Which antiarrhythmic drugs are known to prolong the QT interval and carry a risk of torsades de pointes?

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Multiple Choice

Which antiarrhythmic drugs are known to prolong the QT interval and carry a risk of torsades de pointes?

Explanation:
QT prolongation with torsades de pointes risk happens when drugs delay ventricular repolarization by blocking the hERG potassium channels, lengthening the action potential. Among antiarrhythmics, strong potassium-channel blockers—class IA agents like quinidine and procainamide, and class III agents such as sotalol, dofetilide, and ibutilide—prolong the QT and raise the risk of torsades de pointes, especially with electrolyte disturbances or bradycardia. Amiodarone also lengthens the QT, but its torsades risk is comparatively low because of its multiple effects on different ion channels. In contrast, adenosine, digoxin, and calcium-channel blockers like diltiazem and nifedipine do not carry the same QT-prolonging or torsades risk profile.

QT prolongation with torsades de pointes risk happens when drugs delay ventricular repolarization by blocking the hERG potassium channels, lengthening the action potential. Among antiarrhythmics, strong potassium-channel blockers—class IA agents like quinidine and procainamide, and class III agents such as sotalol, dofetilide, and ibutilide—prolong the QT and raise the risk of torsades de pointes, especially with electrolyte disturbances or bradycardia. Amiodarone also lengthens the QT, but its torsades risk is comparatively low because of its multiple effects on different ion channels. In contrast, adenosine, digoxin, and calcium-channel blockers like diltiazem and nifedipine do not carry the same QT-prolonging or torsades risk profile.

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