QT-Verlängerung und Torsade de pointes-Tachykardie bei Therapie mit Maprotilin
| Autor: | M L Rao, G. Bauriedel, R Schröder, Berndt Lüderitz, S. Lentini |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Tachycardia
Bradycardia medicine.medical_specialty Ejection fraction medicine.diagnostic_test business.industry General Medicine medicine.disease Ventricular tachycardia QT interval Internal medicine Heart failure cardiovascular system medicine Cardiology cardiovascular diseases medicine.symptom Maprotiline business Electrocardiography medicine.drug |
| Zdroj: | DMW - Deutsche Medizinische Wochenschrift. 126:1396-1400 |
| ISSN: | 1439-4413 0012-0472 |
| DOI: | 10.1055/s-2001-18880 |
| Popis: | History and admission findings A 69-year-old somnolent woman developed severe heart failure, aggravated by recurrent episodes of ventricular tachycardia. The patient showed central and peripheral edema. 24 hours earlier, she had suffered cerebral seizures that were successfully terminated by phenytoin. For 13 years, persistent atrial fibrillation had been frequency-controlled with antiarrhythmic drugs (verapamil and glycosides) and treated by oral anticoagulation. In addition, there had been long-term anti-depressant therapy with the tetracyclic agent maprotiline. Investigations Torsade de pointes tachycardia was documented in the electrocardiograms. In addition, the QT interval was extensively prolonged (QTc = 0.70 sec). Neither electrolyte disturbances nor acute cardiac ischemia were seen. Echocardiography revealed a highly reduced ejection fraction of 25 % and a moderately dilated left ventricle. Angiography showed a collateralized occlusion of the right and plaques of the left coronary artery. Treatment and course Repeated torsade de pointes tachycardia resulted in hemodynamic compromise and were terminated by defibrillations. After intravenous magnesium and xylocaine administration as well as with termination of maprotiline and antiarrhythmic co-medication, QT prolongation decreased. In addition, the recurrent torsade de pointes tachycardia stopped. Subsequently, however, there were several bradycardia episodes, QT duration remained long. Accordingly, a VVI pacemaker was implanted. Up to now, the patient is doing well. Conclusions With antidepressant therapy, a risky constellation including comorbidity and interactions with potentially arrhythmogenic drugs may lead to QT prolongation. Medication that delays conduction or causes bradycardia may generally favour torsade de pointes tachycardia. In case of indispensable multi-drug therapy, regular clinical as well as electrocardiographic monitoring with special emphasis on QT interval is mandatory. |
| Databáze: | OpenAIRE |
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