Disopyramide, antiarrhythmic action

Mechanism of action - Disopyramide is a class lA antiarrhythmic agent that decreases the rate of diastolic depolarization (phase 4), decreases the upstroke velocity (phase 0), increases the action potential duration of normal cardiac cells, and prolongs the refractory period (phases 2 and 3). It also decreases the disparity in refractoriness between infarcted and adjacent normally perfused myocardium and does not affect alpha- or beta-adrenergic receptors. 

Mechanism of action. Na -channel blocking antiarrhythmics resemble most local anesthetics in being cationic amphiphilic molecules (p.206 exception phenytoin, p.191). Possible molecular mechanisms of their inhibitory effects are outlined on p.202 in more detail. Their low structural specificity is reflected by a low selectivity toward different cation channels. Besides the Na channel. Carotid 1C channels are also likely to be blocked. Accordingly, cationic amphiphilic antiarrhythmics affect both the depolarization and repolarization phases. Depending on the substance, AP duration can be increased (Class IA), decreased (Class IB), or remain the same (Class IC). Antiarrhythmics representative of these categories include Class IA—quinidine, procainamide, ajmaline, disopyramide Class IB—lidocaine, mexile-tine, tocainide Class IC—flecainide, propafenone. 

PARACETAMOL ANTIARRHYTHMICS Disopyramide and propafenone may slow the onset of action of intermittent-dose paracetamol Anticholinergic effects delay gastric emptying and absorption Warn patients that the action of paracetamol may be delayed. This will not be the case when paracetamol is taken regularly... 

ANTIARRHYTHMIC agents (Class I agents, e.g. disopyramide, flecainide. lignocaine. procainamide, quinidine) are sodium-channel blockers and are mainly used to treat atrial and ventricular tachycardias (see antiarrhythmic agents). ANTIEPILEPTICS have a number of mechanisms of action, but some appear to have a component involving modulation of sodium-channel function, e.g. carbamaxepine and phenytoin (see anticonvulsants). 

Disopyramide is metabolized to nordisopyramide (monodealkylated) by the action of CyP 2D6 nordisopyramide has antiarrhythmic activity approximately 25% that of disopyramide. Under normal circumstances, nordisopyramide accumulates to concentrations ranging from 0.2 to l.Opg/mL, and the compound does not accumulate out of proportion to disopyramide in situations of reduced hepatic or renal function. Therefore little additional therapeutic information is gained by monitoring nordisopyramide. 

Disopyramide is an antiarrhythmic agent that deaeases the rate of diastolic depolarization decreases upstroke velocity inaeases action potential duration and prolongs refractory period. It is indicated in suppression and documented prevention of ventricular arrhythmias considered to be life threatening. 

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