Aside from lifestyle and conventional pharmacological interventions in heart failure, a number of other treatment options have become available or are under investigation. Device therapy involving pacing the heart is now an established option, whereas more novel treatments such as ultrafiltration and the identification and treatment of sleep-apnoea have an evolving role. Future treatment modalities such as gene therapy are investigational. This module reviews these other treatment options.
Cardiac resynchronisation therapy
Cardiac resynchronisation therapy (CRT) devices have become significant adjuncts to optimal medical therapy in the management of patients who have left ventricular systolic dysfunction (LVSD) with an ejection fraction (EF) ≤35%, commonly referred to as severe LVSD. Multiple large-scale randomised controlled trials (RCT) have demonstrated a significant benefit of CRT in reducing mortality and heart failure related hospitalisations whilst meaningfully improving patient symptoms, functional state and quality of life (QoL).
What is CRT?
Many patients with LVSD have a delay in the electrical conduction through the heart. This electrical conduction delay is identified on a 12-lead electrocardiogram (ECG) by a widened QRS complex, often meeting criteria for bundle branch block (BBB). Over 30% of patients with LVSD have left bundle branch block (LBBB) in comparison to <1% of the general population (see figure 1). Around 10% of patients with normal conduction develop new LBBB each year. Atrio-ventricular nodal disease, particularly first degree heart block, is also common in LVSD.
The prolonged QRS duration, particularly LBBB, has a mechanical consequence: late activation and contraction of the lateral left ventricular (LV) wall, leading to (a) late LV relative to right ventricular (RV) contraction (inter-ventricular dyssynchrony); and (b) inco-ordinate LV systolic contraction (intra-ventricular dyssynchrony).
Patients” prognosis and symptoms can be improved by the implantation of a cardiac re-synchronisation (CRT) device, which can pace the RV apex (or septum) and LV free wall simultaneously, thereby shortening the QRS duration. It is commonly assumed that this translates to more co-ordinate LV systolic contraction.
There are two types of CRT device: CRT-pacemakers (CRT-P) and CRT-defibrillators. A CRT-P will resynchronise ventricular depolarisation by simultaneously depolarising RV and LV free wall. Some patients with LVSD are also at high-risk of ventricular arrhythmias and a device delivering pacing and defibrillation therapy (CRT-D) can be offered. Implantable cardioverter defibrillator (ICD) therapy is not covered in this article.
CRT improves patients’ functional state as assessed subjectively by New York Heart Association (NYHA) class and/or objectively by six-minute walk test distance or cardiopulmonary exercise testing. CRT improves QoL questionnaire scores in over two-thirds of the patients undergoing the procedure. Patient survival is also significantly improved whilst hospitalisation rates due to decompensated heart failure are significantly reduced. There is an increase in systolic arterial pressure and myocardial efficiency and a reduction in LV chamber size (LV end-systolic and end-diastolic dimensions), mitral regurgitation and LV mass, all of which are markers of reverse modelling. In some patients, ‘super-responders’, LV systolic function may normalise.
Some 20–30% of patients treated with CRT do not appear to benefit in terms of either symptomatic improvement or improvement in LV size or function. There is no universally agreed definition of “response,” and it’s not clear if lack of response translates into lack of mortality benefit from CRT. The best predictors of response to CRT are:
- QRS complex ≥150ms
- LBBB morphology
- Non-ischaemic cardiomyopathy
- Female sex.
Despite the established benefits of CRT therapy, the UK implant rates for the devices remain amongst the lowest in Europe.