In recent years, management of chronic heart failure has advanced considerably, especially the optimisation of key pharmacological strategies (angiotensin-converting enzyme inhibitors, β-blockers) and multimodal management. In parallel, there has been a quieter revolution: the use of therapeutic pacing and defibrillator devices in patients with heart failure has moved from experimental and clinical research to everyday clinical practice. Milestones include landmark trials establishing the definitive mortality benefit of implantable defibrillators in ischaemic cardiomyopathy,1 the clinical utility of electronically synchronising contraction of both ventricles,2 and mortality benefits of cardiac resynchronisation therapy (CRT).3 Nonetheless, therapeutic pacing and defibrillator devices appear to be underutilised,4 perhaps due to lack of awareness of their clinical benefits and concerns regarding cost.

What are the established modalities? Sudden cardiac death is a significant risk in patients with impaired left ventricular function. The use of implantable cardioverter defibrillators (ICDs) is established in primary and secondary prevention of sudden cardiac death in chronic heart failure — large randomised controlled studies have demonstrated a significant mortality benefit.1,5 American6 and Australian7 guidelines for heart failure management state that an ICD may be used after cardiac arrest, ventricular tachycardia or ventricular fibrillation; ≥ 40 days after myocardial infarction in patients with New York Heart Association (NYHA) class I, II or III symptoms and left ventricular ejection fraction (LVEF) ≤ 30%; and in patients with ischaemic or non-ischaemic cardiomyopathy, NYHA class II or III symptoms and LVEF ≤ 35%. Newer “risk stratifiers” are being explored to better identify patients likely to benefit from ICD therapy.8

The implantation procedure for an ICD is identical, in principle, to that of a pacemaker, with some exceptions: the lead is larger (thus stiffer), so care is required during its manipulation within the heart; the battery is larger, so it requires careful positioning to avoid skin erosion; and testing of the device involves inducing ventricular fibrillation to ensure adequate sensing of arrhythmia and an adequate safety margin in terms of the threshold of defibrillation. Also, the sophisticated programming of ICD therapy requires a cardiac electrophysiologist. ICDs can be programmed to treat ventricular arrhythmias with either antitachycardia pacing (which is painless) or shock therapy. After the patient experiences their initial therapy, which unfortunately may involve a potentially distressing shock while the patient is conscious, individualised adjustments may be needed.

Despite the survival benefit associated with ICDs, their impact on quality of life is uncertain. In contrast to other heart failure therapies, ICDs do not improve cardiac function. They would not be expected to improve a patient’s exercise capacity or ability to perform activities of daily living. Also, implantation can be associated with various immediate and late complications, including device infection, failure and inappropriate discharge.9

The failing heart is frequently characterised by abnormalities of mechanical synchrony, often reflected by abnormalities of electrical conduction. Based on adverse consequences of ventricular dyssynchrony in heart failure, researchers have sought to resynchronise the failing myocardium. One approach, CRT, involves pacing both ventricles in a coordinated manner to restore the normal physiological chronology of left- and right-sided contraction. Ventricular dyssynchrony can be crudely detected on an electrocardiogram by QRS prolongation.10 Epidemiologically, QRS prolongation has been associated with worsening of clinical outcomes in patients with heart failure. Echocardiography has been proposed as a better tool for evaluating mechanical dyssynchrony.11

The implantation of a CRT device extends the standard pacemaker or ICD implantation procedure by placement of a left ventricular pacing lead. This requires specialised sheaths to access the coronary sinus, angiographic identification of an appropriate lateral branch, and careful positioning of the lead. Several factors determine the ideal position for the lead, including proximity to the lateral wall at a position furthest from the right ventricular lead, stability of lead placement, presence of viable myocardium that can be captured by pacing at the site, and avoidance of diaphragmatic pacing. The procedure requires an experienced operator and a service that can optimise programming.

CRT has undergone considerable evaluation and, according to American and Australian guidelines, it is indicated in patients with NYHA class III or IV symptoms, LVEF ≤ 35% and QRS duration on electrocardiogram > 120 ms.6,7 More than 4000 patients have been evaluated in randomised single- or double-blind controlled trials of CRT in heart failure and, in systolic heart failure, CRT has consistently been associated with improved patient wellbeing and ventricular systolic function, and reduced recurrent hospitalisation for heart failure. Meta-analyses and a stand-alone study have shown reduced all-cause mortality with CRT.3,12 These benefits add to those of standard drug therapies for systolic heart failure, and may be further enhanced by use of a defibrillator. Indeed, most CRT devices used in Australia include a defibrillator function.

Ideally, patients should be in sinus rhythm for maximum benefits from this therapy. Some evidence suggests that CRT is also beneficial in patients with atrial fibrillation, and that this cohort may be better optimised with atrioventricular node ablation.13 However, current Australian Government Department of Health and Ageing guidelines do not support the use of these devices in patients with atrial fibrillation.14 In addition, not all patients who meet the criteria for CRT benefit from the therapy. There is a 20%–30% “non-response rate”, in that patients do not feel better or ventricular function does not improve.14 The reason for this is elusive, but improved evaluation of dyssynchrony, using measures more sophisticated than QRS duration (eg, echocardiography, magnetic resonance imaging), may reduce the non-response rate, and CRT trials that base entry criteria on results of imaging alone are underway. Nonetheless, CRT has gained popularity in recent years, particularly for patients who remain severely symptomatic despite drug therapy.

What other modalities are being evaluated? Cardiac contractility modulation (a new form of electrical therapy) is currently being evaluated in patients with heart failure. A recent clinical study demonstrated improved exercise tolerance and quality of life,15 but these data need to be confirmed in large, randomised controlled studies.

Ventricular pacing alone has also been trialled, but can result in deleterious mechanical effects. In patients with impaired left ventricular function, right ventricular pacing can cause further deterioration.16 Adverse effects may be minimised by pacing the right ventricular outflow tract or high septum rather than the apex.17 Perhaps more importantly, atrioventricular synchrony can be maintained, and many pacemakers allow minimisation of ventricular pacing by various programmable algorithms.

What is needed now? Over the past decade, many pacing therapies have been rigorously evaluated in patients with chronic heart failure, and there are now proven indications for their application in clinical practice. The clinical outcomes, potential problems and costs of CRT, ICD and right-sided pacing are summarised in the Box. Doctors should be aware of these therapies and consider referring individual patients who meet the criteria for their use.