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Biomedical subjects

J Gallastegui

Publications and source records attributed to J Gallastegui.

12 recordsLinked to original sources
PubMed1987

Interaction of steady-state procainamide with H2-receptor antagonists cimetidine and ranitidine.

This study was designed to compare the effects of equivalent therapeutic doses of two H2 antagonists, cimetidine and ranitidine, on steady-state procainamide pharmacokinetics. Six healthy men were given 500 mg sustained-release procainamide every 6 h, for a total of 13 doses, on three occasions. Subjects were randomly assigned to three treatments by a Latin-square design: cimetidine 1,200 mg/day, ranitidine 300 mg/day, and no H2-receptor antagonist (control) for 4 days. Cimetidine significantly increased the procainamide area under the serum concentration-time curve by 43%, decreased renal clearance by 36%, and decreased the ratio of systemic clearance of procainamide to bioavailability by 28%. Ranitidine did not significantly alter procainamide steady-state pharmacokinetics.

Acecainide↗
PubMed1987

Flecainide-induced sustained ventricular tachycardia successfully treated with lidocaine.

A 69-year-old man had new sustained ventricular tachycardia caused by flecainide which promptly responded to intravenous lidocaine therapy. Discontinuation of the lidocaine infusion resulted in the reappearance of ventricular tachycardia which again immediately terminated after lidocaine was given. In this case, lidocaine effectively reversed the proarrhythmic effects of flecainide.

Aged↗
PubMed1986

Long-term therapy with disopyramide phosphate: side effects and effectiveness.

In this study, the safety and efficacy of long-term therapy with disopyramide phosphate were evaluated in 40 patients with documented, recurrent, symptomatic tachyarrhythmias. Twenty-one (53%) of the patients had organic heart disease, and nine of these patients had compensated congestive heart failure. The tachyarrhythmias which were treated were paroxysmal supraventricular tachycardia (21 patients), paroxysmal atrial fibrillation (six patients), and paroxysmal ventricular tachycardia (13 patients). In each patient there was evidence, from continuous ECG monitoring or electrophysiologic testing, that disopyramide would be effective therapy, and each patient was able to tolerate disopyramide (no side effects or tolerable side effects) during an initial trial period of 1 to 2 weeks. Dosages of disopyramide were 400 to 1600 mg/day (994 +/- 320 mm/day). During long-term therapy, side effects were reported by 28 (70%) of the patients. The side effects were usually anticholinergic, and were usually a continuation of side effects noted during the initial trial period. None of the patients had idiosyncratic reactions to disopyramide. Most of the patients found side effects to be tolerable; however, in seven patients it was necessary to discontinue disopyramide after 1 to 8 (6 +/- 3) months. Actuarial incidence of intolerable side effects was 21 +/- 7% at 12 months. Nine (22%) of the 40 patients had symptomatic recurrences of tachyarrhythmia after 3 to 32 (15 +/- 9) months of therapy. Actuarial incidence of drug ineffectiveness was 32 +/- 10% at 24 months. Disopyramide was both effective and tolerated in 24 (60%) of the patients, who were followed for 2 to 64 (23 +/- 16) months.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Paroxysmal fascicular tachycardia and ventricular tachycardia due to mechanical stimulation by a mitral valve prosthesis.

Electrophysiologic studies were performed in a woman who had two varieties of paroxysmal wide QRS tachycardia after mitral valve replacement with a Starr-Edwards prosthesis. One tachycardia originated in the left anterior fascicle; QRS complexes were 100 ms wide and resembled right bundle branch block with left posterior fascicular block, and a His bundle potential preceded each QRS by an interval of 20 ms (compared with 50 ms during sinus rhythm). The other tachycardia originated in the left ventricle. Clinical and echocardiographic observations suggested that the tachycardias were caused by mechanical stimulation of the interventricular septum by the mitral prosthesis.

Adult↗
PubMed1984

Pulmonary toxicity of amiodarone.

Mild pleuroparenchymal fibrosis associated with amiodarone pulmonary toxicity is reported in a 63-year-old white man; partial radiographic resolution and complete symptomatic resolution with decreasing the daily dosage to 200 mg permitted continued anti arrhythmic therapy.

Amiodarone↗
PubMed1983

Concordance and discordance of drug responses in atrioventricular reentrant tachycardia.

Whether the results of some drug studies could be used to predict the results of other drug studies was examined during serial electrophysiologic drug testing in patients with sustained atrioventricular reentrant tachycardia. The drugs studied were intravenous propranolol, 0.1 mg/kg; intravenous ouabain, 0.01 mg/kg; the combination of propranolol plus ouabain; intravenous procainamide, 0.75 to 1.5 g; oral quinidine, 1.2 to 2.4 g/day; and oral disopyramide, 0.8 to 1.6 g/day. Response was inability to induce sustained tachycardia after administration of a drug. Responses due to increased anterograde limb refractoriness. Six of 10 patients with response to propranolol plus ouabain versus 0 of 9 patients without response to this combination had response to propranolol alone (p less than 0.01). Seven of 14 patients with response to the combination versus 0 of 9 patients without response to the combination had response to ouabain alone (p less than 0.05). Responses due to increased retrograde limb refractoriness. Eight of 9 patients with response to procainamide versus 2 of 17 patients without response to this drug had response to quinidine (p less than 0.01). There was not a significant relation between response to procainamide and response to disopyramide, or between response to quinidine and response to disopyramide. Anterograde limb versus retrograde limb. There was not a significant relation between response to propranolol plus ouabain and response to any class I drug. In conclusion, there are relations between drug responses during electrophysiologic studies in patients with atrioventricular reentrant tachycardia. Thus, it should be possible to simplify these studies.

Adolescent↗
PubMed1982

Determination of left ventricular ejection fraction by visual estimation during real-time two-dimensional echocardiography.

It has been shown that the measured reduction in the cross-sectional area of the left ventricle (LV), as viewed in the short axis, closely approximates its ejection fraction (EF). We assessed the reliability of using two-dimensional echocardiography (2DE) to visually estimate the EF during real-time viewing, without the need of digitizers, planimetry, or calculations. Twenty-five adult hospitalized patients with either suspected or known cardiac disease were evaluated prospectively. Each patient also had gated nuclear angiography during the same admission, and 14 had cardiac catheterization with left ventriculography. The EF was determined by 2DE using a visual estimate of the percent area reduction of the LV cavity in the short-axis view at the level of the papillary muscles. All 2 DE studies were read by two or more blinded reviewers, with a value for the EF to the nearest 2.5% determined by consensus. These values correlated closely to the values determined in all 25 patients with gated nuclear angiography (r = 0.927) and the 14 patients who had left ventriculography (r = 0.935). We believe that this method of visually estimating the LVEF will enable echocardiographers to easily use 2 DE for a reliable and instantaneous assessment of ventricular function, without the need of sophisticated analytical equipment.

Adult↗
PubMedDate not supplied

Bethanidine sulfate in paroxysmal ventricular tachycardia: toxicity and antifibrillatory actions.

Programmed ventricular stimulation was used to test oral bethanidine sulfate in 10 patients with life-threatening ventricular arrhythmias. These patients had previously documented, recurrent, sustained ventricular tachycardia (VT) and/or ventricular fibrillation (VF) complicating stable heart disease. During control electrophysiologic studies, VT could be induced in all 10 patients: 6 with nonsustained VT, 3 with sustained VT, and 1 with VT/VF. After control, bethanidine 20-30 mg/kg was administered orally and beginning 60 minutes later, programmed ventricular stimulation was repeated. After bethanidine administration, VT could be induced in nine patients; in four, the VT was essentially unchanged from that induced during control studies. In four others, worse VT was induced after bethanidine. The remaining two patients had a potentially beneficial response to the drug. Bethanidine was poorly tolerated: seven patients had symptomatic orthostatic hypotension that persisted for several days despite concurrent protriptyline therapy. Furthermore, in four patients, spontaneous VT or VT/VF occurred 3-8 hours after the last dose. Nausea, vomiting, flushing, and blood pressure elevation were also noted. Bethanidine sulfate in the dosages used usually does not prevent the induction of VT by programmed ventricular stimulation and frequently causes serious toxicity. These findings suggest that the drug would be ineffective and poorly tolerated for long-term therapy in patients with serious ventricular arrhythmias.

Administration, Oral↗