Introduction

Cardiac resynchronisation therapy (CRT) is an established treatment for heart failure patients with left ventricular dysfunction complicated by left ventricular (LV) conduction delay. In patients who are candidates for CRT, the LV stroke volume is diminished both by cardiomyopathy and by a dyssynchronous contraction pattern caused by conduction delay (figure 1). Left bundle branch block (LBBB) is the category of LV conduction delay in cardiomyopathy patients where CRT is most effective as a therapy. Although other patterns of LV conduction delay may also respond to CRT, the pathophysiology of dyssynchrony tied to LV conduction delay is best understood by examination of the constellation of cardiomyopathy and LBBB. By stimulation of opposing sides of the left ventricle (figure 1), a more synchronised contraction can be achieved, and the LV stroke volume can be augmented to achieve clinically meaningful improvements in heart failure outcomes. Beyond the acute haemodynamic effects of CRT that improve heart failure symptoms, long-term beneficial changes at the myocardial cellular and transcriptional level lead to LV reverse remodelling and a direct impact on the natural history of systolic heart failure. Because of this, CRT is now routinely used in patients whose heart failure symptoms are mild to avoid progression of their cardiomyopathy and heart failure symptoms. Despite two decades for evolution of CRT implantation techniques and technology, CRT has been plagued with a non-response rate in the range of 30% that has varied little over time. Recent developments, particularly with multisite LV …