Cases reported "Syncope"

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1/62. Lamotrigine for startle-induced seizures.

    Startle-induced seizures are reflex seizures precipitated by a sudden, surprising stimulus, usually auditory. Aetiologies, electroencephalographic correlates, and brain structural abnormalities are variable. Because of the frequent tonic component at onset, falling is a major clinical problem. There is no established drug of choice, and therapy is often unsatisfactory. Adjunctive lamotrigine therapy was used in four consecutive patients with this syndrome seen in a referral epilepsy practice. All four had been refractory to virtually every other drug, but responded dramatically to lamotrigine with elimination of falls from seizures. This observation may serve as pilot data for trials of lamotrigine for startle-induced or other varieties of reflex epilepsies, as adjunctive or monotherapy.
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2/62. syncope caused by nonsteroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors.

    A 85-year-old woman with diabetes mellitus and prior myocardial infarction was transferred to the emergency room with loss of consciousness due to marked bradycardia caused by hyperkalemia. The T wave during right ventricular pacing was tall and tent-shaped while the concentration of serum potassium was high, and its amplitude during pacing was decreased after correction of the serum potassium level. Simultaneously with the correction, normal sinus rhythm was restored. The cause of hyperkalemia was considered to be several doses of loxoprofen, a nonsteroidal anti-inflammatory drug (NSAID), prescribed for her lumbago by an orthopedic specialist, in addition to the long-term intake of imidapril, an angiotensin-converting enzyme inhibitor (ACEI), prescribed for her hypertension by a cardiologist. This case warns physicians that the combination of NSAID and ACEI can produce serious side effects in aged patients who frequently suffer from hypertension, diabetes mellitus, ischemic heart disease, and degenerative joint disease.
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3/62. Transient nature of interference effects from heterophile antibodies: examples of interference with cardiac marker measurements.

    Two-site immunoassay methods have become the standard technique for measurement of a wide variety of drugs, hormones, and cell proteins. One limitation of these methods is their susceptibility to interference from heterophilic antibodies present in the sera of some patients. Human anti-murine antibodies represent a common heterophile antibody that can bind to mouse immunoglobulin and as well as to immunoglobulin from other species. While the mechanism of human anti-murine antibody interference has been well characterized, the time course over which this interference occurs and the susceptibility of different immunoassay procedures to human anti-murine antibody interference from patients with human anti-murine antibody have not been as well described. We report on the time course of interference in assays for cardiac markers for two patients with human anti-murine antibodies. We measured creatine kinase MB isoenzyme (CKMB) and troponins I and T using three different vendors' immunoassay procedures. Our results demonstrate that assay interference due to human anti-murine antibody interference is a transient phenomenon. In one of our patients, human anti-murine antibody interference appeared suddenly, peaked approximately 9 days following its appearance, and gradually resolved over the next 3 weeks. In addition, we found that immunoassay methods from different vendors can show highly variable interference effects when human anti-murine antibody-containing specimens are analyzed.
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4/62. syncope associated with concurrent amitriptyline and fluconazole therapy.

    OBJECTIVE: To report on a 12-year-old white male with prostatic rhabdomyosarcoma who experienced episodes of syncope attributed to concurrent amitriptyline and fluconazole therapy, confirmed by readministration. CASE REPORT: The patient began experiencing syncopal episodes periodically over a seven-month period. These repeated episodes occurred when fluconazole was administered for periodic mucositis secondary to chemotherapy. The patient had received fluconazole in the past with no difficulty and had been receiving a stable dose of amitriptyline for neuropathic pain. On discontinuation of amitriptyline, no further episodes were noted. DISCUSSION: Concurrent administration of fluconazole with amitriptyline likely resulted in the decreased metabolism of amitriptytine. Three case reports presented in the literature of adults receiving concurrent amitriptyline and fluconazole have shown an increase in serum amitriptyline concentrations with concurrent administration of fluconazole; however, none of these patients were rechallenged. literature available on amitriptyline overdose confirms that syncope and the adverse events noted in the case studies may result from elevated amitriptyline plasma concentrations. CONCLUSIONS: The consistent presentation of syncope in our patient during readministration of amitriptytine and fluconazole strongly suggests a drug-drug interaction.
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5/62. syncope in patients with atrial flutter during treatment with class Ic antiarrhythmic drugs.

    We describe 2 atrial flutter (AFL) patients with syncope during treatment with class Ic antiarrhythmic drugs. During the syncope, 1:1 atrioventricular (AV) conduction during AFL preceded a wide QRS tachycardia. The class Ic drugs, flecainide and pilsicainide, slowed the atrial rate, resulting in AFL with 1:1 AV conduction, and the width of the QRS complexes became wider during the tachycardia. syncope was abolished after successful radiofrequency catheter ablation of the AFL. These potential proarrhythmic effects of the class Ic drugs should be taken into account in AFL patients, and concomitant use of beta-blocking agents would be critical to prevent proarrhythmias.
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6/62. Polymorphic ventricular tachycardia in a woman taking cesium chloride.

    A 47-year-old patient presented with syncope and recurrent episodes of polymorphic ventricular tachycardia. She had evidence of prolonged QT interval by ECG and had been taking cesium as a dietary supplement. Correction of the hypokalemia and discontinuation of the cesium resulted in normalization of the QT interval during follow-up with no further recurrence of ventricular arrhythmias. The use of this drug is potentially hazardous as it may induce fatal ventricular arrhythmias.
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7/62. Hypoglycemic syncope induced by a combination of cibenzoline and angiotensin converting enzyme inhibitor.

    A 65-year-old Japanese woman with dilated cardiomyopathy, hypothyroidism and refractory sustained ventricular tachycardia experienced a near-death hypoglycemic syncope. The attack seemed to be induced by a high level of serum insulin, probably due to cibenzoline and by concomitant use of an angiotensin converting enzyme inhibitor (ACEI). Additionally, decreased food intake because of a severe toothache may have contributed to the deterioration of her condition. This case warns cardiologists that a combined cibenzoline and ACEI therapy can provoke serious adverse effects such as hypoglycemic syncope in the elderly. Therefore, the possibility of a hypoglycemic attack associated with these drugs should be explained to patients who are in poor condition.
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8/62. levofloxacin induced polymorphic ventricular tachycardia with normal QT interval.

    Polymorphic ventricular tachycardia (PVT) is a form of ventricular tachycardia characterized by QRS complexes that seem to change direction during the tachycardia. If associated with a prolonged QT interval, it is called torsades de pointes. In the absence of a congenital long qt syndrome, torsades is seen with certain drugs such as antiarrhythmic agents (Class IA, IC, III), psychotropic medications, antidepressants, antihistamines, and electrolyte disturbances. We report the first case of polymorphic ventricular tachycardia with normal QT interval associated with the oral use of levofloxacin in the absence of other etiologies known to cause these arrhythmias.
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9/62. catheter ablation of a monofocal premature ventricular complex triggering idiopathic ventricular fibrillation.

    A 62 year old man was admitted for evaluation of recurrent episodes of syncope. A surface ECG showed frequent repetitive premature ventricular complexes of right ventricular outflow tract origin. ventricular fibrillation was inducible by programmed electrical stimulation but otherwise cardiac evaluation was unremarkable. A diagnosis of idiopathic ventricular fibrillation was made and an implantable cardioverter-defibrillator (ICD) was installed. However, spontaneous ventricular fibrillation recurred, requiring repeated ICD discharges. The ventricular fibrillation was reproducibly triggered by a single premature ventricular complex with a specific QRS morphology. Radiofrequency catheter ablation was carried out to eradicate this complex. No ventricular fibrillation has developed after this procedure, and the patient does not require drug treatment.
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10/62. citalopram-induced bradycardia and presyncope.

    OBJECTIVE: To report a case of symptomatic bradycardia and hypotension that resulted from the therapeutic use of citalopram and to review any previous reports in the literature, from the manufacturer, and the Australian Drug Reaction Advisory Committee (ADRAC). CASE SUMMARY: A 60-year-old white woman who had been taking citalopram 20 mg/d for two weeks presented to the hospital with a heart rate of 39 beats/min, mild hypotension (systolic BP 105 mm Hg), and a normal electrocardiogram (QTc < 440 msec), following a presyncopal episode. The patient was admitted for cardiac monitoring, and citalopram was discontinued. The bradycardia and hypotension resolved in the 48-hour period following cessation of citalopram. No other medical or pharmacologic cause was found for the adverse drug reaction. DISCUSSION: bradycardia has been reported rarely with citalopram in therapeutic doses, but this is the first detailed case with a dose of only 20 mg. The manufacturer reports bradycardia as an infrequent adverse effect (0.1-1%) of citalopram. There have been no reports to ADRAC or to the manufacturer in postmarketing surveillance. There is a case report of asymptomatic bradycardia in a patient whose dose was increased to 40 mg. In the case reported here, there was no QTc prolongation consistent with previous reports. The sinus bradycardia reported more often with therapeutic doses would appear to be distinct to QT abnormalities seen with citalopram overdose. CONCLUSIONS: citalopram should be used with care in the elderly and in persons with a history of heart disease. heart rate and blood pressure should be monitored in the first week of therapy and when doses are modified.
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