Biomedical subjects

R Jarandilla

Publications and source records attributed to R Jarandilla.

7 recordsLinked to original sources

PubMed1992

Prolonged asystole during head-up tilt table testing after beta blockade.

Neurally mediated vasodepressor syncope is a common clinical problem. The diagnosis is generally associated with a benign prognosis, however, a less common "malignant" form has been identified. Head-up tilt table testing is helpful in the confirmation of the diagnosis of neurally mediated vasodepressor syncope and may be useful in the selection of therapy. One form of therapy commonly used is beta blockade. In this case report we describe a patient with neurally mediated vasodepressor syncope who developed asystole during head-up tilt table testing after treatment with a beta blocker.

Adrenergic beta-Antagonists↗

PubMed1988

The efficacy, electrophysiologic and electrocardiographic effects of intravenous pirmenol, a new class I antiarrhythmic agent, in patients with ventricular tachycardia: comparison with procainamide.

UNLABELLED: The electrophysiologic and electrocardiographic effects of intravenous pirmenol were compared with intravenous procainamide in 17 patients with symptomatic ventricular tachycardia. Pirmenol was found to prolong the PR interval, the QRS duration, the QTc interval, the HV interval, the atrial effective refractory period, and the ventricular effective refractory period. The sinus cycle length decreased following pirmenol administration. The sinus node recovery time, the PA interval, the AH interval, the Wenckebach cycle length, and the AV nodal ERP were unchanged. In patients whose ventricular tachycardias remained inducible on pirmenol, the cycle length was significantly prolonged compared to baseline. These changes were similar to those seen following the administration of procainamide. All 17 patients had sustained ventricular tachycardia inducible during programmed ventricular stimulation in the baseline state. In four patients the ventricular tachycardia was suppressed with both primenol and procainamide. In the remaining 13 patients ventricular tachycardia remained inducible on procainamide. Of these 13 patients, an additional two patients had their ventricular tachycardias rendered noninducible on pirmenol. IN CONCLUSION: (1) the electrophysiologic and electrocardiographic effects of pirmenol are similar to those of procainamide; (2) although ventricular tachycardia inducibility following procainamide was similar to that of pirmenol, an occasional patient with ventricular tachycardia inducible on procainamide had ventricular tachycardias suppressed on pirmenol.

Administration, Oral↗

PubMed1988

Long-term efficacy, safety and survival of patients with potentially lethal ventricular arrhythmias treated with low-dose amiodarone.

The effect of low-dose amiodarone was prospectively evaluated in 110 patients with potentially lethal ventricular arrhythmias and structural heart disease. The patient population had frequent and high-grade ventricular premature complexes (VPCs) (greater than or equal to 39/h) (multifocal, couplets, nonsustained ventricular tachycardia) refractory to conventional antiarrhythmic drugs. All patients had structural heart disease (coronary artery disease in 61%) and also a decreased left ventricular ejection fraction (LVEF) (43 +/- 16%). Patients were treated with low-dose amiodarone (maintenance dose of 275 +/- 102 mg/day.) During follow-up over a period of 15 +/- 11.5 months, 24 patients died of cardiac cause and, of these, 13 died of sudden death. Ventricular arrhythmia suppression at 1, 2, 3, and 4 years was 69%, 80%, 78%, 92% for VPCs, respectively; 96%, 90%, 92%, and 98% for couplets, respectively, and 57%, 57%, 97%, and 91% for nonsustained VTs (NVTs), respectively. Intolerable, reversible side effects requiring withdrawal were encountered in 24 patients (22%) (neurologic 10%, gastrointestinal 6.5%, skin 3.7%, proarrhythmic 0.9%, and cardiac 0.9%). Except for keratopathy (less than or equal to grade II) seen in all patients, the tolerable side effects were transient with dose adjustment. The study population was divided into two groups according to LVEF: Group A (LVEF greater than or equal to 40%, mean 54.4 +/- 9.7) and Group B (LVEF less than 40% mean, 27.7 +/- 7.2). The patients were further classified into responders (suppression of at least 70% of VPCs, 90% of couplets, and 100% of NVTs) and nonresponders. The difference in survival between responders and nonresponders in groups A and B was not statistically significant. Cumulative survival at 1, 2, 3, and 4 years was 90%, 85%, 85%, and 85%, respectively. In conclusion, low-dose amiodarone treatment: 1) Is effective in controlling VPCs and its complex forms and maintains long-term arrhythmia suppression. 2) The side effect profile compares favorably with conventional antiarrhythmics; severe side effects associated with high dosages (pulmonary, hepatic, neurologic, etc.) were rare or absent. 3) Amiodarone improves survival of patients with potentially lethal ventricular arrhythmias.

Aged↗

PubMed1987

Amiodarone in the management of refractory atrial fibrillation.

Thirty-eight patients were studied to evaluate amiodarone hydrochloride in the treatment of refractory atrial fibrillation. Among them were 25 with sustained atrial fibrillation and 13 with paroxysmal atrial fibrillation. All patients were symptomatic and refractory to therapeutic doses of at least two conventional drug trials, and patients with atrial fibrillation had relapsed from electroversion. Amiodarone hydrochloride was administered in doses of 5 mg/kg intravenously, then 600 to 800 mg/d for seven to ten days, followed by 200 to 400 mg/d. Holter recordings were obtained every one to three months. The effect of amiodarone on the ventricular rate during sustained atrial fibrillation was evaluated in 18 patients and decreased from 99/min (range, 72/min to 143/min) at baseline to 75/min (range, 60/min to 102/min) at follow-up before conversion. Conversion to normal sinus rhythm occurred in 19 patients (76%), including 11 with and eight without direct-current cardioversion. During long-term treatment, sinus rhythm was sustained on an average of 16 months (range, three to 27 months) in 20 patients (53%). This included 11 of 25 patients with sustained atrial fibrillation and nine of 13 patients with paroxysmal atrial fibrillation, with only four of these patients relapsing. Four patients (11%) developed intolerable side effects, but no serious toxic effects were encountered, perhaps because of the relatively low doses of amiodarone hydrochloride that were used (average, 232 +/- 80 mg/d). Amiodarone is a safe and effective alternative to standard therapy in patients with refractory sustained or paroxysmal atrial fibrillation.

Adult↗

PubMed1986

Relation of serum reverse T3 to amiodarone antiarrhythmic efficacy and toxicity.

The relation of serum reverse T3 (rT3) to amiodarone efficacy and toxicity was studied in 31 patients with frequent and complex ventricular arrhythmias. Baseline studies included 48-hour Holter recordings and rT3 levels (normal 33 ng/dl or less). Amiodarone therapy was initiated with a 5 mg/kg infusion followed by 600 to 800 mg/day for 7 to 10 days, then 200 to 400 mg/day. Holters and rT3 levels were repeated every 1 to 3 months and amiodarone was titrated to achieve at least a 70% reduction in total ventricular premature complexes, at least a 90% reduction in couplets and abolition of ventricular tachycardia. The baseline rT3 level was 18 +/- 7 ng/dl (range 10 to 30) and patients were followed 12 +/- 9 months. Arrhythmia control was achieved in 25 patients (81%), including 21 patients with elevated rT3 levels (36 to 105 ng/dl) and 4 patients with normal rT3 (15 to 33 ng/dl). Six patients were uncontrolled with rT3 (27 to 90 ng/dl) and 14 patients had minor side effects with rT3 (27 to 123 ng/dl). Three of 4 patients in whom rT3 levels exceeded 130 ng/dl died suddenly (137 to 174 ng/dl before the event). Thus, amiodarone efficacy and minor toxicity occurs at rT3 levels less than 105 ng/dl and sudden death may be associated with levels greater than 130 ng/dl.

Aged↗

PubMed1986

Intravenous lorcainide versus lidocaine in the treatment of frequent and complex ventricular arrhythmias.

Thirty patients with frequent (greater than or equal to 30/hr) and repetitive ventricular premature beats (VPBs) unassociated with acute infarction were randomized to intravenous lorcainide (LOR) or lidocaine (LID). Following at least 2 hours of baseline Holter monitoring, patients received LOR, 2 mg/kg then 200 mg/24hr, or LID, 1 mg/kg then 2 mg/min, with rebolus if needed. Nonresponders detected by bedside telemetry were crossed over. Clinical response was 6 of 25 (24%) including two of nine crossovers with LOR and 8 of 26 (31%) including 3 of 12 crossovers with LID (p = NS). By computer analysis of 24-hour Holter monitors and asymptotic regression of success rates at hourly intervals, it was projected that greater than or equal to 80% reduction in VPBs occurred in 28% of LOR and in 25% of LID (p = NS), and complete suppression of repetitive VPBs occurred in 102% of LOR and in 92% of LID (p = NS). The mean drug levels were 405 ng/ml (range 371 to 463) with LOR and 3.4 micrograms/ml (range 2.1 to 3.6) with LID. Side effects were similar, occurring in 8 of 25 LOR trials and in 11 of 26 LID trials (p = NS). Thus, LOR and LID effectively suppress repetitive VPBs and to a lesser extent VPB frequency. However, neither drug is superior and each may be an effective alternative when resistance to the other is encountered.

Aged↗

PubMed1986

Arrhythmia control and other factors related to sudden death in coronary disease patients at intermediate risk.

Thirty-three patients with coronary artery disease and frequent, complex ventricular arrhythmias (VA) were followed long-term to evaluate factors related to sudden death (SD). Patients with malignant VA (sustained ventricular tachycardia (VT), resuscitated SD, or acute myocardial infarction) were excluded. Baseline data included angiographic ejection fraction (EF), segmental wall motion, and Holter evidence of frequent (greater than 30/hr) and complex (repetitive) ventricular premature beats (VPBs). Control of VA was attempted with conventional or experimental agents and was defined as greater than or equal to 70% reduction in VPBs, greater than or equal to 90% reduction in couplets, and abolition of nonsustained VT on two consecutive Holter tapes. After 24 +/- 15 months of follow-up on the single most effective agent, 18 patients survived while 15 patients died suddenly. There was no difference between these groups with respect to age, sex, or baseline VA. Survivors had a higher EF (51% vs 34%, p less than 0.001), fewer dyskinetic segments (0.05 vs 1.0, p less than 0.01), and better VA control (83% vs 40%, p less than 0.01) than nonsurvivors. By analysis of variance, VA control was not independent of EF (F = 6.98, p less than 0.01). The 1-, 2-, and 3-year survival rates were 90%, 90%, and 82% for patients with EF greater than or equal to 40% and 22%, 11%, and 11%, for those with EF less than 40% and uncontrolled VA.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗