Prevention of Sudden Death – Implantable Cardioverter Defibrillator and/or Ventricular Radiofrequency Ablation

Sudden cardiac death (SCD) is defined as death from cardiac causes occurring unexpectedly within 1 hour of onset of symptoms. About 80% of SCDs are due to ventricular tachyarrhythmia that is, ventricular tachycardia and ventricular fibrillation. The remaining 20% consists of a number of conditions, including cardiomyopathies (10–15%), other structural heart defects (less than 5%) and bradycardia. SCD is responsible for more deaths than cancer, stroke, and AIDS combined (CDC, 2002). The overall incidence of SCD in the United States and Europe is 1 to 2 per 1000 people (0.1% to 0.2%) annually. Almost 80% of all SCDs occur at home. The 10%-25% survival rate is low and has not been improved by the automatic external defibrillator in patients with moderate risk (de Vreede-Swagemakers, 1997; Bardy, 2008; Myerburg, 2001). On the other hand, several clinical trials showed that the implantable cardioverter defibrillator (ICD) could prevent SCD and reduce overall mortality in some patients with severe left ventrocular dysfunction. For these reasons, ICD therapy has become the first choice strategy to prevent SCD from malignant ventricular tachyarrhythmia in high-risk patients. However, there are numerous well-recognized limitations to ICD therapy. These include the effects and the result of appropriate and inappropriate ICD shocks, the cost of the devices, complications related both to the implantation procedure and to subsequent device function, device malfunction, and restricted efficacy despite normal device function in presence of significant concomitant disease and in particular in presence of severe left ventricular disfunction. Several possible solutions have been proposed in the clinical practice, these include better patients’ selection for ICD implantation, better ICD programmation, better medical therapy and arrhythmic substrate ablation. The role of catheter ablation of ventricular tachycardia in patients with structural heart disease has been increasing in the last 2 decades. The mechanisms of ventricular tachycardia are now clearer, and the electroanatomic mapping systems have made precise activation and substrate mapping more feasible; therefore, the potential for doing catheter ablation of ventricular tachycardia has increased dramatically in the past