QT prolongation and arrhythmia suppression.
It seems possible to draw some overall conclusions from the data on antiarrhythmic drug-induced QT prolongation and its role in drug effects. At one end of the spectrum are patients with highly exaggerated QT responses during therapy, most often in the setting of hypokalemia and long cycle lengths (post-ectopic pauses, bradycardia). These patients may be at high risk for development of arrhythmias during therapy. It should also be remembered that the presence of hypokalemia may render antiarrhythmic agents less effective in general. On the other hand, modest QT prolongation in the course of therapy with an antiarrhythmic drug may well be a marker of reduction of dispersion of action potential durations or refractory periods and hence represent an antiarrhythmic effect. The clinical actions of these drugs in patients with arrhythmias strongly suggest that this is the case. New agents with the ability to reduce dispersion of repolarization or of refractoriness without inducing arrhythmias may well become the agents of choice for the treatment of serious cardiac rhythm disturbances.
Roden
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DM
Woosley
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RL
D000120:Acecainide / Q000627:therapeutic use; D000638:Amiodarone / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects; D001145:Arrhythmias, Cardiac / Q000139:chemically induced / Q000188:drug therapy / Q000209:etiology*; D003638:Deafness / Q000151:congenital; D003645:Death, Sudden; D004562:Electrocardiography; D006325:Heart Atria; D006352:Heart Ventricles; D006801:Humans; D011802:Quinidine / Q000627:therapeutic use; D013015:Sotalol / Q000627:therapeutic use; D013599:Systole / Q000187:drug effects; D013610:Tachycardia / Q000139:chemically induced
D000889:Anti-Arrhythmia Agents; D000120:Acecainide; D013015:Sotalol; D011802:Quinidine; D000638:Amiodarone