Multifocal atrial tachycardia caused by risperidone.

Risperidone, an atypical antipsychotic drug, is one of the most frequently used atypical neuroleptic drugs for the treatment of symptoms of behavioral disorders seen in autism. Although various cardiovascular side effects have been reported with risperidone, to our knowledge, it has not yet been reported that it can also result in multifocal atrial tachycardia. Based on the case reported herein, our aim is to bring awareness that risperidone may cause multifocal atrial tachycardia.

Persistent wandering atrial pacemaker after epinephrine overdosing - a case report.

BACKGROUND: Long-term complications of sympathomimetic drug overdosing have not been adequately investigated in infants and young children. Despite reports discouraging their use in children, these formulations are frequently administered for "cold-like symptoms". Their frequent adverse events are different forms of arrhythmias, including multifocal atrial tachycardia. CASE PRESENTATION: A 3-year-old toddler developed multifocal atrial tachycardia following an iatrogenic overdose of epinephrine accidentally administered intravenously. His ECG showed wandering atrial pacemaker (p-waves with different origins and configurations) that persisted for at least one year. This event demonstrated the sensitivity of young children to the sympathomimetic drugs, especially overdosing. CONCLUSIONS: Health care providers and parents should be warned of toxicities associated with sympathomimetic drug overdosing. Future studies are needed to determine whether wandering atrial pacemaker is a potential long-term complication of high-dose sympathomimetics.

Recurrent atrial ectopic tachycardia following chemotherapy with ifosfamide.

In most pediatric tumors, particularly sarcomas, cyclophosphamide or ifosfamide represent essential first-line chemotherapeutic agents. Whereas cyclophosphamide is known to be associated with a well-defined cardiomyopathy, only a few cardiac complications following ifosfamide chemotherapy have been observed to date. Here we report a patient treated for Ewing sarcoma with multiple pulmonary and osseous metastases who repeatedly developed a supraventricular tachyarrhythmia following administration of ifosfamide as part of a polychemotherapy regimen.

Age-related sensitivity to nicotine for inducible atrial tachycardia and atrial fibrillation.

The influence of nicotine in modulating vulnerability to atrial tachycardia and fibrillation (AT/AF) remains ill defined. The isolated hearts of six young (2-3 mo) and six old (22-24 mo) male Fischer 344 rats were Langendorff perfused at 5 ml/min with oxygenated Tyrode solution at 37 degrees C, and the whole heart was also super-fused with warmed oxygenated Tyrode solution at 15 ml/min. Nicotine prolonged the interatrial conduction time and effective refractory period that were significantly (P < 0.05) higher in the old than in the young rats in a concentration-dependent manner. Nicotine had a biphasic effect on burst atrial pacing-induced AT in both groups, increasing it at 10-30 ng/ml while decreasing it at 50-100 ng/ml (P < 0.01). Nicotine at 10-100 ng/ml increased burst atrial pacing-induced AF in the young rats but suppressed it in the old rats (P < 0.01). Optical mapping showed the presence of multiple independent wavefronts during AF and a single periodic large wavefront during AT in both groups. Nicotine, at concentrations found in the blood of smokers (30-85 ng/ml), exerts biphasic effects on inducible AT/AF in young rats and suppresses it in the old rats by causing high degrees of interatrial conduction block.

Cardiac sensitization testing of the halon replacement candidates trifluoroiodomethane (CF3I) and 1,1,2,2,3,3,3-heptafluoro-1-iodopropane (C3F7I).

Trifluoroiodomethane (CF3I) and 1,1,2,2,3,3,3-heptafluoro-1-iodopropane (C3F7I) have been considered as replacement candidates for halon fire suppressants due to their excellent fire extinguishant capabilities and low ozone depletion potential compared to halon fire extinguishants in use currently. As part of the process to develop environmental and health effects criteria for halon substitutes, a cardiac sensitization test was conducted in beagle dogs. Cardiac sensitization to adrenaline is a phenomenon associated with the inhalation of a number of unsubstituted and halogenated hydrocarbons. Adrenaline was administered by intravenous injection before and during inhalation of the test substance. CF3I was administered to dogs at concentrations in air of 0.1, 0.2, 0.4 or 1% v/v. At each of 0.4 and 1.0% CF3I, the first dog exposed developed fatal ventricular fibrillation, and no further dogs were exposed at these concentrations. There was no cardiac sensitization at 0.1 or 0.2% CF3I. For the C3F7I experiment, dogs were exposed to concentrations in air of 0.1, 0.2 or 0.4% v/v. At each of 0.1 and 0.4% C3F7I, one dog responded with multifocal ventricular ectopic beats. Thus, CF3I and C3F7I are potent cardiac sensitizers in the adrenaline-challenged dog model.

Continuous ambulatory electrocardiography among workers exposed to methylmethacrylate.

Methylmethacrylate (MMA), a widely used monomer in the manufacture of acrylic polymers, has been reported to cause cardiac troubles in industrial workers. The effects of MMA on the heart was assessed by continuous ambulatory electrocardiographic records. The study was performed in 22 occupationally exposed workers and in 18 healthy controls. Our study did not support the hypothesis that MMA is responsible for cardiomyodystrophy. However, supraventricular and ventricular ectopic beats were significantly more frequent among exposed workers versus controls (P < 0.01). Moreover, repolarization changes such as large T waves were noted only in exposed workers (eight cases against none in the control group). Although there was no clear connection between MMA exposure and the recorded cardiac changes in the exposed group, the role of MMA cannot be totally excluded.

[Induction of arrhythmia by licorice abuse]. / Arrhythmieauslösung durch Lakritzabusus.

We report two cases of licorice-induced arrhythmias. In both cases the ingestion of large amounts of licorice caused a marked hypokalemia. The importance of licorice-induced hypokalemia for the development of arrhythmias is underestimated from the small number of published cases. We conclude that patients with a predisposition for arrhythmias should avoid licorice candies.

Cardiovascular rhythm effects of gamma recombinant DNA interferon.

Twenty patients receiving recombinant DNA gamma interferon were prospectively assessed for cardiac rhythm disturbances. All patients were evaluated with baseline electrocardiograms, pretreatment ambulatory monitoring and ejection fraction determination. Each patient was then monitored continuously during drug administration. Quantitative ventricular ectopy was not increased, nor were average heart rate, maximal heart rate, or quantitative supraventricular ectopy when comparing baseline to during therapy parameters. Complex cardiac ectopy and noteworthy cardiac events (NCE) were defined and identified in 2/20 (10%) patients pretreatment, and in 8/18 patients (44%) with normal baseline tracings during treatment (p = .02). This difference was not apparent when corrected for total days monitored pre- and post treatment (p greater than .2). These consisted predominantly of nonsustained short duration ventricular tachycardia (seven of eight patients). We conclude that life threatening cardiac events are uncommon with gamma interferon therapy.

Reevaluation of digoxin-encainide interactions using an animal model.

The effects of intravenous encainide on digoxin-induced atrial ectopic tachycardia (AET) were investigated in the rat using 3-channel simultaneous limb-lead electrocardiography. Pentobarbital-anesthetized (35 mg/kg, intraperitoneal) adult male rats were given digoxin subcutaneously, 30 mg/kg. After onset of AET, rats received either saline (0.5 ml/kg) or encainide; 0.25, 0.5, 1.0, or 2.0 mg/kg intravenously in repeated doses at 15-min intervals. At all doses, encainide converted digoxin-induced AET to ventricular arrhythmias, prolonged recovery time, and increased mortality in comparison to saline-treated animals. An additional group of anesthetized rats was not given digoxin. These animals received encainide (2.0 mg/kg, intravenously) in repeated doses at 15-min interval and developed dose-related increase in the P-R interval only. Blood samples were obtained by cardiac puncture from 12 additional anesthetized, digoxin-treated rats 5 min after the fourth intravenous dose of saline (0.5 ml/kg, n = 6) or encainide (1.0 mg/kg, n = 6). Serum was prepared and analyzed by affinity column-mediated immunoassay. Digoxin levels were the same in both groups. These results suggest that encainide may exacerbate digoxin-induced arrhythmias (proarrhythmic effect) in this species. In view of our findings of digoxin-encainide interactions in the rat, we recommend caution if these drugs are coadministered in humans.