Abstract 3096: Does The Extent Of Non Viable Myocardium, As Identified By Delayed Enhancement Cardiac Magnetic Resonance, Preclude Response After Cardiac Resynchronization Therapy?
Cardiac resynchronisation therapy (CRT) is a recognised treatment for symptomatic left ventricular (LV) failure associated with a broad QRS.It has been suggested that >15% myocardial scarring predicted failure to respond to CRT. To determine if the scar burden is a major determinant in response to CRT, we prospectively studied 50 pts (66± 1 years, ischaemic aetiology 57%) undergoing CRT for standard indications at baseline (NYHA: 3±0.4, EF: 23±0.8%, QRS: 150±7 ms, BNP: 495±461 pmol/l) and 6 months post-CRT. Clinical response was defined by a reduction in NYHA class >1 and in BNP level >30%. Reverse LV remodelling was defined as a reduction in end-systolic volume ≥10%. All patients had an echocardiographic examination, including an assessment of dyssynchrony. Additionally, a Cardiac Magnetic Resonance (CMR) study, with delayed enhancement, was performed in patients without contraindications. Of the 30 patients that had CMR, 23 pts (77%) responded clinically to CRT (reduction in NYHA: 1.6±0.6, reduction in BNP: 34±0.4%) and 19/30 (63%) additionally displayed reverse LV remodelling. Among the clinical responders 8 pts (35% of responders) were found to have extensive full thickness myocardial scarring on CMR (in 7 ±1 segments), predominantly in the anteroseptum and apex (86%). Three of these patients also showed significant echocardiographic reverse remodelling. The mechanism of response to CRT in these patients with extensive infarction was more frequently interventricular resynchronisation (43%) or atrio-ventricular resynchronisation (43%) rather than intra-ventricular resynchronisation (14%).The previously suggested 12 segment dyssynchrony index (DI) would have identified none of these responders with extensive myocardial infarction. The DI identified only 7/23 responders (30%).
Conclusion: Even patients with extensive myocardial scar are potential responders to CRT and should not be excluded if they fulfil the standard AHA/ESC criteria for biventricular pacing. Intraventricular resynchronisation is not the only mechanism by which patients respond to CRT and measures of intraventricular dyssynchrony alone are inadequate for identifying potential response