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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Verapamil, a calcium antagonist, has been used extensively for treatment of cardiac arrhythmias. Concern persists, however, that it may seriously depress myocardial function in cardiac patients. To investigate this possibility, 20 patients with coronary artery disease (CAD) but no heart failure were given intravenous verapamil (0.1 mg/kg bolus, followed by 0.005 mg/kg/min infusion), and studied hemodynamically and angiographically. Verapamil markedly lowered mean aortic pressure (94 +/- 17 to 82 +/- 13 mm Hg, p less than 0.0005) and systemic vascular resistance (1413 +/- 429 to 1069 +/- 235 dyn-sec-cm5, p less than 0.0005). Simultaneously, all indices of left ventricular (LV) performance greatly improved: cardiac index rose from 2.8 +/- 0.6 to 3.1 +/- 0.7 1/min/m2 (p less than 0.0005), mean velocity of circumferential fiber shortening increased from 0.85 +/- 0.39 to 0.97 +/- 0.46 circ/sec (p less than 0.01), and ejection fraction improved from 55 +/- 16 to 61 +/- 18% (p less than 0.01). No significant changes were noted in the heart rate before and after verapamil administration, and verapamil did not worsen the extent of LV asynergy in the majority of patients. In patients with CAD, the intrinsic negative inotropic effect of verapamil is of negligible importance because its potent vasodilatory properties more than compensate for any intrinsic decrease in LV contractility, and thereby improve the overall cardiac function.
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PMID:Effects of verapamil on myocardial performance in coronary disease. 36 90

Experimental studies have demonstrated that the 3 calcium antagonists nifedipine, diltiazem, and verapamil have a comparable effect in the prevention of myocardial damage during ischaemia. Secondary prevention trials after acute myocardial infarction, which aimed at improving survival and preventing reinfarction, nevertheless demonstrated pronounced differences between the 3 drugs. Nifedipine had no effect on reinfarction or death. Diltiazem had no overall effect but prevented first reinfarction or cardiac death (cardiac events) in patients without heart failure, and increased cardiac events in patients with heart failure before randomisation. Verapamil prevented first reinfarction or death (major events); the most pronounced effect was found in patients without heart failure before randomisation. Verapamil did not have detrimental effects in patients treated for heart failure before randomisation. Differences between trials and between drugs explaining the different clinical findings are evaluated.
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PMID:Secondary prevention with calcium antagonists after acute myocardial infarction. 128 82

Recent multicentre studies evaluating the therapeutic value of calcium antagonists in reducing the incidence of cardiovascular complications after myocardial infarction (secondary prevention) and in retarding the development of atherosclerosis in coronary artery disease (tertiary protection) are reviewed. The prognosis of patients after acute myocardial infarction can be improved not only by interventional measures such as aortocoronary bypass surgery or percutaneous transluminal catheter angioplasty, but also by various drugs. Numerous studies have shown that beta-blockers and platelet aggregation inhibitors can reduce mortality and reinfarction rates. Calcium antagonists in secondary prevention trials after acute myocardial infarction, however, have produced variable results. Whereas the Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) [Israeli SPRINT Study Group 1988] with nifedipine showed no beneficial effect of the drug, studies with verapamil in the Danish Verapamil Infarction Trial II (DAVIT II) [Danish Study Group on Verapamil in Myocardial Infarction 1990] and diltiazem in the Multicentre Diltiazem Postinfarction Trial (MDPIT) [Multicenter Diltiazem Postinfarction Trial Research Group 1988] as secondary prevention have demonstrated improvements in survival and cardiovascular complications, but these improvements were restricted to patients without heart failure. In view of the ability of calcium antagonists to reduce atheroma progression in coronary artery disease in animal models, the antiatherosclerotic effects of these agents in clinical studies have generally been disappointing. In the International Nifedipine Trial on Antiatherosclerotic Therapy (INTACT) [Lichtlen et al. 1990], however, nifedipine treatment was associated with a 28% reduction in new lesion development, but did not affect the development of severe lesions. Similar results have been obtained with nicardipine.
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PMID:Secondary and tertiary prevention with calcium antagonists in coronary artery disease. 137 87

Between 1969 and 1991, 11 patients were followed up for permanent junctional reciprocating tachycardia. The average age at diagnosis was 2 years and 4 months (1 day to 14 years). The tachycardia was diagnosed at routine examination in 5 cases and following an episode of cardiac failure in the other 6. Digitalis was prescribed in all patients with 4 good results, 5 average and 2 poor results. One patient, who remained in mild cardiac failure with digitalis therapy, died suddenly at the age of 9 years. In more recent cases, amiodarone was used from the onset or secondarily with good results in all patients. In 2 patients, in whom amiodarone was withdrawn after 3 months and 3 years' treatment, there was a recurrence of the tachycardia. No side effects of amiodarone therapy were observed in this series. Three patients were prescribed flecainide with 1 good and 2 average results. Propranolol, used in 2 cases, was associated with 1 average and 1 poor result. Disopyramide and Verapamil were ineffective. These results suggest that amiodarone is the drug to choose in permanent junctional reciprocating tachycardia but it must be given long term. The persistence of cardiac failure, poor control of the tachycardia or secondary effects of drug therapy should lead to consideration of non-medical management of the tachycardia.
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PMID:[Permanent junctional reciprocating tachycardia in children and adolescents. Efficacy of medical treatment]. 153 Mar 93

Treatment of patients with heart failure due to major ventricular systolic dysfunction should aim not only at symptomatic but also at prognostic improvement. If correction of the underlying problem is not possible, treatment should slow down the progression of cardiac failure and eliminate triggers for sudden cardiac death due to electromechanical dissociation or arrhythmias. In every patient with chronic congestive heart failure screening for myocardial ischemia and complete revascularization is mandatory, if possible. In patients with coronary artery disease and diminished systolic function, beta-blockade may improve prognosis by reducing ischemic events and sudden cardiac death. The incidence of life-threatening arrhythmias in patients with heart failure may be reduced by eliminating facilitating factors like electrolyte disturbances, altered autonomic tone and raised intracardiac pressure rather than by antiarrhythmic medical treatment itself. One of the most important prognostic aspects in treatment is the interference with the development of the cardiomyopathy of overload, uniformly observed in chronic congestive heart failure. Modification of mechanical and neuroendocrine stimuli may postpone myocardial hypertrophy and interstitial hyperplasia as a consequence of altered gene expression. Early treatment with ACE inhibitors and in certain patients with betablockers are the most promising strategies to delay the progression of the disease. In contrast, positive inotropic drugs, including digitalis and phosphodiesterase inhibitors, do not improve prognosis. Calcium antagonists should also be used with restriction, as Verapamil and Diltiazem, but also Nifedipine may adversely affect the outcome in congestive heart failure patients.
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PMID:[Prognostic aspects in the treatment of chronic heart insufficiency]. 173

In vitro and in vivo studies have demonstrated many similarities between the three calcium antagonists verapamil, nifedipine, and diltiazem in relation to protection of the myocardium during hypoxia. Important clinical differences exist between the three drugs when they are used during or after an acute myocardial infarction with the purpose of preventing death and reinfarction. The balance between the negative inotropic and the vasodilator properties and concomitant treatment with beta blockers may explain the results of clinical trials with the three calcium antagonists. Patients not treated with beta blockers. Nifedipine has been demonstrated to be no better than placebo both during and after an acute myocardial infarction. No placebo-controlled studies exist with diltiazem. Verapamil had no effect during the acute phase of a myocardial infarction. After a myocardial infarction, verapamil improved survival and reduced the reinfarction rate, an effect primarily found in patients without heart failure in the coronary care unit. Patients also treated with beta blockers. Nifedipine prevents the development of myocardial infarcts in patients with unstable angina. Diltiazem probably prevents reinfarction in the first two weeks after non-Q-wave infarction. Secondary prevention with diltiazem after an acute myocardial infarction had no overall effect on death or cardiac events (i.e., reinfarction or cardiac death). Subgroup analysis demonstrated in diltiazem-treated patients, compared with placebo-treated patients, a significant reduction of cardiac events in patients without and a significant increase of cardiac events in patients with heart failure. At present no indications exist for nifedipine during or after a myocardial infarction; further studies are needed with diltiazem, and verapamil may be used in secondary prevention of death and reinfarction.
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PMID:Calcium antagonists and myocardial infarction. 188 90

More and more patients with coronary heart disease (CAD) are admitted to intensive care units. The drugs used to treat these patients have various effects on the myocardium which must be known in order to avoid worsening the CAD. This review examines the metabolic effects on the myocardium of the most commonly used drugs in intensive care. The physiology of myocardial oxygen supply is first recalled with regard to the coronary circulation, myocardial oxygen extraction and consumption. Digitalis glycosides do not affect the coronary circulation, but the decrease myocardial oxygen consumption in patients with heart failure, mainly by lowering heart rate. Dihydropyridine calcium blockers (nifedipine, nicardipine) increase coronary blood flow, despite a decrease in arterial blood pressure. Their effects on myocardial oxygen consumption are mediated by a sympathetic reflex. Verapamil decreases the heart rate and myocardial inotropism, and is responsible for coronary vasodilation. The result is a decrease in myocardial oxygen consumption. Diltiazem and bepridil have almost similar effects: they decrease myocardial oxygen consumption and increase blood supply to the heart. It has been recently shown that verapamil was the most depressant calcium channel blocking agent, and that it resulted in the most important decrease in myocardial metabolism. Beta-blocking agents decrease myocardial metabolism, except those with an important intrinsic sympathomimetic activity, such as pindolol. Amiodarone can be considered as an alpha and beta blocking drug: its main effect is to counteract the effects of endogenous catecholamines on myocardial metabolism. The sympathomimetic amines (noradrenaline, adrenaline, isoprenaline, dopamine, dobutamine) increase, to different extents, myocardial oxygen consumption. Vasodilators, such as the nitrates or sodium nitroprusside, decrease cardiac filling pressures, and increase myocardial blood flow, thus lowering myocardial oxygen consumption. Phosphodiesterase inhibitors (amrinone, enoximone) have both an inotropic and a vasodilating effect. They decrease cardiac afterload, and increase blood supply to the myocardium; this compensates for the increase in myocardial oxygen consumption due to the increase in myocardial contractility. Because all the drugs used in intensive care have different effects on myocardial metabolism, their reasoned use should avoid an inappropriate increase in oxygen demand.
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PMID:[Changes in myocardial metabolism induced by drugs used during intensive care]. 197 Apr 63

Normal left ventricular systolic performance with impaired left ventricular diastolic filling may be present in a substantial number of patients with congestive heart failure (CHF). To evaluate the effect of oral verapamil in this subset, 20 men (mean age 68 +/- 5 years) with CHF, intact left ventricular function (ejection fraction greater than 45%) and abnormal diastolic filling (peak filling rate less than 2.5 end-diastolic volumes per second [edv/s]) were studied in a placebo-controlled, double-blind 5-week crossover trial. All patients underwent echocardiography to rule out significant valvular disease, and thallium-201 stress scintigraphy to exclude major active ischemia. Compared to baseline values, verapamil significantly improved exercise capacity by 33% (13.9 +/- 4.3 vs 10.7 +/- 3.4 minutes at baseline) and peak filling rate by 30% (2.29 +/- 0.54 vs 1.85 +/- 0.45 edv/s at baseline) (all p less than 0.05). Placebo values were 12.3 +/- 4.0 minutes and 2.16 +/- 0.48 edv/s, respectively (difference not significant for both). Improvement from baseline in an objective clinico-radiographic heart failure score (scale 0 to 13) was significantly greater with verapamil compared to placebo (median improvement in score: 3 vs 1, p less than 0.01). Mean ejection fraction and systolic blood pressure were unchanged from baseline; diastolic blood pressure and heart rate decreased to a small degree. Verapamil may have therapeutic efficacy in patients with CHF, preserved systolic function and impaired diastolic filling.
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PMID:Usefulness of verapamil for congestive heart failure associated with abnormal left ventricular diastolic filling and normal left ventricular systolic performance. 222 Jun 22

The complementary antihypertensive effects of the beta-blocker/calcium antagonist combination has to be weighed against their additive and potentially detrimental negative inotropic, chronotropic, and dromotropic effects inherent in both classes of drugs. We reviewed the main adversity, particularly electrophysiological and hemodynamic effects, of combined treatments with beta-blockers and the calcium antagonists verapamil, diltiazem, and nifedipine. In patients with coronary artery disease, a different picture emerged between the verapamil and nifedipine combination with a beta-blocker. Verapamil was more often associated with conduction problems (up to 9%) and dyspnea or heart failure (up to 8%). These problems had rarely been reported with nifedipine but ankle edema (up to 11%), flushing (up to 11%), and headaches (up to 7%) predominated. The cardiovascular unwanted effects led to withdrawal in 5-8% for the verapamil/beta-blocker or nifedipine/beta-blocker combination. Although there was little cardiac adversity with the nifedipine/beta-blocker combination, the intravenous administration of verapamil in patients on beta-blockers is contraindicated and the oral verapamil/beta-blocker combination should not be sought in patients with impaired left ventricular function and when conduction disturbances are likely to occur. In treating hypertensive patients without overt coronary artery disease, there is no argument against the use of the nifedipine/beta-blocker combination but there is a need for definitive studies of the verapamil/beta-blocker combination.
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PMID:Review of the cardiovascular adversity of the calcium antagonist beta-blocker combination: implications for antihypertensive therapy. 241 10

A 61-year-old woman who was being treated with verapamil because of atrial fibrillation with rapid ventricular rate, went into anaphylactic shock. Verapamil is safe and effective for treating supraventricular tachyarrhythmias and serious adverse effects are uncommon. However, hypotension, cardiogenic shock, bradycardia and precipitation or aggravation of heart failure have been described. The patient presented was successfully treated with corticosteroids and antihistaminics.
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PMID:[Anaphylactic shock after i.v. verapamil]. 257 50


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