Ventricular arrhythmia has for decades been considered as a premonitory sign and risk marker of sudden death. Novel theories about arrhythmogenesis and conditions for the occurrence of sudden death, as well as evidence about proarrhythmic effect of antiarrhythmic drugs, have changed the views on the treatment of ventricular arrhythmia. Ventricular tachycardia (VT) is most often associated with structural heart disease: ischemic heart disease and previous myocardial infarction, cardiomyopathy (dilated and hypertrophic), arrhythmogenic right ventricular dysplasia, valvular heart disease (mitral valve prolapse), heart failure, condition after surgical correction of a congenital heart disease. Sometimes VT occurs without structural heart disease (congenital LQTS, Brugada syndrome, idiopathic VT). Today's standpoint is to treat only symptomatic and/or prognostically significant arrhythmias. Prognostic significance of VT mostly depends on the type and degree of structural heart disease and on global cardiac function. In patients with asymptomatic non-sustained VT and low risk for sudden death no treatment is needed or antiarrhythmics are administered. Conversely, in high risk patients implantation of automatic cardioverter-defibrillator is indicated. In the treatment of acute attack of VT the following can be used: electroconversion, cardiac pacing (overdrive), lidocaine, amiodarone, beta-blockers, and occasionally magnesium or verapamil. In the prevention of recurrent arrhythmia and sudden death we can use: amiodarone, sotalol, mexiletin, phenytoin, beta-blockers, radiofrequency ablation, implantable cardioverter-defibrillator, and in specific patients verapamil, pacemaker or left ganglion stellatum denervation.