Will electrocardiographic detection of myocardial fibrosis work?

Sudden cardiac death (SCD) is a major cause of premature mortality worldwide, and intensive research efforts have focused on finding ways to recognise high-risk individuals before the fatal event. Ventricular tachycardia degenerating into ventricular fibrillation is the most common pathophysiological cascade leading to sudden death from arrhythmia. Presence of myocardial fibrosis leads to susceptibility for life-threatening reentrant ventricular arrhythmias by creating anatomical and/or functional abnormalities in the electrical impulse conduction that may serve as an arrhythmogenic substrate. Therefore, detecting cardiac fibrosis has been under considerable interest, as this could help to identify patients with cardiac disease at high risk of SCD. Late gadolinium enhancement (LGE) in cardiac magnetic resonance (CMR) acts as an in vivo marker of replacement fibrosis and scar. The presence of fibrosis in CMR has been emerging as a powerful prognostic tool, and several studies have demonstrated increased risk of arrhythmias in cardiac patients with LGE. This risk appears to be at least partly independent from reduced left ventricular ejection fraction (LVEF), SCD risk marker that is currently used to guide implantable cardioverter-defibrillator (ICD) therapy for primary prevention. In a recent meta-analysis, fibrosis detected by LGE was associated with a fourfold risk of ventricular arrhythmias or SCD in ischaemic as well as in non-ischaemic cardiomyopathy, and the risk was similar both in LVEF ≤35% and LVEF >35% patients.1 In hypertrophic cardiomyopathy, extensive LGE increases the risk of …