Background: Cardiac resynchronisation therapy (CRT) is an effective treatment for heart failure however, 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 ventricle (LV). However, around 30% of patients with dilated cardiomyopathy (DCM) also possess 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 6 months after CRT implantation. Patients were implanted in accordance with current HRS/ESC guidelines; QRS duration of >130 ms 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 CMR in addition to clinical history and angiographic findings. 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, NICM n=38) were analysed. Echocardiographic response rates were significantly higher in patients with DCM versus ICM (70.2% versus 39.5%;
p=< 0.001). Absolute LV remodelling was also significantly higher in DCM patients (53 ± 39mls versus 33 ± 31mls; p=< 0.01), see Figure 1.
Amongst ICM patients, 22/37 (59.5%) were scar+. Amongst DCM patients, CMR scanning showed evidence of fibrosis in only 5/38 (13%). In both ICM and DCM patients, scar+ patients exhibited a similar response rate (ICM scar+ 31.8% versus DCM scar+ 40%; p=> 0.05). Scar– ICM and DCM patients also demonstrated a similar degree of LV remodelling (ICM scar– 56.6 ± 20.5 mls versus DCM scar– 71.3 ± 45.5 mls; p=>0.05). In addition, regardless of aetiology, scar- patients demonstrated greater reductions in LVESV (scar–
68 ± 42 mls versus scar+ 38 ± 35 mls; p=0.01), see Figure 1.
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. Scar+ DCM and ICM patients display similarly poor rates of response, whilst scar – patients display greater remodelling across both aetiologies. Our findings would suggest the presence or absence of scar and not aetiology predict response to CRT and this system of classifying patients may prove more useful when guiding therapy.