Cardiac Resynchronization Therapy (CRT) restores mechanical synchrony to a structurally diseased heart when coexisting electrical conduction disease is present, a condition that affect 270,000 patients yearly. A CRT procedure is typically performed in a laboratory under X-ray where three pacing leads are implanted in the cardiac chambers through venous access and connected subcutaneously to a pulse generator that is either a pacemaker (CRT-P) or an implantable cardiac defibrillator with pacing function (CRT-D). The His-Purkinje System (HPS) of the heart ensures that electrical activation across the entire heart is synchronized to provide maximal mechanical efficiency during a ventricular contraction cycle. Disease affecting the proximal end of the HPS may result in a complete left bundle branch block (LBBB), effectively eliminating the normal electrical connection to the left ventricle. This has a profound effect of delaying electrical activation throughout the entire left ventricle, with the greatest delay in activation occurring in the lateral wall region. The result of this is mechanical dyssynchrony that is visible and quantifiable both within each and between both ventricles. In the long term, mechanical dyssynchrony may lead to progressive cardiac dysfunction and failure. CRT can correct delayed activation through pacing at late sites in the left ventricle, reducing or in some cases eliminating the mechanical dyssynchrony. A patient with positive response to CRT has improved cardiac function and in the long term, improved activity tolerance, reduced HF-related rehospitalizations1 and lower mortality.
A major challenge in the CRT field is the rate of treatment failure. Up to 30% of CRT recipients experience no clinical benefit, resulting in 60,000 failed implants and $6B in wasted healthcare spending annually. Inappropriate CRT patient selection is a key contributing factor to this high rate of treatment failure. There is strong evidence that CRT is effective primarily in patients with complete LBBB and ineffective or even detrimental in right bundle branch block or uniform diffuse ventricular conduction delays. The accurate diagnosis of complete LBBB by ECG is complicated by overlapping similarity of the ECG morphology found in other cardiac disorders. Accurate interpretation of complete LBBB using strict criteria on a standard 12-lead electrocardiogram (ECG) is a skill often relegated to specialists and is a declining art. Direct electro-anatomic mapping studies, which displays actual LV electrical activation pattern, have also brought into question the specificity of more commonly applied LBBB criteria currently in use. These criteria are more generalized, with more relaxed observance of the QRS morphology criteria and a greater reliance on the QRS duration measurement. As such, up to one-third of patients currently diagnosed to have LBBB on ECG do not meet the published strict criteria for complete LBBB. The effect is that a significant proportion of patient’s implanted for CRT have presumed but not proven complete LBBB. To improve complete LBBB detection we believe visualizing late activation of the typical complete LBBB patient in a 3-d model would assist cardiologists to identify and diagnose this important CRT substrate with greater specificity. Improved patient selection for CRT will reduce treatment failures and improve clinical outcomes for 60,000 patients with HF each year.