Current aspects of cardiac resynchronisation therapy

ent using echocardiographic parameters, CRT was harmful in those patients with narrow QRS complexes [8]. In more than 20 years of experience with CRT-related issues, we have deepened our knowledge about indication, implantation, evaluation, and optimisation of CRT. With the rapid development of the CRT technology new challenges arise. This special issue of the Netherlands Heart Journal elucidates current aspects of cardiac resynchronisation therapy. Wiegerinck et al. [9] describe the pathophysiological relationship between LBBB and dyssynchronous mechanical activation which creates LV dysfunction by ‘wasted work’. The worsening of LV function causes remodelling by neurohumoral activation and asymmetric hypertrophy. The fact that these remodelling processes are caused by changes in the regulation of gene expression raises the question whether genetic predisposition can also play a role in CRT response. Possible answers to this question are discussed in the review article by Lahrouchi and Bezzina [10]. They found different expressions of genes encoding components of Ca2 + handling, β-adrenergic receptors, contractile proteins, and myocardial natriuretic peptide preand post-CRT. It remains unclear whether these changes in gene expression are truly induced by CRT itself or whether they are the result of improvement in LV function. Because of the complexity of the phenotype ‘CRT responder’ and the intricate underlying genetic architecture, large studies will be necessary to identify genetic factors associated with volumetric CRT response. Versteeg et al. [11] showed in a prospective study of 139 CRT patients that patient-reported outcome assessed prior to CRT independently identifies poor survival and hospitalisation. It seems logical to assess patient-perceived symptoms of heart failure, functional limitations, and quality of life routinely before CRT implantation and during follow-up to improve their management. In the accompanying editorial comment ‘Patients predict their own outcome’, Kronborg In 1993, the cardiac surgeon Bakker et al. [1] introduced biventricular pacing as a novel method to treat heart failure by synchronous stimulation of the right and left ventricle. After this first-in-man implantation, the rapid development of transvenous left ventricular (LV) leads and the implementation of biventricular pacing in implantable cardioverter/defibrillators have established cardiac resynchronisation therapy (CRT) as a standard treatment of heart failure with systolic LV dysfunction and broad QRS complexes. Although the milestone trials have proven the benefit of CRT (reduction in mortality and morbidity, reverse remodelling, improvement of LV function), the prediction of CRT response still remains a challenge [2–6]. Because of the high number of CRT non-responders, especially in patients with unspecific widening of the QRS complex, class I indication for CRT was restricted to heart failure patients with typical left bundle branch block (LBBB) in the European Heart Rhythm Association guidelines update of 2013. Two-dimensional echocardiography is the most widely used noninvasive method for the evaluation of LV function and assessment of reverse remodelling after CRT; however it has as yet failed to play an additional role in determining the indication for CRT [7]. Furthermore, even though mechanical dyssynchrony was thought to be pres-