A 55-year-old man with past medical history significant for hypertension (HTN), hyperlipidemia, and type 2 diabetes mellitus, was admitted to the coronary care unit 3 months ago with non-ST-elevation myocardial infarction (NSTEMI). Coronary angiography then revealed 95% narrowing in the proximal left anterior descending coronary artery. He underwent successful percutaneous coronary intervention and stent placement with excellent angiographic results and resolution of his symptoms. His left ventricular ejection fraction (LVEF) was 25% by left ventriculography performed at the time of the intervention. He was established on dual antiplatelet therapy, statin, and guideline-directed medical therapy for heart failure (HF). Beta blocker and angiotensin-converting enzyme (ACE) inhibitor were gradually titrated to the maximally tolerated doses during the next few months after discharge. He returned for his 3-month post discharge visit reporting no angina. An echocardiogram in the office revealed an LVEF of 30%. His 12-lead electrocardiogram (ECG) showed normal sinus rhythm (NSR), normal intervals, old septal infarct, and QRS of 110 ms. His medications include carvedilol 25 mg by mouth twice daily, lisinopril 10 mg by mouth twice daily, spironolactone 25 mg by mouth once a day, aspirin 81 mg by mouth once a day, clopidogril 75 mg by mouth once a day, and atorvastatin 80 mg by mouth before bed. He resides in NYHA functional class II. What is the single most important therapy you recommend to improve his survival?

Sudden cardiac death (SCD) is a major public health problem and the cause of death in approximately 500,000 patients every year in the United States. An implantable cardioverter defibrillator (ICD) is a device-based therapy designed to detect and treat lethal ventricular arrhythmias and has shown to decrease mortality in high-risk populations, including those who survived prior cardiac arrests. Among patients without prior history of cardiac arrest or sustained ventricular arrhythmias, the LVEF of 35% or less has been identified as the single best predictor of SCD risks. Several randomized clinical trials have enrolled patients with low ejection fraction, various clinical HF profiles without history of cardiac arrest or sustained ventricular arrhythmias, and shown survival benefits from prophylactic ICD implantation when compared to conventional therapy alone. In this chapter we will discuss the risks of SCD among HF patients, major components and basic functions of the intravenous ICD system, the ICD implant procedure, and possible complications. We will also discuss the clinical trials that led to the introduction of ICD as a lifesaving therapy in certain patient populations and highlight recent indications and contraindications of ICD therapy according to the most recent guidelines.

ICDs are surgically implanted devices with the ability to continuously monitor cardiac rhythm, as well as detect and terminate life-threatening arrhythmias. The ICD system consists of a pulse generator that is implanted subcutaneously in the subpectoral fascia medial to the deltopectoral groove and connected to a single ventricular lead (single-chamber ICD) or dual atrial and ventricular leads (dual-chamber ICD). Leads are introduced to the central venous system through semirigid vascular catheters inserted in the subclavian or axillary veins over a guidewire. In single-chamber ICDs, the lead is advanced to the right ventricular apex and secured into the endocardium. In dual-chamber ICDs, an additional pacing lead can be secured in the right atrium if sequential A-V pacing is desired (Figure 30-1).

When compared to standard pacing devices, the ICD pulse generator is bigger in size, which allows enough space to host a large battery capable of generating high-voltage current during shock delivery. In addition to all pacing microcomponents and software programs included in the standard pacemaker pulse generator, the ICD pulse generator encloses high-voltage capacitors and a very complex system of microprocessors.

The ICD lead distal terminal is equipped with a pacing tip electrode for sensing and pacing purposes, similar to the standard pacing leads. In contrast to pacing leads, the ICD ventricular lead is surrounded by 1 or 2 shock coils that correspond to locations in the right ventricle and superior vena cava when the lead is fully deployed (Figure 30-2). Some leads are designed to be equipped with a single coil only in the right ventricle (single-coil leads).

All ICD devices have pacing capability with features that are comparable to those of traditional pacemakers. Because excessive pacing from the right ventricular apex is proven to be deleterious to the cardiac function, most primary prevention ICDs are generally programmed to minimize ventricular pacing when patients have no pacing indication. Application of a magnet over the ICD pulse generator will disable the ICD detection tachy therapy and leave the pacing capability intact. This is used during urgent surgical procedures to prevent unnecessary shocks from electromagnetic interference.

The ICD’s main role is to directly treat cardiac tachydysrhythmia. When the device senses a ventricular rate that is above the programmed threshold, the ICD will attempt to terminate it either by performing antitachycardia pacing (ATP) or defibrillation. With ATP, the ICD fires a programmed sequential number of rapid pacing impulses (in ramp or burst fashion) in an attempt to terminate the ventricular tachycardia. If ATP was unsuccessful, or if the tachycardia rate fell in the preprogrammed cut-off for ventricular fibrillation (VF), the device will immediately perform a cardioversion/defibrillation. Some device models are capable of performing ATP while charging for defibrillation out of VF (Figure 30-3).

Cardiac resynchronization therapy (CRT) is another device-based therapy that is beginning to occupy a central part in HF management through its proven effects on reducing morbidity and mortality among patients with symptomatic HF with evidence of electrical dyssynchrony, defined as wide QRS > 120 ms with left bundle branch morphology. CRT is delivered by simultaneous pacing of the right and left ventricles (LVs) through an additional lead that is advanced through the coronary sinus (CS) to a posterolateral location of the LV wall. When equipped with CRT functions, a pacemaker device is called a CRT-P and an ICD device is called a CRT-D (Figure 30-4).

At the time of the implant procedure, evaluation of adequate sensing of cardiac intrinsic activities and assessment of the pacing and defibrillation thresholds are usually performed once the system is assembled and the pulse generator is connected to the lead. This is done to confirm device integrity and ensure successful detection and termination of induced VF. Ensuring that the ICD device is sensing adequate R waves is essential to increase device sensitivity to discriminate between intrinsic ventricular activities and other signals (ie, T waves or myopotentials) (Figure 30-5).

The ICD implant procedure is mostly done under moderate sedation with the exception of checking the defibrillation threshold, at which time deep sedation is required. On average, the implant procedure takes 1 to 2 hours and requires an overnight stay for observation. However, there is an increasing trend among operators to discharge patients the same day, especially in low-risk patients who underwent uncomplicated procedures.

The most common complications are hematoma (1.1% of implantations), lead dislodgement (1.0%), and pneumothorax (0.5%); the cumulative major complication rate is 1.5%.¹ The procedure is routinely performed by cardiac electrophysiologists; however, it can also be performed by general cardiologists and cardiac surgeons who received sufficient training in device implantation and programming.

Secondary prevention is a term commonly used when the indication of ICD is to prevent SCD in patients who already have survived a prior cardiac arrest or in patients with documented long episodes of sustained and hemodynamically unstable ventricular tachycardia (VT). The term primary prevention of SCD, however, is usually used when ICD therapy is used prophylactically against SCD in populations at higher risk for having cardiac arrest because of cardiac disease but who have not yet experienced sustained VT or VF.

Early ICD trials tested the efficacy of device therapy versus antiarrhythmic medications, mostly amiodarone or sotalol, in improving survival among very high-risk populations. These trials evaluated the role of ICDs as secondary preventive measures in patients who either had documented ventricular arrhythmias or cardiac arrest or were post-myocardial infarction (MI) without advanced HF. ICD therapy was proven to be superior to antiarrhythmic medications in this secondary prevention population.

The secondary prevention strategy was founded on the observation of high incidences of VT or VF in patients who survived cardiac arrest. To test the benefits of ICD therapy in this group, 3 secondary-prevention ICD trials were conducted in the late 1980s and early 1990s, including the Antiarrhythmics Versus Implantable Defibrillator (AVID) trial,² the Canadian Implantable Defibrillator (CIDS) trial,³ and the Cardiac Arrest Study Hamburg (CASH) trial.⁴ The AVID trial was the first among those 3 trials to show a statistically significant survival benefit for ICD over antiarrhythmic drugs (mostly amiodarone), with an absolute risk reduction of 7% over a follow-up of 2 years.

Following the result of AVID, the CIDS trial was stopped early due to its similar design to AVID. The CASH study was much smaller, and terminated prematurely due to adverse outcomes in 1 of its arms. A meta-analysis of the pooled data from all 3 trials showed a significant survival improvement with the ICD over antiarrhythmic medications (Table 30-1).⁵