Implantable cardiac defibrillators
Death from heart failure (HF) is usually related to pump failure or ventricular arrhythmia (Figure 8.1). Left ventricular ejection fraction (LVEF) is the major predictor of outcome and sudden death. The majority of clinical trials have shown an increased risk of ventricular arrhythmias when LVEF is reduced to 30–35% or lower. A number of clinical trials have shown a mortality benefit in patients receiving an implantable cardiac defibrillator (ICD) either as primary or secondary prevention (Table 8.1).
Figure 8.1 Data from the MERIT-HF trial show that the risk of sudden death is greatest when patients are NYHA class II and that death from pump failure is greater in advanced symptomatic heart failure (NYHA class IV). CHF, chronic heart failure; NYHA, New York Heart Association. Source: Lancet 1999;353:2001–7, reproduced with permission from Elsevier © 1999.
TABLE 8.1 Recommendations for ICD implantation* |
Primary prevention • LV dysfunction (LVEF ≤ 35%), prior MI/IHD and at least 40 days after acute MI • LV dysfunction (LVEF ≤ 35%) of non-ischemic etiology • High risk of sudden cardiac death (e.g. familial long QT, some cases of hypertrophic myopathy) Secondary prevention • Survivor of cardiac arrest due to VF/VT, after excluding reversible cause • Structural heart disease with sustained VT • Syncope, LVEF ≤ 35% and inducible sustained VT/VF at electrophysiological study *Assuming patient has an overall life expectancy > 1 year, with good functional status. ICD, implantable cardiac defibrillator; IHD, ischemic heart disease; LV, left ventricular; LVEF, left ventricular ejection fraction; MI, myocardial infarction; VF, ventricular fibrillation; VT, ventricular tachycardia. |
Approximately 10% of patients who have an ICD for primary prevention receive an appropriate shock in the first 2 years after the device is implanted. Patients who receive an ICD for secondary prevention have a high risk of recurrence without treatment, with a rate of sudden death of up to 40% 1 year after presentation. Pharmacological therapy (e.g. amiodarone) is not effective at preventing sudden death and an ICD is superior therapy.
Defibrillators in non-ischemic cardiomyopathies. Although there is a clear mortality benefit for prophylactic ICDs in patients with systolic HF related to coronary artery disease (CAD), evidence for benefit in HF that is not due to CAD has been less than convincing. Since the early ICD trials, optimal medical management as well as cardiac resynchronization therapy (CRT) for HF has significantly improved outcome. In a recent large scale study, patients with LVEF ≤ 35% without CAD were randomized to receive either an ICD or optimal clinical care (including CRT) and were followed for a median of 67.6 months. Sudden cardiac death rates were low in both groups and the ICD did not confer a significant benefit compared with standard care. This study suggests that the decision to implant a prophylactic automated ICD can be safely delayed in patients with non-ischemic cardiomyopathy in favor of 6–12 months’ intensive pharmacological management. Not infrequently, the significant reversal of LV remodeling may obviate the need for device therapy.
Cardiac resynchronization therapy
Hypertension, myocardial infarction (MI) and ischemia can all cause myocardial cell damage and areas of fibrosis. Ischemia and fibrosis can damage the conduction system of the heart, slowing ventricular depolarization by promoting cell-to-cell conduction, a much slower depolarizing process. This results in a widening of the QRS complex on the surface ECG, often with a left bundle branch block type morphology. In many cases this results in a differential effect in the contractile function of the ventricles known as ventricular dyssynchrony, in which parts of the ventricle no longer achieve maximum contractility and move at different rates and with a different contractile force to other parts. There are two types of ventricular dyssynchrony:
• intraventricular dyssynchrony, in which the muscle fibers within the left ventricle contract at differing rates and speeds
• interventricular dyssynchrony in which the left and right ventricles no longer contract simultaneously.
Dyssynchrony results in a loss of efficient ventricular contraction and impairs stroke volume and cardiac output. Often there is also dyssynchrony of contraction of the papillary muscles that control mitral valve function, resulting in mitral valve regurgitation which further impairs cardiac output (see page 29).
To improve overall cardiac function and resynchronize the heart, the right and left ventricles need to be paced simultaneously. Right ventricular (RV) pacing is a well-established, safe and effective technology. Placing a pacing lead within the left ventricular (LV) cavity is also feasible, but it is fraught with potential problems, particularly thromboembolism to the systemic circulation. Instead, a pacing lead is placed into the coronary sinus, which runs under the heart between the left atrium and ventricle, and then into the peripheral veins under the left ventricle so that the myocardium can be paced reliably. Accessing these veins has been a technical challenge but with better delivery tools the success rate of placing a lead in a satisfactory position is now high.
The technology. In patients with sinus rhythm, three pacing leads are inserted: one to the right atrium, one to the right ventricle and one within the coronary sinus to access a posterolateral vein underneath the left ventricle (Figure 8.2). (In patients with permanent atrial fibrillation there is no requirement for an atrial lead.) The coronary sinus ostium is accessed using a specialized sheath system. Once the sheath is placed within the body of the sinus a balloon occlusive catheter is inserted. The balloon is expanded to occlude the vein and contrast is injected through the catheter and a venogram taken (Figure 8.3). This allows the anatomic details of the side veins of the coronary sinus to be documented (see Figure 8.3). A pacing lead and guide wire are then inserted into the sheath and the lead is advanced over the wire into its final position (Figure 8.4).
Figure 8.2 Cardiac resynchronization therapy. Anterior–posterior chest X-ray showing final lead positions: a pacing lead to the high right atrium (HRA), a defibrillating lead at the right ventricular apex (RVA) and a pacing lead within the posterolateral coronary sinus vein (PLV).
Figure 8.3 Venogram showing the positioning of a balloon occlusive catheter in the coronary sinus and the location of the posterolateral coronary side vein.
Figure 8.4 Chest X-ray showing the position of the pacing lead within a sheath, which slides over the guide wire. Once the lead is in position and stable the sheath is removed by cutting it away from the lead.
The leads are connected to a pacing generator. During sinus rhythm, the device senses the underlying p wave and via a short atrioventricular (AV) delay (this must be shorter than intrinsic AV nodal conduction) ‘force’ paces the ventricles. The ventricles are continuously driven or paced by the device and intrinsic conduction is suppressed.
Types of device. The basic requirement for CRT is to be able to pace both ventricles simultaneously. It is recommended that the device should pace the ventricles at least 98% of the time to exert its full benefit. A device may be either a pacemaker (CRT-P) or a pacemaker and defibrillator (CRT-D), but there is some controversy about which device is best. Patients with less symptomatic HF (NYHA class II or III) are at relatively greater risk of sudden death, whereas patients with ambulatory class IV are more likely to suffer pump failure. There is therefore an argument to implant a CRT-D in patients with fewer symptoms and a CRT-P in those with advanced HF.
The landmark CARE-HF study showed that most of the survival benefit of the device was related to CRT-P, while the COMPANION study showed no significant difference between CRT-P and CRT-D in terms of reduction in sudden deaths. Although there are no convincing data of a significant benefit of CRT-D, in the real world a CRT-D device is usually implanted because all patients will have impaired LV function.
Cost implications. CRT is considerably more expensive than standard pacing, often three to four times the cost; there is also a significant cost difference between the CRT-P (AUS$15 000) and CRT-D (AUS$35 000) devices (see above). As the incidence of HF increases, there will be a need for more implants, substantially increasing the cost to society.
Does CRT reduce mortality? The CARE-HF trial studied 813 patients with symptomatic NYHA class II or III HF despite optimal medical treatment; 50% were randomized to continue optimal medical treatment with angiotensin-converting enzyme (ACE) inhibitors/beta-blockers and diuretics, and 50% additionally underwent implantation of a CRT pacemaker. Mortality was reduced by 32% in the CRT group (Figure 8.5). The readmission rate with decompensated HF was also significantly reduced, as were sudden deaths and overall mortality. As a result, CRT is now standard therapy for patients with HF, broad QRS complexes and symptoms despite optimal medical treatment (Table 8.2).
Figure 8.5 The results of the CARE-HF study show a significant mortality reduction (p < 0.002) in patients with HF implanted with a CRT pacemaker compared with those who received optimal pharmacological treatment only (see text). Adapted from Cleland JGF et al. N Engl J Med 2005;352:1539–49.
TABLE 8.2 Inclusion criteria for cardiac resynchronization therapy |
• Impaired LV function: LVEF < 35% • NYHA class II, III and ambulatory class IV symptoms of HF despite optimal medical treatment with ACE inhibitors or ARBs/beta-blockers/diuretics and spironolactone • Wide QRS complexes > 120 ms, preferably with a LBBB morphology (> 150 ms with non-LBBB QRS morphology) • Reasonable expectation of life > 1 year • Sinus rhythm or atrial fibrillation* • CRT-D (defibrillation) or CRT-P (pacemaker) depends on clinical judgment |
*CRT for patients with atrial fibrillation, provided pacing occurs for more than 92% of the time. If not, consider atrioventricular nodal ablation. ACE, angiotensin-converting enzyme; ARB, angiotensin-receptor blocker; HF heart failure; LBBB, left bundle branch block; LVEF, left ventricular ejection fraction; NYHA, New York Heart Association. |
Does CRT improve morbidity? Many studies have consistently shown an improvement in NYHA symptoms, usually decreasing by at least one class, sometimes two or even three. These changes are maintained for at least 2 years and there is evidence that the improvements occur over the duration of the device.
Possible contraindications are shown in Table 8.3. Cost-effectiveness for ICDs is significantly reduced in patients over 75–80 years old (Figure 8.6), and clinical judgment should be used in very elderly patients. The results of the Reverse and MADIT-CRT trials suggest that early implantation of the device slows down the progression of HF and allows positive LV remodeling. Increasingly, CRT is used earlier in treatment.
TABLE 8.3 Possible contraindications for CRT device implantation |
• Poor ventricular rate control in atrial fibrillation (AV nodal ablation is recommended to ensure pacing is constant) • Right bundle branch block • Full-thickness posterior MI (can affect lead positioning) • Narrow QRS complexes (< 120 ms) • Mild symptoms |
AV, atrioventricular; CRT, cardiac resynchronization therapy; MI, myocardial infarction. |
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