Sotalol testing unmasks altered repolarization in patients with suspected acquired long-QT-syndrome?a case-control pilot study using i.v. sotalol
S KAAB
Abstract
S KAAB
Abstract
AIMS: The aim of this pilot study was to evaluate provocative sotalol testing to unmask abnormal repolarization due to altered myocardial electrical properties as the key feature in acquired Long-QT-Syndrome. Reliable diagnosis and risk stratification for the individual patient are complicated by the multitude of mechanisms involved in acquired QT-prolongation. The combined influence of all components determines susceptibility to arrhythmias related to QT-prolongation. METHODS: Twenty consecutive patients who had experienced torsades de pointes in association with QT-prolonging drugs were tested with i.v. D,L-sotalol (2mg/kg) with 24-h intensive care monitoring to evaluate the repolarization process by determining QT- and QTc-prolongations. Results were compared to age and sex matched controls. RESULTS: At baseline, no differences between control and study population with regard to QT and QTc were detected. After sotalol infusion, QTc increased from 422+/-17 to 450+/-22ms in controls and from 434+/-20 to 541+/-37ms in the study population. Torsades de pointes occurred in three out of 20 patients (15%) in the study population but in none of the control patients following i.v. sotalol testing. CONCLUSIONS: Controlled exposure to sotalol successfully identifies patients with normal QTc intervals but altered myocardial repolarization. This may be useful for clarifying diagnosis and pathogenesis of acquired Long-QT-Syndrome.
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AIMS: The aim of this pilot study was to evaluate provocative sotalol testing to unmask abnormal repolarization due to altered myocardial electrical properties as the key feature in acquired Long-QT-Syndrome. Reliable diagnosis and risk stratification for the individual patient are complicated by the multitude of mechanisms involved in acquired QT-prolongation. The combined influence of all components determines susceptibility to arrhythmias related to QT-prolongation. METHODS: Twenty consecutive patients who had experienced torsades de pointes in association with QT-prolonging drugs were tested with i.v. D,L-sotalol (2mg/kg) with 24-h intensive care monitoring to evaluate the repolarization process by determining QT- and QTc-prolongations. Results were compared to age and sex matched controls. RESULTS: At baseline, no differences between control and study population with regard to QT and QTc were detected. After sotalol infusion, QTc increased from 422+/-17 to 450+/-22ms in controls and from 434+/-20 to 541+/-37ms in the study population. Torsades de pointes occurred in three out of 20 patients (15%) in the study population but in none of the control patients following i.v. sotalol testing. CONCLUSIONS: Controlled exposure to sotalol successfully identifies patients with normal QTc intervals but altered myocardial repolarization. This may be useful for clarifying diagnosis and pathogenesis of acquired Long-QT-Syndrome.
Key concepts: Sotalol, Torsades de pointes, Medicine, QT interval, Cardiology, Long QT syndrome, Internal medicine, Repolarization