**3. Implantable cardioverter defibrillator**

**2. Sudden cardiac death**

60 Cardiac Defibrillation

lar tachyarrhythmias [29].

Sudden cardiac death (SCD) is generally defined as a sudden and unexpected death from a cardiovascular cause in a person with or without preexisting heart disease. The specificity of this definition varies depending on whether the event was witnessed; however, most stud‐ ies include cases that are associated with a witnessed collapse, death occurring within 1 hour of an acute change in clinical status, or an unexpected death that occurred within the previous 24 hours [8-10]. Despite the significant decline in coronary artery disease (CAD), the overall burden of SCD in the population remains high. In the second half of the 20th cen‐ tury, SCD continues to claim 250.000 to 300.000 US lives annualy [11,12]. In North America and Europe the annual incidence of SCD ranges between 50 to 100 per 100.000 in the general population [13-16]. However, even in the presence of advanced first responder systems for resuscitation of out-of-hospital cardiac arrest, the overall survival to hospital discharge was recently estimated to be only 7,9% [17]. In addition, the majority of SCDs occur at home, of‐ ten where the event is unwitnessed [18,19]. SCD can manifest as ventricular tachycardia (VT), ventricular fibrillation (VF), that accounting for approximately three-quarters of cases, the rest 25% caused by bradyarrhythmias or asystole [20-22]. In a significant proportion of patients, SCD can present without warning or a recognized triggering mechanism. The mean age of those affected is in the mid 60s, and at least 40% of patients will suffer SCD before the age of 65 [14].There is also strong evidence from studies in North America and Europe that there are significantly altered trends in the presenting arrhythmia observed by first responders among SCD cases [23,24]. The prevalence of SCD cases presenting with VF is decreasing with a corresponding increase in the proportion of cases presenting with pulseless electric activity (PEA). Given the extremes of resuscitation outcome based on pre‐ senting arrhythmia (>25% survival for VF and <2% for PEA) [14], it is important to improve our understanding of the determinants of these altered trends. Moreover for some segments of the population rate of SCD are not decreasing and may actually be increasing [23, 25].

More recent studies suggest that the incidence of VF or VT as the first recorded rhythm in out-of-hospital cardiac arrest has declined to perhaps even <30% in the past several decades [17,23,26]. The risk of SCD in myocardial infarction (MI) survivors has also declined signifi‐ cantly over the past 30 years, presumably due to early reperfusion and optimal medical therapy practices [27]. Recurrent ischemia may not be significantly associated with SCD, whereas heart failure due to MI markedly increases the risk of SCD [27]. Interestingly, acute ischemia is an established cause of VF and polymorphic VT [28], whereas cardiac death in patients with nonischemic dilated cardiomyopathy and functional class IV heart failure is more often due to bradyarrhythmia or electromechanical dissociation than due to ventricu‐

As a result, automated external defibrillators (ICD), which improve resuscitation rates for witnessed arrests only due to VT/VF [30], may have limited effectiveness on reducing over‐ all mortality from SCD because SCD represent a current epidemic that is not exclusively due to ventricular tachyarrhythmias. These observations may have important implications when

considering both secondary and primary SCD prevention by implantable ICDs [31].

The ICD has emerged as a generally accepted therapy for prevention of SCD in selected cat‐ egories of patients. Nearly 4 decades elapsed between the original notion that an ICD might be a useful clinical strategy, its subsequent development, and its current acceptance in vari‐ ous clinical settings based on randomized trial data. Each decade played a distinctive role in the evolution of ICD therapy. From the late 1960s until the first patient implant in 1980 [32], Mirowski's concept of a "standby automatic defibrillator" [33,34] met with skepticism [35] and concern about the practical difficulties in designing and manufacturing such a device [36,37]. After the first human device implant in 1980, clinical acceptance of the concept was initially slow, but began to accelerate after Food and Drug Administration approval in 1985 and Medicare coverage for limited indications in 1986. The early scientific support for the clinical value of the ICD was limited to a series of nonrandomized observational studies in‐ volving cohorts of high-risk patients. They were counterbalanced by contemporary interest in studies exploring the value of antiarrhythmic drug therapy guided by ambulatory ar‐ rhythmia monitoring or electrophysiological testing, and antiarrhythmic surgical techni‐ ques. This created uncertainty and intense debate in the electrophysiology community that continued even after the publication of the CAST (Cardiac Arrhythmia Suppression Trial) study [38,39] highlighted the potential dangers of empiric treatment with membrane-active antiarrhythmic drugs. Nonetheless, the CAST study was seminal in both constituting a turn‐ ing point of the concept of antiarrhythmic drug therapy for prevention of SCD and serving as a catalyst for the recognition of the importance of randomized trial data to validate the potential for ICD benefit.
