Results of a medical study known as the Cardiac Arrhythmia Suppression Trial (CAST) demonstrated that patients with structural heart disease (such as a history of MI (heart attack), or left ventricular dysfunction) and also patients with ventricular arrhythmias, should not take this drug. The results were so significant that the trial was stopped early and preliminary results were published. The dose may need to be adjusted in certain clinical scenarios. As with all other antiarrhythmic agents, there is a risk of proarrhythmia associated with the use of<unk> . This risk is probably increased when<unk>  is co-administered with other class Ic antiarrhythmics, such as encainide. The risk of proarrhythmia may also be increased by hypokalemia. The risk of proarrhythmia is not necessarily associated with the length of time an individual is taking<unk> , and cases of late proarrhythmia have been reported. Because of the role of both the liver and the kidneys in the elimination of<unk> , the dosing of<unk>  may need to be adjusted in individuals who develop either liver failure or kidney failure. Because of the negative inotropic effects of<unk> , it should be used with caution in individuals with depressed ejection fraction, and may worsen congestive heart failure in these individuals. It should be avoided in people with ischaemic heart disease and the elderly. As with all class I antiarrhythmic agents,<unk>  increases the capture thresholds of pacemakers. Heart Due to the narrow therapeutic index of<unk> , physicians should be alert for signs of toxicity before life-threatening arrhythmias occur like torsades de pointes. While the toxic effects of<unk>  are closely related to the plasma levels of the drug, it is unfeasible to check the plasma concentration in an individual on a regular basis. Signs of<unk>  toxicity include marked prolongation of the PR interval and widening of the QRS duration on the surface ECG. There may be signs and symptoms attributable to overt heart failure secondary to sudden decreased myocardial contractility. Treatment Treatment of<unk>  cardiac toxicity involves increasing the excretion of<unk> , blocking its effects in the heart, and (rarely) institution of cardiovascular support to avoid impending lethal arrhythmias. Modalities that have had success include administration of a beta-sympathomimetic agent, and administration of a sodium load(often in the form of hypertonic sodium bicarbonate). Placing the individual on cardiopulmonary bypass support may be necessary in order to temporarily remove the need for a beating heart and to increase blood flow to the liver. Lungs<unk>  has a very high affinity for lung tissue and is associated with drug-induced interstitial lung disease.
Flecainide
Tocainide
Procainamide
Acecainide
Amiodarone
Ibutilide
Verapamil
Dofetilide