Title Left ventricular scar predicts remodeling in patients undergoing cardiac resynchronisation therapy – a retrospective analysis from a large tertiary centre Background Cardiac resynchronization therapy (CRT) has emerged as one of the few effective treatments for heart failure however, between 30%-50% of patients fail to respond. Ischaemic cardiomyopathy (ICM) has been identified as a negative predictor of response to CRT, in part due the presence of scar within the left ventrical (LV). However, around 30% of patients with dilated cardiomyopathy (DCM) also posses evidence of late gadolinium enhancement (LGE) on Cardiac Magnetic Resonance (CMR), which correlates with LV fibrosis/scar. Quantitative data evaluating the impact of aetiology and/or the presence of scar on LV reverse remodelling is currently lacking. Purpose We set out to compare rates of volumetric remodelling in patients undergoing CRT. We wished to evaluate two hypotheses; firstly that amongst patients with ICM, rates of LV reverse remodelling would prove inferior to those with DCM. In addition, we sought to evaluate whether the presence of scar, regardless of aetiology, would corelate with reductions in LV reverse remodelling. Methods A retrospective analysis of patients who attended both the CRT Pre-Assessment Clinic (CRT PAC) and CRT Optimisation Clinic at our institution was undertaken. Optimisation assessments were performed six months after CRT implantation. Patients were implanted in accordance with current HRS/ESC guidelines; QRS duration of >130ms with left bundle branch block morphology, a left ventricular ejection fraction of <35% and New York Heart Association class III—IV). Aetiology was assessed using clinical history, angiography and CMR appearance. LGE CMR sequences were obtained in order to ascertain the presence of LV scar and patients were classified as either having evidence of scar (scar+) or being free of scar (scar-). Patients were considered echocardiographic responders to CRT if they exhibited a 15% reduction in their LV end systolic volume (LVESV). Results Seventy five patient datasets (ICM n=37, DCM n=38) were analysed. Echocardiographic response rates were significantly higher in patients with DCM vs ICM (70.2% vs 39.5%; P<0.001). Absolute LV remodelling was also significantly higher in DCM patients (53 ± 39mls vs 33 ± 31mls; P<0.01), see Figure 1a. Amongst ICM patients, 22/37 (59.5%) were scar+. Amongst DCM patients, CMR scanning showed evidence of fibrosis in only 5/38 (13%). Across both aetilogies in scar+ patients, the response rate was similar (ICM; 31.8% vs DCM; 40%). In addition, regardless of aetiology, scar- patients demonstrated greater reductions in LVESV (scar- 68 ± 42mls vs scar+ 38 ± 35mls; P = 0.01), see Figure 1b. Figure 1A. Absolute change in LVESV (mls) in patients with DCM and ICM. Figure 1B. Absolute change in LVESV (mls) in scar+ and scar- patients. Conclusion Patients with DCM display greater LV reverse remodelling than patients with ICM. This may in part be explained by the higher burden of scar+ ICM patients. Amongst scar+ DCM & ICM patients, rates of response were similarly poor. Our findings would suggest the presence or absence of scar and not aetiology predicting response to CRT and this system of classifying patients may prove more useful when guiding therapy.