TABLE 77.1 Class I and IIa Indications for Implantable Cardioverter-Defibrillator Therapy | ||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
Cardiac Electronic Implantable Device Therapy
Cardiac Electronic Implantable Device Therapy
Yang Yang
Irakli Giorgberidze
Lorraine Cornwell
INTRODUCTION
The first case of successful defibrillation in a human was performed in 1947 by Dr Claude Beck, a cardiothoracic surgeon, on a 14-year-old boy whose rhythm had degenerated into ventricular fibrillation (VF) during surgery for pectus excavatum.1 Based on the contemporary studies of Carl Wiggers, who showed that timely defibrillation restored sinus rhythm in animals with VF,2 Beck applied a direct shock to the heart cardioverting it back to sinus rhythm.
With time, both open- and closed-chest defibrillation became the mainstay of resuscitation from cardiac arrest. Michel Mirowski and Morton Mower invented and built the first implantable cardioverter-defibrillator (ICD)3 that was implanted in February 1980.4 The first ICD weighed over 200 g and used large epicardial patches for defibrillation while requiring a thoracotomy for implantation.
Over time the ICD attained indications for sudden death prevention in patients who survived ventricular tachycardia (VT) or cardiac arrest (secondary prevention) and those with left ventricular (LV) systolic dysfunction at risk of sudden death (primary prevention).5 Subsequently, studies demonstrated that simultaneously pacing both right and left ventricle (ie, biventricular pacing) in electrically dyssynchronous ventricles could improve mechanical synchrony, LV systolic function, and the functional status of patients6 and decrease mortality.7 With those findings, biventricular pacing or cardiac resynchronization therapy (CRT) has become the standard of care for heart failure patients with a wide QRS complex on the electrocardiogram. Thus, the benefits of ICD therapy in sudden death prevention and the benefits of CRT in the improvement of heart failure led to the combination of biventricular pacing with defibrillation (ie, implantable CRT-defibrillators [CRT-D] device).
Due to the initial limitations of both generator size and need for epicardial patches, the earliest ICDs required cardiothoracic and abdominal wall surgery. With advances in technology, the device (ie, generator) is now a fifth its original size and implanted via minimally invasive surgery via the creation of small subcutaneous pocket in a pectoral region. Epicardial patches have been replaced by intracardiac leads (wire electrodes) that use sheath-based introducer techniques for transvenous implantation under fluoroscopic guidance.
ICDs consist of a pulse generator and up to three intracardiac leads for CRT-D systems. The pulse generator—also known as “the can”—contains the high-voltage capacitor, battery, and sensing circuitry for the device. Contemporary ICDs function as a defibrillator and also incorporate all functions of a pacemaker. The defibrillator lead, which consists of a pace/sensing electrode and one or two coils for defibrillation, is usually implanted into the right ventricle. In dual-chamber ICDs, a regular pacing lead is also implanted into the right atrium. With CRT devices, LV pacing is accomplished by a lead that is advanced into one of the epicardial LV veins via the coronary sinus (CS).
Contemporary techniques for ICD and CRT-D implantation are minimally invasive procedures that use local anesthesia and conscious sedation, percutaneous venous access through the Seldinger technique and only one incision for the creation of the generator pocket. The right ventricular and right atrial leads are then guided into the appropriate location under fluoroscopic guidance. Specially designed guiding sheaths are used for delivery of the LV lead to the selected branch of the CS. The generator is secured in either a subcutaneous or submuscular pocket. The whole procedure can be done on a same-day basis requiring minimal hospitalization.
INDICATIONS
Table 77.1 lists the current indications for ICD implantation for both primary and secondary prevention.
Secondary Prevention
Early observations showed both VF and VT are leading causes of sudden cardiac death (SCD), and patients who survived the initial event remained at high risk of recurrent life-threatening arrhythmias. Accordingly, patients with documented VT or VF were among the first to be enrolled in clinical trials demonstrating the effectiveness of ICDs in reducing mortality.
The first trial to enroll sudden death survivors was the Cardiac Arrest Study Hamburg (CASH), which evaluated 346 patients with prior cardiac arrest. Patients were randomized to either ICD, metoprolol, amiodarone, or propafenone. Propafenone therapy was discontinued early due to excess mortality secondary to the presumed increased proarrhythmic effect of the drug. At a mean follow-up of 57 months, the trial demonstrated a trend toward a decrease in total mortality when comparing ICD to antiarrhythmic drugs (36.4% vs 44.4%, P = .08).8
Similarly, the Canadian Implantable Defibrillator Study (CIDS) randomized patients with prior cardiac arrest, hemodynamically significant or sustained VT, and LV ejection fraction (LVEF) < 35% to either ICD (N=328) or amiodarone (N = 331). At 5 years, a trend toward decreased mortality with ICD therapy (8.3% per year in ICD group vs 10.2% per year in amiodarone group, P = .14) was observed.9
The Antiarrhythmics Versus Implantable Defibrillators (AVID) trial provided the crucial evidence which prior trials were hinting toward. It compared ICD therapy with antiarrhythmic drug therapy (amiodarone or sotalol) in 1016 patients with LVEF < 40% and life-threatening arrhythmias (ie, either prior VF or sustained VT with syncope or signs of hemodynamic compromise). The study was stopped early at 18 months when it showed a significant mortality benefit for ICD therapy (15.8% vs 24.0%).10
Primary Prevention
Patients with LV dysfunction, prior myocardial infarction, and frequent ventricular ectopy are known to be at increased risk of life-threatening arrhythmias.11,12 Based on these observations, studies were designed to evaluate the efficacy of ICD in reducing mortality in “high-risk” patients who had not yet suffered cardiac arrest (ie, primary prevention).
The first such patients studied were those with spontaneous nonsustained VT who had inducible sustained VT in the electrophysiology laboratory. The Multicenter Automatic Defibrillator Implantation Trial (MADIT) enrolled 196 patients with LVEF ≤ 35%, nonsustained VT, and inducible and nonsuppressible (with procainamide) sustained VT induced during electrophysiologic study and randomized them to ICD versus optimal medical therapy (including antiarrhythmics). After a mean follow-up period of 27 months, there was a significant reduction in all-cause mortality with ICD (38.6% vs 15.8%, P = .009).13
The Multicenter Unsustained Tachycardia Trial (MUSTT) randomized patients with recent myocardial infarction (ranging from 4 days to 3 years before randomization), LVEF ≤ 40%, spontaneous nonsustained VT, and inducible VT to either conservative treatment (angiotensin-converting enzyme inhibitors/β-blockers) or antiarrhythmic therapy (intervention arm). Patients randomized to the intervention group received antiarrhythmic drug therapy (Class I agent, amiodarone, or sotalol) and underwent repeat testing for inducible sustained VT. Those who failed multiple drugs received an ICD. Overall, 46% of patients received ICDs. At a mean follow-up of 39 months, there was a significant difference in mortality between non-ICD and ICD patients regardless of antiarrhythmic therapy (24% vs 55%, P < .001).14
Moving beyond risk stratification by electrophysiology testing, the MADIT II trial enrolled 1232 postmyocardial infarction patients with LVEF ≤ 30%—regardless of prior ventricular ectopy—to receive prophylactic ICD or conventional medical therapy. The trial was terminated early at 20 months due to significant reduction in overall mortality in the ICD group (14.2% vs 19.8%, P = .016), driven almost entirely by reduction in SCD (3.8% vs 10.0%, P < .01).15