Cases reported "Atrial Fibrillation"

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1/151. adenosine-induced atrial pro-arrhythmia in children.

    adenosine has become the preferred acute treatment for common types of supraventricular tachycardia because of its efficacy and safety. There have been a few reports of serious proarrhythmic events associated with its use, including the induction of atrial fibrillation in adult patients. Three instances of adenosine-induced atrial proarrhythmia (two atrial fibrillation and one atrial flutter) have been observed in children with manifest or concealed wolff-parkinson-white syndrome at the Hospital for Sick Children, Toronto, ontario since 1990, which indicates a previously unreported risk of atrial arrhythmia for children as well. Because adenosine may enhance antegrade bypass tract conduction, its use carries a risk of ventricular acceleration, including progression to ventricular fibrillation. Because of such rare and potentially life-threatening adverse effects, appropriate monitoring and precautions are required during the administration of the drug to children and adults.
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2/151. ST segment elevation in the right precordial leads induced with class IC antiarrhythmic drugs: insight into the mechanism of brugada syndrome.

    We evaluated two patients without previous episodes of syncope who showed characteristic ECG changes similar to brugada syndrome following administration of Class IC drugs, flecainide and pilsicainide, but not following Class IA drugs. Patient 1 had frequent episodes of paroxysmal atrial fibrillation resistant to Class IA drugs. After treatment with flecainide, the ECG showed a marked ST elevation in leads V2 and V3, and the coved-type configuration of ST segment in lead V2. A signal-averaged ECG showed late potentials that became more prominent after flecainide. Pilsicainide, a Class IC drug, induced the same ST segment elevation as flecainide, but procainamide did not. Patient 2 also had frequent episodes of paroxysmal atrial fibrillation. Pilsicainide changed atrial fibrillation to atrial flutter with 2:1 ventricular response, and the ECG showed right bundle branch block and a marked coved-type ST elevation in leads V1 and V2. After termination of atrial flutter, ST segment elevation in leads V1 and V2 continued. In this patient, procainamide and quinidine did not induce this type of ECG change. In conclusion, strong Na channel blocking drugs induce ST segment elevation similar to brugada syndrome even in patients without any history of syncope or ventricular fibrillation.
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3/151. Left ventricular ischemia due to coronary stenosis as an unexpected treatable cause of paroxysmal atrial fibrillation.

    We present a patient with exercise-induced paroxysmal atrial fibrillation who was eventually scheduled for a Cox-maze operation due to persistence of his complaints of fatigue, impaired exercise tolerance, and predominantly exercise-related irregular palpitations despite treatment with several antiarrhythmic drugs. A preoperative exercise stress test without antiarrhythmic or negative chronotropic drugs, however, showed clear evidence of myocardial ischemia. After coronary angioplasty of a significant stenosis in the left anterior descending artery, there was no recurrence of atrial fibrillation during a follow-up of 7 months.
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4/151. hypoglycemia induced by interaction between clarithromycin and disopyramide.

    A 59-year-old man receiving hemodialysis was hospitalized due to severe hypoglycemic attack. The patient had been treated with disopyramide (50 mg/day) because of paroxysmal atrial fibrillation. hypoglycemia occurred after taking clarithromycin (CAM, 600 mg/day), a macrolide antibiotic. The serum disopyramide concentration reached 8.0 micrograms/ml (23.6 microM) in the presence of CAM, while it was 1.5 micrograms/ml before the addition of CAM. A 75 g oral glucose tolerance test and daily profiles of blood glucose value showed that blood glucose levels were significantly lower in the presence of CAM and disopyramide compared to that in the absence of these drugs. The Turner index in the presence of CAM and disopyramide was significantly higher than that in the absence of these drugs, suggesting that a toxic concentration of disopyramide enhanced insulin secretion, resulting in the induction of hypoglycemic attacks, in which the inhibitory effects of CAM on the hepatic chytochrome P-450 might be involved. QT and QTc intervals were prolonged in the presence of CAM and disopyramide, but torsades de points were not observed in this patient receiving nicorandil (15 mg/day). Thus, it should be taken into account that life-threatening hypoglycemia may result from the interaction between clarithromycin and disopyramide.
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5/151. procainamide-induced postoperative pyrexia.

    procainamide is an effective antiarrhythmic that is often used to convert atrial fibrillation to normal sinus rhythm. A side effect of procainamide, rarely reported in the surgical literature, is pyrexia. The pyrexia is a manifestation of an allergic response to this medication. If unrecognized, procainamide-induced pyrexia can lead to unnecessary testing, hospitalization, and treatment. We present a case of a post-coronary artery bypass surgery patient who repeatedly displayed pyrexia when reexposed to procainamide indicating an allergic response to this drug.
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6/151. Using ibutilide to convert atrial fibrillation and flutter.

    Ibutilide fumarate injection is the first antiarrhythmic drug approved by the food and Drug Administration for acute conversion of atrial fibrillation and flutter of recent onset (up to 90 days). This drug will find its greatest use in critical care units and emergency departments. critical care nurses monitor the patients, recognize and assist in treating adverse events, and evaluate patient outcomes. Advanced practice nurses will find this information useful for teaching patients, colleagues, and new critical care nurses.
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7/151. Potentiation of oral anticoagulation and hemarthrosis associated with nabumetone.

    Concomitant therapy with warfarin and nonsteroidal antiinflammatory drugs (NSAIDs) is of concern due to the potential for increased bleeding. Nonsteroidal antiinflammatory drugs may alter patient response to warfarin by pharmacodynamic or pharmacokinetic interactions. A man receiving long-term, stable warfarin therapy experienced a significant increase in international normalized ratio 1 week after nabumetone was added to his regimen. Despite prompt reduction of the warfarin dosage, he experienced hemarthrosis of his right knee. Previous reports suggested lack of interaction between nabumetone and warfarin. Caution and close monitoring are advisable when the two agents are administered concomitantly.
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8/151. epistaxis associated with elevation of INR in a patient switched to generic warfarin.

    A 61-year-old man with atrial fibrillation receiving Coumadin brand warfarin was switched to Barr brand warfarin without his knowledge as a result of a retail pharmacy dispensing error. The patient took the same dosage for 6-7 days and experienced severe epistaxis that required two visits to the emergency room. Previously, his coagulation values were within therapeutic range, but when tested at the emergency room the international normalized ratio was elevated. The patient denied changes in therapy compliance, diet, alcohol ingestion, or use of other drugs. His only other drug, taken periodically, was sildenafil for erectile dysfunction. Clinicians should be aware of differences between branded and generic compounds.
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9/151. Development of rapid atrial fibrillation with a wide QRS complex after neostigmine in a patient with intermittent wolff-parkinson-white syndrome.

    We report the case of a 67-yr-old man with intermittent Wolff-Parkinson-White (WPW) syndrome in whom neostigmine produced life-threatening tachyarrhythmias. The patient was scheduled for microsurgery for a laryngeal tumour. When he arrived in the operating room, the electrocardiogram showed normal sinus rhythm with a rate of 82 beat min-1 and a narrow QRS complex which remained normal throughout the operative period. On emergence from anaesthesia, the sinus rhythm (87 beat min-1) changed to atrial fibrillation with a rate of 80-120 beat min-1 and a normal QRS complex. We did not treat the atrial fibrillation because the patient was haemodynamically stable. neostigmine 1 mg without atropine was then administered to antagonize residual neuromuscular block produced by vecuronium. Two minutes later, the narrow QRS complexes changed to a wide QRS complex tachycardia with a rate of 110-180 beat min-1, which was diagnosed as rapid atrial fibrillation. As the patient was hypotensive, two synchronized DC cardioversions of 100 J and 200 J were given, which restored sinus rhythm. No electrophysiological studies of anticholinesterase drugs have been performed in patients with WPW syndrome. We discuss the use of these drugs in this condition.
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10/151. Exit block of focal repetitive activity in the superior vena cava masquerading as a high right atrial tachycardia.

    An unusual case of atrial tachycardia (AT) originating from the superior vena cava (SVC) is reported. A 34-year-old man without structural heart disease underwent catheter ablation for drug-resistant AT. During the tachycardia, low-amplitude spiky electrograms with a cycle length of 120 to 175 msec were recorded in the SVC and exhibited 2:1 exit block to the atria, masquerading as the atrial activation observed with high right AT. These spiky electrograms also were observed during sinus rhythm, but they appeared immediately after the local atrial electrograms. The spikes were traced to a point 3 cm above the junction of the right atrium. Radiofrequency ablation at the site of the earliest appearance of the spike in the SVC successfully eliminated the tachycardia. During the following 15 months, no clinically significant atrial arrhythmias, including atrial fibrillation, occurred. This report indicates that careful mapping, including inside the SVC, will be a requisite in patients with high right atrial tachyarrhythmias.
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