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Disopyramide
Disopyramide (INN, trade names Norpace and Rythmodan) is an antiarrhythmic medication used in the treatment of Ventricular Tachycardia.〔Guyton, Arthur C., Hall, John E. (2006). Textbook of Medical Physiology (11th ed.). Philadelphia: Elsevier Saunders〕 It is a sodium channel blocker and therefore classified as a Class 1a anti-arrhythmic agent.〔Rizos, I. I., et al. "Effects of Intravenous Disopyramide and Quinidine on Normal Myocardium and on the Characteristics of Arrhythmias: Intraindividual Comparison in Patients with Sustained Ventricular Tachycardia." European heart journal 8.2 (1987): 154-63. Biological Sciences. Web. 10 Feb. 2012〕’〔Kim, S. Y. SY, and N. L. NL Benowitz. "Poisoning due to Class IA Antiarrhythmic Drugs. Quinidine, Procainamide and Disopyramide." Drug safety : an international journal of medical toxicology and drug experience 5.6 (1990): 393-420. Biological Sciences; Environmental Science and Pollution Management. Web. 12 Feb. 2012.〕 Disopyramide has a negative inotropic effect on the ventricular myocardium, significantly decreasing the contractility.〔Levites, R. R., and G. J. GJ Anderson. "Electrophysiological Effects of Disopyramide Phosphate during Experimental Myocardial Ischemia." American Heart Journal 98.3 (1979): 339-44. Biological Sciences. Web. 15 Feb. 2012.〕'〔Mathur, P. P. PP. "Cardiovascular Effects of a Newer Antiarrhythmic Agent, Disopyramide Phosphate." American Heart Journal 84.6 (1972): 764-70. Biological Sciences; Environmental Science and Pollution Management. Web. 15 Feb. 2012〕 Disopyramide also has an anticholinergic effect on the heart which accounts for many adverse side effects. Disopyramide is available in both oral and intravenous forms, and has a low degree of toxicity.〔Mathur, P. P. PP. "Cardiovascular Effects of a Newer Antiarrhythmic Agent, Disopyramide Phosphate." American Heart Journal 84.6 (1972): 764-70. Biological Sciences; Environmental Science and Pollution Management. Web. 15 Feb. 2012〕
== Mechanism of Action ==
Disopyramide’s Class 1a activity is similar to that of Quinidine in that it targets sodium channels to inhibit conduction.〔Mathur, P. P. PP. "Cardiovascular Effects of a Newer Antiarrhythmic Agent, Disopyramide Phosphate." American Heart Journal 84.6 (1972): 764-70. Biological Sciences; Environmental Science and Pollution Management. Web. 15 Feb. 2012.〕’〔Kim, S. Y. SY, and N. L. NL Benowitz. "Poisoning due to Class IA Antiarrhythmic Drugs. Quinidine, Procainamide and Disopyramide." Drug safety : an international journal of medical toxicology and drug experience 5.6 (1990): 393-420. Biological Sciences; Environmental Science and Pollution Management. Web. 12 Feb. 2012.〕 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.〔Kim, S. Y. SY, and N. L. NL Benowitz. "Poisoning due to Class IA Antiarrhythmic Drugs. Quinidine, Procainamide and Disopyramide." Drug safety : an international journal of medical toxicology and drug experience 5.6 (1990): 393-420. Biological Sciences; Environmental Science and Pollution Management. Web. 12 Feb. 2012.〕 Disopyramide prolongs the PR interval by lengthening both the QRS and P wave duration.〔Mathur, P. P. PP. "Cardiovascular Effects of a Newer Antiarrhythmic Agent, Disopyramide Phosphate." American Heart Journal 84.6 (1972): 764-70. Biological Sciences; Environmental Science and Pollution Management. Web. 15 Feb. 2012.〕 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.〔Hulting J, Rosenhamer G: Hemodynamic and electrocardiographic effects of disopyramide in patients with ventricular arrhythmia. Acta Med Scand 199:41-51, 1976.〕 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.〔Mathur, P. P. PP. "Cardiovascular Effects of a Newer Antiarrhythmic Agent, Disopyramide Phosphate." American Heart Journal 84.6 (1972): 764-70. Biological Sciences; Environmental Science and Pollution Management. Web. 15 Feb. 2012.〕
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