Cases reported "Bradycardia"

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1/95. nicorandil, a potassium channel opener, abolished torsades de pointes in a patient with complete atrioventricular block.

    TdP is a serious complication of AV block. We report a case of complete AV block with QT prolongation who had bouts of TdP resistant to lidocaine and isoproterenol. Temporary pacing could not be performed, because insertion of a pacing lead triggered TdP that deteriorated into ventricular fibrillation. nicorandil, a potassium channel opener, shortened the QT interval and abolished TdP. This may suggest that potassium channel opening drugs are clinically effective against TdP associated with bradycardia-dependent QT prolongation.
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2/95. Treatment of the bradycardia-tachycardia syndrome with permanent demand pacing.

    The bradycardia-tachycardia syndrome (paroxysmal supraventricular tachycardia alternating with sinus bradycardia and episodes of sinus node arrest) has previously presented a complicated therapeutic dilemma when excitatory and suppressive drugs have been utilized. A patient with this syndrome successfully treated with a permanent ventricular transvenous demand pacemaker is presented. Various aspects of this syndrome as well as facets of diagnosis and treatment have been reviewed and discussed. Significant underlying cardiac disease was ruled out in this patient by the usual diagnostic methods including left heart catheterization and coronary angiography. An interesting possibility of the relationship of vagal stimulation secondary to hiatus hernia as an etiologic factor in this syndrome has been discussed. The opinion is expressed that the currently preferred method of treatment is the insertion of a permanent transvenous pacemaker alone or in conjunction with antiarrhythmic drugs, preferably digitalis and propranolol.
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3/95. 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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4/95. Profound bradycardia and hypotension following spinal anaesthesia in a patient receiving an ACE inhibitor: an important 'drug' interaction?

    An 86-year-old man on whom a transurethral resection of prostate was performed under spinal anaesthesia developed profound bradycardia and hypotension with disturbance of consciousness during transfer to the recovery room. Initial treatment with atropine produced rapid improvement in cardiovascular and cerebral function. A further hypotensive episode (without bradycardia) occurred approximately 1 h later but responded rapidly to methoxamine. The patient made a full recovery during an overnight stay on the High Dependency Unit. Possible mechanisms for this event are discussed, with the proposal that the concomitant administration of captopril and the relative unavailability of angiotensin ii may have significantly contributed to the problem.
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5/95. The 12-lead electrocardiogram in anorexia nervosa: A report of 2 cases followed by a retrospective study.

    anorexia nervosa (AN) has been associated with various cardiac disorders and several electrocardiographic abnormalities, the most prominent being sudden death and prolonged QT duration and dispersion. We report 2 cases of AN with marked repolarization abnormalities, the first clearly related to electrolyte imbalance, the second without a good explanation from metabolic, electrolytic or pharmacological sources. A retrospective analysis of 47 other consecutive patients with AN showed that sinus bradycardia was the most common ECG finding, but that QT or QTc interval prolongation was not a typical feature, being present in only 1 patient. The sole variable slightly correlated with QTc duration was the serum potassium concentration. Consequently, marked repolarization changes (QT interval and/or T wave morphology) in AN should not be taken as a feature of the disease, but should call for the search of potential causes such as metabolic and electrolytic disturbances, drug effects, or a possible genetic component.
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6/95. gout, bradycardia, and hypercholesterolemia after renal transplantation.

    Approximately 17,000 solid organ transplantations are done annually in the united states. Increasingly, care of these patients will be provided by primary care physicians. In this report, we illustrate the complexity of common medical problems in a patient who had cellulitis and who had had a cadaveric renal transplantation 10 years earlier. Immunosuppressive therapy was cyclosporine (100 mg twice a day) and prednisone (10 mg once a day). The patient's hospital course was complicated by acute gout and symptomatic bradycardia. In both instances, usual treatment--full-dose indomethacin for gout and withholding verapamil for bradycardia--could have had significant interaction with the cyclosporine. At the time of discharge, a therapeutic plan for long-term management of hypercholesterolemia included possible drug interactions with cyclosporine. The potential for drug toxicity in the transplant patient necessitates careful monitoring of immunosuppressive drug levels. Ongoing communication with the transplant center is also needed.
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7/95. Asymptomatic bradycardia associated with amisulpride.

    Well-known adverse effects of amisulpride include nausea, insomnia or tiredness, gastrointestinal, extrapyramidal and endocrine symptoms. Cardiac disorders, however, appear to be an extremely rare complication of the drug. Only a few case reports on this complication have been published so far, which deal with QT prolongation, hypotension, hypertension and palpitations. bradycardia has not yet been mentioned. Here, we will report on a case of asymptomatic bradycardia that developed subsequent to therapeutic doses of amisulpride in a 25-year-old male patient with chronic paranoid-hallucinatory schizophrenia. The patient had been rehospitalized for an acute exacerbation of the psychosis. When the patient failed to respond at the beginning of hospitalization, the treatment was changed from clozapine to amisulpride. After a complete switchover to amisulpride, the patient's ECG showed sinus bradycardia and QT prolongation. When the daily dose of amisulpride was reduced from 800 mg/d to 600 mg/d, the patient's ECG quickly normalized (including blood pressure and pulse rate) within a few days. The patient did not report any cardiovascular-related complaints. Since the cardiovascular-specific diagnostics did not yield any indicative results, bradycardia may be a rare complication of amisulpride treatment.
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8/95. 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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9/95. hypotension and bradycardia in a healthy volunteer following a single 5 mg dose of olanzapine.

    Olanzapine is an atypical antipsychotic medication indicated for the treatment of schizophrenia and other manifestations of psychotic illness. Common side effects include somnolence, constipation, weight gain, and postural hypotension. The authors report a case of hypotension accompanied by bradycardia in a normal, healthy volunteer participating in an olanzapine pharmacokinetic study following a single 5 mg dose. A venous catheter allowed for serial blood sampling of olanzapine concentrations before, during, and after the adverse event. The subject experienced a rapid absorption of the drug and higher than anticipated maximum plasma concentrations. This case suggests that atypical antipsychotics, although generally better tolerated than conventional agents, may still result in untoward reactions that may be partially due to individual differences in drug absorption and metabolism.
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10/95. poisoning with calcium channel blockers--a case report and review of the literature.

    The incidence of poisoning with calcium channel blockers, accidental or intentional, has increased in recent years, associated with more frequent use. We present a clinical case of bradycardia and shock of unknown cause, which came to be revealed a poisoning by 3240 mg of slow-release diltiazem, managed with temporary transvenous pacing and dopamine in high concentration. We make a review of the cardiovascular manifestations of the three classic calcium channel blockers: verapamil, diltiazem and nifedipine; namely, hypotension, rhythm and conduction disturbances. We point out the late appearance of the beginning of manifestations with the use of slow releasing formulations. The toxicity by calcium channel blockers can lead to a wide variety of manifestations in the central nervous system, gastrointestinal system, endocrine-metabolic, hematologic and respiratory systems. There is a high clinical suspicion when the following factors are present: hypotension with bradycardia, mental state disturbances, lactic acidosis, hyperglycemia, sinus pauses and refractory shock. Treatment is based on general measures of intoxication support, decreasing the drug absorption and improvement of cardiac function. The bradyarrhythmias are corrected with the use of intravenous calcium, glucagon, atropine and pacemaker. If the intoxication causes depression of cardiac contractility, the use of calcium or/and glucagon is indicated. If there is refractoriness with these measures, catecholamines should be employed. There are alternative and adjuvant drugs such as amrinone, insulin-glucose, 4-aminopyridine and calcium entry promoters. charcoal hemoperfusion can be useful in the overdose of sustained release preparations, but hemodialysis is unworthy of therapeutical interest.
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