Cases reported "Atrial Fibrillation"

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1/109. 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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2/109. Atrial infarction is a unique and often unrecognized clinical entity.

    A patient with heart failure and acute atrial fibrillation received the final diagnosis of atrial infarction associated with ventricular infarction based on clinical findings of ischemia in association with atrial fibrillation and heart failure (mechanisms probably involved: contractile dysfunction and loss of atrial contribution). Although a transesophageal echocardiography, which could refine the diagnosis of anatomic abnormalities, was not performed, all evidence led to the diagnosis of atrial involvement. Electrocardiographic findings were consistent with Liu's major criterion 3. Therapy with digitalis, quinidine and angiotensin-converting enzyme inhibitors was chosen, as the patient had acute pulmonary edema. The use of beta-blockers and verapamil was res-tricted. No other complications, such as thrombo-embolism or atrial rupture, were noted.
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3/109. Familial skeletal myopathy with atrioventricular block.

    OBJECTIVE: We studied familial cases of skeletal myopathy with atrial fibrillation (Af) and atrioventricular (AV) block to compare the clinical features to other myopathies associated with cardiac abnormalities. methods: Neurologic, cardiologic, electrophysiologic, muscle pathology, and genetic studies were performed on the patients showing muscle weakness. patients: Four patients (a 63-year-old mother, 30 and 32-year-old sisters, and their maternal grandmother) and three healthy family members from three generations were studied. The mode of inheritance was suspected as autosomal dominant. RESULTS: Two sisters with congenital myopathy without rigid spine developed Af and AV block at the age of 28 and 18, respectively. The mother showed AV block, and underwent pacemaker implantation at the age of 63. The maternal grandmother had dilated cardiomyopathy, Af and severe lordosis. She died of stroke attacks and congestive heart failure at the age of 78. Muscle biopsy obtained from the mother and sisters showed myopathic changes without characteristic abnormalities. No mitochondrial dna mutations were found. Other inherited myopathies with cardiac complications were not suspected in this family. CONCLUSION: This Japanese family appears to belong to a new genetically heterogeneous group of autosomal dominant skeletal myopathy with severe AV block and Af.
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4/109. 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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5/109. 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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6/109. Gemcitabine-induced atrial fibrillation: a hitherto unreported manifestation of drug toxicity.

    BACKGROUND: Gemcitabine is an antimetabolic drug for solid tumors. Although its pharmacokinetics as well as its side-effects are well known, paroxysmal atrial fibrillation associated to the administration of this drug has not yet been described. patients AND methods: We describe the case of a 78-year-old man with pancreatic adenocarcinoma who presented repeated paroxysmal atrial fibrillation episodes 18-24 hours after every gemcitabine infusion which resolved with antiarrhythmic drugs. This clinical history was positive for a remote brief episode of atrial fibrillation, which resolved spontaneously, and the patient had no predisposing factors for supraventricular arrhythmias (systemic hypertension, diabetes or coronary artery disease). RESULTS: Cardiac work-up revealed only a mild mitral-valve prolapse and complete right bundle branch block. During the arrhythmia episodes no other precipitating factors were reported. The close temporal relationship of the arrhythmia to drug administration and the recurrence of arrhythmia upon rechallenge allowed to hypothesize an intrinsic pro-arrhythmic effect of gemcitabine or its metabolite 2',2'-difluorodeoxyuridine. CONCLUSIONS: The occurrence of atrial fibrillation during the administration of gemcitabine may be considered as a cardiac arrhythmia drug-related toxicity. This side-effect of gemcitabine infusion is a previously unreported sign of drug toxicity; therefore, a high level of awareness to this problem is warranted when this drug is administered.
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7/109. Premature depolarization concealed in two pulmonary veins.

    A case is presented in which a premature depolarization emanated from a partially activated left inferior pulmonary vein, activated the entire left superior pulmonary vein, but did not activate the atria ("concealed"). The site of conduction block between each vein and the left atrium was the anatomic atriovenous junction. At times, the same depolarization would activate the atria and initiate atrial fibrillation. The shortest depolarization coupling interval that activated the atria was significantly longer than the atrial fibrillation cycle length recorded in either vein. Observations in this case support two concepts: (1) the existence of myocardial "tracts," extending into and between pulmonary veins; and (2) a "mismatch" between pulmonary vein activation ingress and egress.
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8/109. A case of sinus pause due to the proarrhythmia of pilsicainide.

    A 74-year-old man received oral administration of pilsicainide, a pure sodium channel blocker with slow recovery kinetics, to convert paroxysmal atrial fibrillation to sinus rhythm and developed loss of consciousness two days later. The ECG monitoring revealed sinus pause with markedly prolonged PQ interval and QRS width. Two days after the drug was discontinued, the duration of the QRS complex was normalized. This drug is rapidly absorbed from the gastrointestinal tract, most of which is excreted from the kidney. The plasma concentration of pilsicainide, although not measured, must have been very high, since his renal function was impaired. When pilsicainide is prescribed in patients with coronary artery disease or renal dysfunction, close attention must be paid to avoid life-threatening arrhythmias due to high plasma concentrations of the drug. This is an interesting case because the proarrhthmia of the drug was not tachyarrhythmia, such as ventricular tachycardia or torsades de pointes, but sinus pause.
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9/109. Donor-to-recipient decremental conduction of atrial fibrillation following orthotopic heart transplantation: insights into the mechanism of atrioatrial conduction.

    We describe the unique case of a heart transplant patient with type I atrial fibrillation that arose in the donor atrium during a late acute rejection episode and conducted to the recipient atrium with second-degree type I local block. After internal cardioversion, programmed stimulation showed bidirectional decremental conduction across the suture line with nearly equal atrioatrial interval, whereas the recipient atrium showed progressively delayed intra-atrial conduction. These findings strongly suggest that the mechanism of atrioatrial conduction may be electrical propagation along viable myocardium bridging the surgical scar and that the electrophysiologic characteristics of the recipient atrium are involved in decremental conduction across the suture line.
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10/109. Apparent bradycardia-dependent right bundle branch block associated with atrial fibrillation: concealed electrotonic conduction as a possible mechanism.

    A 79-year-old woman with atrial fibrillation was reported in whom apparent bradycardia-dependent right bundle branch block was suggested. When a conducted supraventricular impulse occurred within a critical period after the preceding conducted impulse, the impulse was blocked in the right bundle branch except when it fell in the supernormal period of the right bundle branch. When the conducted impulse occurred between the critical period and another longer period, it was conducted without bundle branch block. When the impulse occurred beyond that longer period, it was usually blocked in the bundle branch again. However, when the impulse occurred beyond a still longer period, it was conducted without bundle branch block again. These findings suggest that when impulses fell in the right bundle branch shortly after the preceding conducted impulses, they were blocked in both bundle branches; however, it seemed that concealed electrotonic conduction of the blocked impulses affected conduction of the subsequent impulses.
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