<p>Drug-induced long&#xa0;QT syndrome is a&#xa0;modifiable cause of fatal ventricular arrhythmias. Common drugs such as antiarrhythmics, psychotropic drugs, and antibiotics prolong the QTc interval via potassium channel (hERG/<i>I</i><sub>Kr</sub>) inhibition and promote torsade de pointes tachycardias. A&#xa0;prerequisite for the diagnosis is an accurate QTc measurement, which is associated with high error rates in automated analysis. In case of suspicion, manual QT measurement is advised, followed by the use of an appropriate formula for heart rate correction. Differential diagnosis should consider congenital long&#xa0;QT syndrome, electrolyte disturbances, intoxication, and structural heart disease, with diagnosis based on the modified Schwartz score. For medication lists and new therapies, drug lists and interaction analyses should be used, particularly to identify high-risk drug interactions such as psychotropic drugs combined with antibiotics and/or diuretics. In cases of increased risk at a&#xa0;QTc interval ≥ 500 ms, trigger substances must be immediately discontinued, and electrolyte, heart rate, and volume status normalized. In acute situations with torsade de pointes tachycardia, treatment using magnesium, isoproterenol, overdrive stimulation, and (if necessary) defibrillation is indicated. Follow-up electrocardiograms before, during, and (if discontinued due to QT prolongation) after therapy until QT normalization, avoidance of further trigger substances, regular follow-up controls, genetic counseling in the case of suspected congenital long&#xa0;QT syndrome, and comprehensive patient education form the basis of aftercare for this condition.</p>

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Praktischer Umgang mit dem arzneimittelinduzierten Long-QT-Syndrom

  • Pascal Syren,
  • Patrick A. Schweizer

摘要

Drug-induced long QT syndrome is a modifiable cause of fatal ventricular arrhythmias. Common drugs such as antiarrhythmics, psychotropic drugs, and antibiotics prolong the QTc interval via potassium channel (hERG/IKr) inhibition and promote torsade de pointes tachycardias. A prerequisite for the diagnosis is an accurate QTc measurement, which is associated with high error rates in automated analysis. In case of suspicion, manual QT measurement is advised, followed by the use of an appropriate formula for heart rate correction. Differential diagnosis should consider congenital long QT syndrome, electrolyte disturbances, intoxication, and structural heart disease, with diagnosis based on the modified Schwartz score. For medication lists and new therapies, drug lists and interaction analyses should be used, particularly to identify high-risk drug interactions such as psychotropic drugs combined with antibiotics and/or diuretics. In cases of increased risk at a QTc interval ≥ 500 ms, trigger substances must be immediately discontinued, and electrolyte, heart rate, and volume status normalized. In acute situations with torsade de pointes tachycardia, treatment using magnesium, isoproterenol, overdrive stimulation, and (if necessary) defibrillation is indicated. Follow-up electrocardiograms before, during, and (if discontinued due to QT prolongation) after therapy until QT normalization, avoidance of further trigger substances, regular follow-up controls, genetic counseling in the case of suspected congenital long QT syndrome, and comprehensive patient education form the basis of aftercare for this condition.