Molecular Problem: Tachycardia Tachycardia is a rapid heart rate of over 100 beats/minute. Abnormalities in the heart lead to rapid rhythmical impulses that travel in all directions throughout the heart. Common causes of Tachycardia include increased body temperature, sympathetic stimulation of the heart or ischemia which occurs during myocardial infarction.^[7] The presence of a series of ventricular premature beats one after the other on an electrocardiogram signifies a Ventricular Tachycardia. Ventricular tachycardia occurs after significant ischemic damage to the ventricle, and if left untreated can lead to ventricular fibrillation.^[8]

Mechanism of Action: Disopyramide’s Class 1a activity is similar to that of Quinidine in that it targets sodium channels to lengthen the action potential.^[9]’^[10] Disopyramide depresses the increase in sodium permeability of the cardiac Myocyte during Phase 0 of the cardiac action potential, in turn decreasing the inward sodium current. This results in an increased threshold for excitation and a decreased upstroke velocity.^[11] Disopyramide prolongs the PR interval by lengthening both the QRS and P wave duration.^[12] This effect is particularly well suited in the treatment of ventricular tachycardia as it slows the action potential propagation through the atria to the ventricles. Disopyramide does not act as a blocking agent for beta or alpha adrenergic receptors, but does have a significant negative inotropic effect on the ventricular myocardium.^[13] As a result, the use of disopyramide may reduce contractile force up to 42% at low doses and up to 100% in higher doses leading to heart failure.^[14] Levites proposed a possible secondary mode of action for Disopyramide, against reentrant arrhythmias after an ischemic insult. Disopyramide decreases the inhomogeneity between infarcted and normal myocardium refractory periods; in addition to lengthening the refractory period.^[15]This decreases the chance of re-entry depolarization, because signals are more likely to encounter tissue in a refractory state which can’t be excited.^[16] This provides a possible treatment for atrial and ventricular fibrillation, as it restores pacemaker control of the tissue to the SA and AV nodes.