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Biomedical subjects

P Podrid

Publications and source records attributed to P Podrid.

7 recordsLinked to original sources
PubMed1990

Efficacy and safety of moricizine in patients with congestive heart failure: a summary of the experience in the United States.

Patients with ventricular premature beats (VPBs) and congestive heart failure (CHF) have an increased risk of sudden death, yet suppression of arrhythmia in this population is frequently complicated by proarrhythmia and by the negative inotropic effects of antiarrhythmic drugs. The purpose of this study was to evaluate the safety and efficacy of moricizine in patients with clinical CHF. The New Drug Application data base submitted to the Food and Drug Administration was analyzed. A total of 908 patients were treated with moricizine for ventricular arrhythmias; CHF developed in 49 of them (5.4%). Of the 908 patients, 374 had a history of CHF, 326 of whom tolerated moricizine for a mean of 97 +/- 217 days. New-onset CHF occurred only once (1/546 = 0.2%). Recurrence or exacerbation of clinical CHF during treatment with moricizine occurred in 48 of 374 patients (12.8%), 28 of whom continued to take moricizine with alteration in CHF therapy. The mean left ventricular ejection fraction (LVEF) of those patients in whom CHF developed was 26%. It is important to note that patients with a history of CHF were as likely to have suppression of VPBs (defined as greater than or equal to 75% reduction) as those without a history of CHF. In fact, suppression of arrhythmia was achieved as often in patients with LVEF less than 30% as in those with more preserved LVEF. Of the 374 patients with a history of CHF, 15 (4%) had a proarrhythmic event within 14 days of therapy. The incidence of sudden cardiac death in this group was 0.8%. These proarrhythmia rates compare favorably with those of other antiarrhythmic drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1984

Effects of oral mexiletine on left and right ventricular function.

Malignant ventricular arrhythmias often occur in patients with left ventricular (LV) dysfunction. Antiarrhythmic drugs may further impair LV function in these patients. Mexiletine, a lidocaine congener, is an effective antiarrhythmic drug, but when administered orally, its effect on LV and right ventricular (RV) function is unknown. To determine the hemodynamic effects of mexiletine, LV and RV ejection fraction (EF) were measured by radionuclide ventriculography in 10 patients with LV dysfunction (LVEF less than 50%). Symptom-limited exercise tests were also performed. Patients were studied before and during therapy with oral mexiletine. There was no significant change in LVEF (28% vs 27%) or RVEF (46% vs 41%). Also, heart rate at rest, exercise duration and peak heart rate during exercise were unchanged. Thus, in patients with LV dysfunction, oral mexiletine does not significantly affect LV or RV function.

Adult↗
PubMed1984

Effects of acetyl-strophanthidin on left ventricular function and ventricular arrhythmias.

Digitalis drugs can suppress ventricular arrhythmias. It is uncertain whether this effect results from improved left ventricular (LV) function. We utilized radionuclide scanning techniques to evaluate changes in LV ejection fraction (EF) after an infusion of acetyl-strophanthidin in 43 patients with frequent ventricular premature beats (VPBs) (44 to 2400/hr). Acetyl-strophanthidin suppressed ventricular arrhythmia in 17 patients, but LVEF increased in only six of these patients (57% to 67%), while it was unaltered in 11 patients (28% to 30%). In 26 patients ventricular arrhythmia was not suppressed. Fifteen of these patients had an increase in LVEF (60% vs 71%), while this was unchanged in 11 patients (27% vs 29%). Thus no correlation was observed between the positive inotropic and antiarrhythmic action of acetyl-strophanthidin on ventricular arrhythmia and LVEF. We conclude that the suppression of VPBs by acetyl-strophanthidin is independent of the drug's effects on LV function. Evidence is reviewed suggesting that the antiarrhythmic effect of acetyl-strophanthidin on ventricular ectopic activity is due to its vagotonic action.

Adult↗
PubMed1984

Lorcainide in patients with refractory ventricular tachyarrhythmia.

Lorcainide, a new antiarrhythmic agent with local anesthetic or membrane-stabilizing properties similar to those of quinidine, was tested in 76 patients with diverse types of heart disease and recurrent ventricular tachycardia or ventricular fibrillation. Lorcainide was administered for 72 to 96 hours in a dose ranging from 200 to 400 mg daily. Evaluation of drug efficacy involved ambulatory monitoring and exercise stress testing in 60 patients who had high grade ventricular arrhythmia. Invasive electrophysiologic testing was carried out in the remaining 16 patients who exhibited infrequent ventricular ectopic activity during control studies. Lorcainide was effective in 21 (38%) of 56 patients evaluated for suppression of ventricular ectopic activity and in 6 (40%) of 15 who had invasive testing. In five patients, the drug was discontinued because of toxic reactions. Thus, 27 (38%) of the 71 patients who completed the drug study responded to lorcainide. Side effects, reported by 42 patients (55.3%), consisted primarily of insomnia and gastrointestinal symptoms; 7 experienced aggravation of arrhythmia. Fifteen patients were discharged while receiving lorcainide therapy, but in four the treatment was discontinued after 2 months because of side effects. Three patients died, one suddenly. It is concluded that lorcainide is of value in a small subset of patients with life-threatening ventricular arrhythmias who have proven refractory to conventional drugs. Its usefulness is limited by the high frequency of insomnia.

Adolescent↗
PubMed1982

Aggravation and provocation of ventricular arrhythmias by antiarrhythmic drugs.

Antiarrhythmic drugs may aggravate or even induce ventricular arrhythmias. This type of adverse reaction is becoming more prevalent as the use of antiarrhythmic agents becomes more widespread. In a retrospective analysis of antiarrhythmic drug action, a worsening of arrhythmia was observed in 80 of 722 (11.1%) antiarrhythmic drug tests in 53 of 155 patients being treated for ventricular tachyarrhythmias. Aggravation of arrhythmias was defined by occurrence of a fourfold increase in the frequency of ventricular premature complexes, a 10-fold increase in repetitive forms, or the first emergence of sustained ventricular tachycardia coincident with time course of action of the particular drug under study. Such aggravation was noted with each of nine drugs tested: quinidine, procainamide, disopyramide, propranolol, metoprolol, aprindine, mexiletine, tocainide and pindolol. The frequency of this complication for a specific drug ranged from 5.9-15.8%. Blood drug concentrations were consistently in the therapeutic range. A study of the variability of ventricular arrhythmia during 48-hour Holter monitoring and exercise stress testing in no instance showed arrhythmia enhancement commensurate with that defining aggravation. Our data suggest that this potentially serious complication is not readily predictable and requires a systematic approach to antiarrhythmic drug testing before a patient is prescribed a long-range maintenance program.

Adolescent↗
PubMed1977

Hyperthyroidism after propranolol withdrawal.

Classic features of thyrotoxicosis developed in three patients with no prior history of thyroid disease shortly after the discontinuation of therapy with or decrease in doseage of propranolol hydrochloride. Graves' disease probably developed fortuitously after propranolol therapy was instituted, but the beta-adrenergic blockade masked the clinical features of hyperthyroidism. On discontinuation of propranolol therapy or decrease in propranolol dosage, previously latent thyrotoxicosis became manifest. If hyperthyroidism masked by beta-blockade is not recognized before withdrawal of propranolol therapy in patients with ischemic heart disease, the sudden appearance of thyrotoxicosis may lead to symptoms of increased myocardial ischemia.

Adult↗