Disopyramide reduces membrane responsiveness in atrial muscle and the amplitude of the action potential. Excitability of atrial muscle is decreased. These changes decrease atrial muscle conduction velocity. Action potential duration in atrial muscle fibers is prolonged by disopyramide administration. This occurrence increases ERP. Postrepolarization refractoriness does not occur with disopyramide, and it appears to differ from quini-dine and procainamide in this respect.

Abnormal atrial automaticity may be abolished at disopyramide plasma concentrations that fail to alter either conduction velocity or refractoriness. Disopyramide increases atrial refractoriness in patients pretreated with atropine, suggesting that the primary action of disopyra-mide is a direct one and not a consequence of its anti-cholinergic effect.

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