complications. Calcium antagonists are effective therapy for some types of silent ischemia, and they are also used to relieve the symptoms of unstable angina, but few studies have evaluated the effects of intravenous administration of these agents. The effectiveness of intravenous administration of diltiazem, a calcium channel blocker, was compared with that of nitroglycerin, a vasodilator, in 18 patients with unstable angina. The diltiazem-treated group had significantly fewer episodes of ischemia than the nitroglycerin-treated group. The findings confirm earlier reports that vasodilators control the symptoms of angina, but are less effective in controlling episodes of asymptomatic ischemia in unstable angina. Intravenous diltiazem controlled both types of ischemia (angina and silent ischemia). It was also found that heart rate did not increase before or during ischemia, most ischemic episodes in patients with unstable angina are asymptomatic, and that monitoring the electrocardiogram (for ST depressions) is essential in assessing unstable angina. Intravenous diltiazem may be used for patients with unstable angina before they undergo procedures to increase the blood supply to the heart. The persistence of silent ischemia is an indication of poorer outcomes in patients with unstable angina, therefore controlling ischemia may help improve their prognosis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Calcium antagonists impede the entry of calcium into myocytes and inhibit myocardial contraction. Calcium antagonists differ in their relative negative inotropic potency and can provoke baroreceptor stimulation that modulates left ventricular (LV) performance. Calcium antagonists are uniformly well tolerated in patients with normally LV function. Use of these agents in patients with suspected LV function impairment has yielded results ranging from hemodynamic improvement to clinical deterioration and increased mortality. Reports of clinical deterioration when calcium antagonists were combined with [Beta] blockers underscore the importance of reflec adrenergic support for the myocardium. Atthough calcium antagonists are potent vasodillators and produce short-term hemodynamic improvement, they are not useful as primary treatment in patients with congestive heart failure (CHF). They may have a place in the treatment of coexistent problems in patients with LV dysfunction. Short-term use of calcium antagonists for myocardial ischemia or rapid atrial fibrillation is probably safe in the presence of LV dysfunction and over CHF. Calcium antagonists appear to have a role in the treatment of patients with diastolic dysfunction of diverse etiologies., Calcium channel blockers, also known as calcium antagonists, are effective in treating hypertension, arrhythmias (abnormal heart rhythms), and angina pectoris (chest pain caused by inadequate blood flow to the heart). Because these drugs have a strong suppressing effect on heart muscle contraction, they have not been used in patients with depressed left ventricular function. (The left ventricle pumps blood to the body.) However, the beneficial effects of calcium channel blockers have convinced researchers to evaluate their use in selected patients with left ventricular dysfunction. While these agents produce short-term improvement, they have not been used as primary treatment of congestive heart failure because they may adversely affect older patients and those with severe illness. The effects of the calcium channel blockers nifedipine, verapamil, diltiazem, nitrendipine and isradipine were compared. At this time, there is little information about the effects of calcium antagonists in patients with impaired left ventricular function who also suffer from angina pectoris. Short-term use of calcium antagonists for myocardial ischemia (inadequate blood supply to the heart) and atrial fibrillation (an abnormal heart rhythm) is considered safe even in patients who suffer from chronic heart failure. However, diltiazem is not recommended after a heart attack if the patient has pulmonary vascular congestion (congestion of the lung vessels). (Consumer Summary produced by Reliance Medical Information, Inc.)

A randomized, placebo-controlled, double-blinded trial was performed to evaluate the usefulness of empiric therapy with a calcium antagonist in patients who undergo corenary angioplasty. A total of 201 patients were randomized to placebo or to high-dose diltiazem (mean dose, 329 mg/day). Treatment began 24 hours before angioplasty. Restenosis was assessed by percent area stenosis as determined by quantitative angiographic techniques before, immediately and 1 year after angioplasty. All patients also received aspirin and dipyridamole before angioplasty. Heparin and verapamil were administered intravenously during the procedure. The 2 groups were similar with respect to age, extent of coronary artery disease, smoking history, and baseline lipid levels. Procedural complications, including death (1 vs 1), Q-wave infarction 0 vs 3), acute occlusion (5 vs 5) and focal spasm O vs 0), were not significantly different in the diltiazem and placebo patients, respectively. Freedom from all acute complications was noted in 85% of patients in both groups. One-year angiographic follow-up was obtained in 60% of patients. Restenosis rates were similar: 36% in the diltiazem group and 32% in the placebo group (p = 0.30). The incidence of late cardiac events (death, Q-wave myocardial infarction, recurrent angina or coronary bypass graft surgery) was similar in the 2 groups. Thus, diltiazem did not influence the overall restenosis rate or prevent late events after coronary angioplasty. (Am J Cardiol 1991;67:373-376), Calcium antagonists are a group of drugs that have been used to treat high blood pressure by virtue of their ability to relax blood vessels and decrease the heart's need for oxygen. It has been suggested that calcium antagonists, which inhibit the flow of calcium ions into muscle cells, may also be useful after coronary angioplasty. Coronary artery disease (CAD) occurs when atherosclerotic coronary arteries, narrowed and blocked by fatty plaques, cause decreased blood flow to the heart. This condition may be effectively treated by percutaneous transluminal coronary angioplasty (PTCA), in which a balloon-tipped catheter is inserted into the affected vessels. The balloon is inflated to dilate (widen) the narrowed arterial segments and restore coronary blood flow. Unfortunately, shortly after and within several months of PTCA, vessels may exhibit tissue damage and restenosis (recurrent narrowing). Calcium antagonists, such as diltiazem, may enhance vascular healing and prevent the development of new atherosclerotic lesions and other complications. The effectiveness of diltiazem in preventing complications and restenosis after PTCA was assessed in 201 patients; 102 patients received diltiazem and 99 were given an inactive placebo. Patient characteristics were similar in both groups. Results of one-year follow-up were obtained for 120 of the patients. The amount of blockage of coronary vessels was similar in both groups: 83 percent before surgery, 50 percent right after surgery, and 63 percent at follow-up. Similar results were observed in both groups following surgery and at follow-up in relation to complications and restenosis. The results demonstrate that diltiazem did not reduce post-PTCA mortality, heart attack, recurrent angina or the need for coronary bypass graft surgery during the study period. (Consumer Summary produced by Reliance Medical Information, Inc.)

To examine the time-course and potential predictors of prolongation of ventricular repolarization with the calcium antagonist bepridil, the effects of bepridil (300 to 500 mg/day; n = 4S) and diltiazem (180 to 300 mg/day; n = 42) on QT and QTc interval duration were analyzed in a randomized double-blind study in patients with angina pectoris. Electrocardiograms were recorded before and 14, 28, 70 and 112 days after treatment was begun. After 14 days, bepridil prolonged QT interval by 26 [+ or -] 35 ms (range, -60 to 120 ms) and QTc (Bazett's formula) by 17 [+ or -] 33 ms (range, -73 to 107 ms) compared to baseline (both p (Am J Cardiol 1990;66:812-817), Calcium antagonists (also called calcium channel blockers) reduce calcium transport across cell membranes, causing muscle tone to relax and blood vessels to become less constricted. The calcium antagonist bepridil has other beneficial properties in the treatment of angina pectoris, or chest pain resulting from decreased circulation to the heart. Still under study in the United States, bepridil has been available in Europe for almost a decade. This agent may be useful for treating ventricular and supraventricular arrhythmias (abnormal heart rhythms). Torsades des pointes, an irregular fast heart rate, is a rare but potentially fatal side effect associated with administration of bepridil. It occurs when the systolic phase lengthens excessively, as indicated by the QT segment of an electrocardiogram (ECG). (The QT interval corresponds to the phase of the heart beat in which the ventricle is contracting and beginning to repolarize.) Although extremely rare, torsades des pointes is a major concern because there is no way to predict who is at risk. The authors had previously compared bepridil with diltiazem in the treatment of patients with stable angina over a period of four months. This analysis is designed to measure the effects of the two drugs on the timing of ventricular repolarization in a subgroup of 87 patients from the original study population of 227. Patients were randomly assigned to receive bepridil or diltiazem. The results of the study confirm that bepridil prolongs ventricular repolarization, but diltiazem does not. This suggests that calcium blocking is not causing the prolongation of the repolarization cycle, which is probably due to blockade of potassium channels. Bepridil had no significant effect on heart rate, offering further evidence that it affects only the repolarization cycle. A short interval and a slow heart rate may predict greater prolongation of the cycle when bepridil is administered, but despite the lengthened QT interval, no torsades des pointes or other abnormal heart rhythms occurred. There is still no agreement about whether QT prolongation promotes or prevents abnormal heart rhythms. (Consumer Summary produced by Reliance Medical Information, Inc.)

Calcinosis, calcium deposits in various body tissues, occurs chiefly in a scleroderma-linked disorder called the CREST syndrome. The CREST syndrome is an acronym for features which characterize it, which include 'Calcinosis', 'Raynaud's phenomenon', 'Esophageal dysfunction', 'Sclerodactyly', and 'Telangiectasia'. The cause of calcinosis is unclear, but appears to be related to an increased affinity for calcium in connective tissues. No consistently effective treatment for calcinosis is known. However, studies with calcium channel blockers such as verapamil or diltiazem, which prevent the entry of calcium into many cells, have shown promise. The effects of diltiazem treatment in a 38-year-old woman who had progressive calcinosis since the age of 15 years are described. Calcinosis caused skin lesions that hardened and often developed inflammation. The patient also had Raynaud's phenomenon with other features of CREST, along with high blood pressure. No abnormalities in calcium metabolism were found. Only two minor lesions occurred during five years of diltiazem treatment. Rather than progressing, calcification in soft tissue and bone decreased. The major side effect was weight gain, which stabilized after one year. Except for possible improvement in symptoms of Raynaud's phenomenon, the underlying connective tissue disorder was not apparently effected. The study suggests that calcium antagonists, such as diltiazem, may be effective in treating in calcinosis, and that altered calcium handling at the cellular level may contribute to the development of the disorder. (Consumer Summary produced by Reliance Medical Information, Inc.)

Invasive haemodynamic monitoring should be considered when hypotension fails to respond to empirical treatments We present a potentially fatal case of diltiazem overdose caused by inappropriate self treatment. We highlight [...]

Therapeutic errors involving calcium channel antagonists (CCA) resulting in death rarely have been reported in detail. We report a fatality from an unintentional overdose of sustained-release (SR) diltiazem including antemortem and postmortem blood concentrations. Case Report. A 65-year-old man with aortic stenosis mistakenly took six tablets of diltiazem 360 mg SR. He developed symptoms of toxicity by 7 hours after ingestion. By 10 hours, he went to the emergency department. Despite a prolonged resuscitative attempt, the patient died 17 hours postingestion. An antemortem blood sample drawn 11.5 hours after ingestion was 2.9 mcg/mL. Postmortem gas chromatography of central blood revealed a diltiazem level of 6 mcg/mL and the peripheral blood sample measured 5 mcg/mL. Conclusion. This case suggests that an unintentional overdose with a CCA may be lethal if the patient's cardiovascular ability to compensate for the toxic effects is compromised. Keywords Fatal; Diltiazem; Antemortem; Postmortem, INTRODUCTION Calcium channel antagonists (CCAs) are prescribed for the treatment of an extensive array of cardiovascular-related diagnoses and therapeutic errors may occur (1,2). We report a fatality from an unintentional [...]

To investigate the antiischemic efficacy of intravenously administered diltiazem, 42 patients were randomlY allocated to receive placebo or active treatment before 1-vessel percutaneous transluminal coronary angioplasty (PTCA). The development of myocardial ischemia was studied using subjective (pain) and objective electrocardiography) parameters. Pretreatment with intravenous diltiazem resulted in a significantly delayed onset of ischemic pain and ST-segment elevation; these variables also returned to baseline earlier after balloon deflation. Thus, intravenous diltiazem prevents or delays the onset of myocardial ischemia during repetitive transient coronary occlusions; improvement of the myocardial blood flow distal to the coronary occlusion or impedance of calcium entry into the ischemic cell are considered as possible mechanisms. Because PTCA is increasingly used in patients with poor left ventricular function and more extensive disease, and because recent evidence suggests that better PTCA results could be obtained by the use of longer inflation times, the addition of diltiazem to the classic armamentarium could be beneficial. (Am J Cardiol 1989;64:1103-1107), Percutaneous transluminal coronary angioplasty (PTCA) is a procedure for treating narrowed coronary arteries, which are the major blood vessels that bring blood to the heart. A catheter or tube-like structure with a small inflatable balloon is inserted into the narrowed portion of the artery, and the balloon is inflated, thereby mechanically dilating the narrowed coronary artery. In PTCA, inflation of the balloon causes transient occlusion, or blockage, of the coronary artery. This leads to regional ischemia, or insufficient blood flow to specific portions of the heart. Medications can be given before PTCA to reduce or prevent regional ischemia. The anti-ischemic effect of the drug diltiazem was assessed in 42 patients who were scheduled to undergo PTCA; half the patients received pretreatment with diltiazem while the other half received an inert placebo. During the PTCA procedure, chest pain and changes in the electrocardiogram, a recording of the electrical activity of the heart, were used as indicators of ischemia. Pretreatment with diltiazem delayed the onset of pain and ECG changes associated with ischemia, and both of these indicators returned to normal after deflation of the balloon more quickly with diltiazem than without. The results show that intravenous diltiazem delays the onset of myocardial ischemia during repetitive and brief blockage of the coronary arteries. Diltiazem may exert its effects by improving blood flow beyond the blocked portion of the coronary artery, or by blocking the entry of calcium into the ischemic cell; diltiazem is a calcium blocking agent. Thus, diltiazem may be a useful medication for delaying the onset of ischemia in patients undergoing PTCA; it may be particularly helpful if longer balloon inflation periods (which may prove to be more effective than briefer periods) are utilized in the future. (Consumer Summary produced by Reliance Medical Information, Inc.)

Angina pectoris is chest pain associated with myocardial ischemia, diminished blood supply to the heart muscle. Angina is precipitated by exertion and can be treated with the drug diltiazem, which prevents the uptake of calcium (a calcium antagonist). The use of a sustained-release formula of diltiazem for the treatment of stable angina pectoris was evaluated in 65 patients during exercise. Patients were given either 120 or 180 mg of sustained-release diltiazem twice a day. For three weeks, exercise tests were performed at the end of each week, twelve hours after the last dose. Angina was reduced and exercise time prolonged in both dosage regimens. There were no differences between the dosages. Mild adverse drug effects included swelling and flushing. One patient experienced severe low blood pressure. It was concluded that sustained released diltiazem is safe and effective treatment for stable angina pectoris. (Consumer Summary produced by Reliance Medical Information, Inc.)

The excretion of protein in the urine (proteinuria) is generally thought to be an indicator of deteriorating kidney function. While drugs which lower high blood pressure (hypertension) may all contribute to the preservation of kidney function, experiments in diabetic rats with hypertension have shown that the drugs which function by inhibiting angiotensin-converting enzyme are more effective in reducing proteinuria than other antihypertensive drugs. Drugs which act as calcium channel antagonists vary in their influence on proteinuria. A study was conducted to measure the effects of the drug diltiazem, a calcium channel antagonist which has effects similar to the angiotensin-converting enzyme inhibitors. In eight patients with noninsulin-dependent diabetes and hypertension, diltiazem was compared with lisinopril. Both drugs significantly decreased the urinary excretion of protein without changing the creatinine clearance, indicating improved kidney function. Both diltiazem and lisinopril were effective at reducing blood pressure during the treatment period. There were no significant differences between diltiazem and lisinopril. A larger study would be required to fully evaluate the effectiveness of these medications in the management of diabetic kidney disease. However, the evidence suggests that these two drugs may be of value, and that diltiazem may serve as a good alternative for diabetic patients with allergy to lisinopril or other reasons why they should not take it. (Consumer Summary produced by Reliance Medical Information, Inc.)

Diltiazem gel heals half of all anal fissures that are resistant to treatment with glyceryl trinitrate ointment, said Marion Jonas and associates at the University of Nottingham (England). A complete [...]

MORAN, Wyo. -- The "pill in a pocket" is an effective management strategy in selected patients with paroxysmal supraventricular tachycardia, Dr. Gordon A. Ewy said at a conference sponsored by [...]