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

Disopyramide is a new antiarrhythmic drug with a pharmacological profile of action similar to that of quinidine and procainamide. In a few controlled therapeutic trails and a large number of uncontrolled studies in patients with arrhythmias, often following a myocardial infarction, disopyramide has been relatively effective (more so in ventricular than in atrial arrhythmias) and usually well tolerated. In treating premature atrial and ventricular contractions, the best-studied area of its therapeutic use, disopyramide was superior to a placebo and of similar efficacy to but better tolerated than quinidine; the drop-out rate due to adverse effects of the disopyramide group (10%) being less than one-third that of the quinidine group (36%). In an open ward setting, disopyramide used prophylactically after myocardial infarction appeared to reduce both the incidence of reinfarction and the mortality rate, while in patients treated in coronary care units although the incidence of reinfarction was lower with disopyramide than with a placebo, the mortality rate was not significantly different. Further well-designed trials with adequate numbers of patients are needed before the routine use of disopyramide in infarct patients treated in either setting can be justified. Comparative studies are also required to determine if disopyramide has advantages over other antiarrhythmic agents in this area of use. Side-effects with disopyramide are usually a result of its anticholinergic activity, a dry mouth and difficulty in urination being the most common. Like other antiarrhythmic agents, disopyramide exerts a negative inotropic action on cardiac muscle, and development of acute heart failure has been reported. Development of worsening of heart block and hypotension have also occurred. Disopyramide is largely excreted unchanged and dosage should be reduced in patients with impaired renal function, in accordance with creatinine clearance values.
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PMID:Disopyramide: a review of its pharmacological properties and therapeutic use in treating cardiac arrhythmias. 35 May 55

The haemodynamic effects of disopyramide have been studied in 11 patients with manifest or imminent heart failure. Disopyramide, 2 mg per kg body weight, was given intravenously during right and left heart catheterisation. The cardiac index decreased by an average of 28% (p less than 0.01); mean maximal left and right ventricular end-diastolic pressures were increased by 5.0+/-0.9 mm Hg (p less than 0.01) and 5.0+/-0.6 mm Hg (p less than 0.05), respectively; and left ventricular systolic pressure fell slightly but significantly (p less than 0.05). No significant change in right ventricular systolic pressure was seen. Pulmonary wedge pressure rose on average by 2.7 mm Hg (p less than 0.05). No significant change in heart rate was observed in 5 patients with sinus rhythm. In 6 patients with atrial fibrillation, there was a significant (p less than 0.01) increase in heart rate; the average increase in heart rate for the entire group was 19.6 beats per minute. The maximum effect on all the parameters occurred 7-11 minutes after the injection, and it gradually subsided during the following 10 minutes. It was concluded that disopyramide had a potentially serious myocardial depressant effect.
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PMID:Haemodynamic effects of intravenous disopyramide in heart failure. 123 15

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

The efficacy of intravenous disopyramide was studied during 200 episodes of supraventricular and ventricular arrhythmias in 160 patients, mainly presenting with acute myocardial infarction or cardiac failure. Disopyramide 50 mg was administered in a few seconds and any remaining dose within 2 to 5 min. The overall success rate was 80.5%. Intravenous disopyramide was more effective in patients with ventricular arrhythmias (85%) than in those with supraventricular arrhythmias (76%). Dose dependent prolongation of the PR interval, QRS time and the QT interval occurred in 16.32 and 20% of the cases, respectively. The adverse effects were aggravation of the arrhythmias, decrease of blood pressure and anticholinergic activity.
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PMID:Efficacy of intravenous disopyramide in acute cardiac arrhythmias. 616 24

The efficacy of disopyramide in the management of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) was evaluated in 50 patients by programmed ventricular stimulation: 38 patients had coronary artery disease (16 with left ventricular aneurysm), 8 had other cardiac diseases, and 4 had no apparent heart disease. Disopyramide was administered orally for 72 hours (dosage 400 to 1,600 mg/day), resulting in a plasma level of 3.6 +/- 1.2 micrograms/ml (mean +/- standard deviation [SD]). Disopyramide prevented induction of sustained ventricular tachyarrhythmias in 17 patients (34%) and failed to prevent induction in 33 patients (66%). Plasma levels were not significantly different regardless of response to disopyramide. The VT cycle length in patients responding to disopyramide was shorter than in nonresponding patients (225 +/- 51 ms versus 281 +/- 70 ms, p = 0.005). Disopyramide increased VT cycle length in those patients in whom it was ineffective (failed to prevent induction) from 281 +/- 70 ms to 347 +/- 64 ms (p less than 0.001). Ventricular refractory periods, QRS, and QTc durations significantly increased after disopyramide administration. Of the 17 patients in whom tachyarrhythmias were noninducible on disopyramide, 11 were discharged on disopyramide and followed up for 19 +/- 9 months; 9 of them remained free of VT. Heart failure developed in 2 of these patients. One other patient in whom disopyramide was ineffective had irreversible heart failure and died. It is concluded that disopyramide (1) prevents induction of ventricular tachyarrhythmias in one third of patients studied and remains clinically effective in approximately 80%, (2) is more frequently effective in rapid tachycardias, (3) prolongs the VT cycle length when ineffective, and (4) may produce marked hemodynamic embarrassment in patients with significant left ventricular dysfunction.
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PMID:Disopyramide: evaluation of electrophysiologic effects and clinical efficacy in patients with sustained ventricular tachycardia or ventricular fibrillation. 682 35

The effects of acute myocardial infarction on the pharmacokinetics of disopyramide were studied. Disopyramide (200 mg) was given orally to nine patients with left-sided cardiac failure due to acute myocardial infarction within 24 h after the onset (phase I). In seven patients the study was repeated 7-14 days later at discharge from the hospital (phase II). Serum concentrations and the 24-h area under the serum concentration-time curve of disopyramide were significantly lower during phase I than during phase II (p less than 0.05 and p less than 0.001, respectively). The peak serum concentrations and the 24-h area under the pulmonary capillary wedge pressure (less than 0.05) in phase I. Rates of absorption and elimination of disopyramide were similar during both phases. Renal clearance of disopyramide showed concentrations and the decrease of 24-h area under the serum concentration-time curve are most probably due to decreased gastrointestinal absorption and are related to the degree of left ventricular failure. Thus, the dosage of oral disopyramide obviously needs to be increased in these patients to achieve therapeutic concentrations in the acute phase.
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PMID:The pharmacokinetics of disopyramide in patients with acute myocardial infarction. 710 76

Two patients abruptly developed congestive heart failure and elevation in serum transaminase levels when given disopyramide phosphate; enzyme abnormalities and hemodynamic status corrected upon withdrawal of the drug. Both patients had underlying ischemic cardiomyopathy. Myocardial infarction, pulmonary embolism, and viral hepatitis were ruled out in both patients. One patient had a liver biopsy documenting central hepatic necrosis with congestion, consistent with hepatic ischemia and not toxic hepatitis. In the other patient, cardiac decompensation and hepatocellular enzyme elevation were reproduced on rechallenge with the drug. Disopyramide should be used with caution in patients with heart failure.
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PMID:Acute cardiac failure and hepatic ischemia induced by disopyramide phosphate. 722 41

Five patients with severe left ventricular failure, renal insufficiency, and recurrent ventricular tachycardia had cardiovascular collapse and died eight hours to 23 days after initiation of the usual doses of disopyramide. Three patients had recent myocardial infarction (12 to 33 days), and one had severe congestive cardiomyopathy. ECG changes antedated appearance of cardiovascular collapse and consisted of lengthening of the QRS (0.10 plus or minus 0.02 to 0.22 plus or minus 0.09; P less than 0.025) and the QTc duration (0.44 plus or minus 0.04 to 0.56 plus or minus 0.09; P less than 0.05). Sinus bradycardia or varying degrees of atrioventricular block or both occurred in all patients. Terminal disopyramide blood concentration (4.9 and 8.1 micrograms/ml) were available in two patients. A syndrome of progressive lengthening of ventricular depolarization and repolarization terminating in cardiovascular collapse and death associated with disopyramide is described. In addition, a high incidence of sinus bradycardia, atrioventricular conduction disturbances, or both was also noted. Disopyramide is contraindicated in patients with severe heart failure and renal insufficiency. Progressive widening of the QRS complex or the QT interval may presage appearance of severe myocardial dysfunction.
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PMID:Cardiovascular collapse associated with disopyramide therapy. 722 32

The effects of intravenous disopyramide phosphate on myocardial function were evaluated by non-invasive indices of cardiac performance (systolic time intervals, STI) in 15 patients with atherosclerotic heart disease and different degrees of cardiac failure. Disopyramide (1.5 mg/Kg) was given intravenously over a period of 5 min. This drug induced in patients in I-II classes of NYHA a significant decrease of LVETc, while PEP, ICT, and PEP/LVET ratio rose significantly. STI were affected much more markedly in patients in III-IV classes of NYHA. Particularly affected were contractility indices (PEP, ICT, PEP/LVET), which were reduced significantly more in patients in III-IV classes as compares to patient in I-II classes. In contrast, LVETc, which correlates to stroke volume and cardiac output, was similarly worsened by the drug in the 2 groups of patients. Therefore, this study shows that disopyramide has relevant depressant effects on myocardial performance, simultaneously reducing stroke volume and contractility, and that the effect on contractility is more marked in patients with severe left ventricular impairment.
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PMID:Effects of intravenous disopyramide on myocardial function in patients with different degrees of cardiac failure. 737 60

Disopyramide as an antiarrhythmic can be prescribed to patients with atrial fibrillation and, owing to its negative inotropic effect, to patients with hypertrophic obstructive cardiomyopathy. It is known that in patients with cardiac conduction disturbances and heart failure, disopyramide can adversely affect heart rhythm and conduction and induce cardiovascular collapse. A patient with hypertrophic obstructive cardiomyopathy and paroxysms of atrial fibrillation is described who was treated with disopyramide and also, during the 5 days before admission, with metoprolol. In spite of normal cardiac conduction and function before disopyramide, this treatment was followed by hypotension, bradycardia, and cardiac conduction disturbances. Our case shows the potential for disopyramide, especially when combined with metoprolol, to induce grave adverse effects even in patients with normal cardiac conduction and ventricular function.
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PMID:Heart conduction disturbances and cardiovascular collapse after disopyramide and low-dose metoprolol in a patient with hypertrophic obstructive cardiomyopathy. 937 12


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