11,23,25 In parallel, activated fibroblasts proliferate and differentiate into myofibroblasts that generate fibrogenic signals, which perpetuate tissue repair and promote collagen deposition resulting in replacement of myocardium with fibrous scar tissue. 9,22–25 The response to ablation injury implies infiltration of immune cells and neovascularisation, with local inflammation and interstitial oedema being observed up to 8 weeks post-ablation. The pathology of radiofrequency (RF) ablation injury is well established in animal models and patients and is characterised by coagulation necrosis, haemorrhage and complete loss of cellular and vascular architecture, apart from a narrow peripheral transition zone. The scope of this article does not include real-time monitoring of lesion formation through intraprocedural MRI, which – despite holding great promise – is still of limited clinical relevance because of current structural and technical limitations related to electromagnetic interference, as well as the relative absence of acute parameters that accurately predict definite lesion formation. This review focuses on the assessment of chronic ablation lesions using LGE-MRI and its utility in clinical practice. 19 In addition, we have generated evidence that the timing of image acquisition with respect to different stages of lesion formation and scar remodelling also has to be considered. 5,6,17,18 This limited reproducibility of promising results across centres may have been because of differences in the methods of image acquisition, post-processing and analysis. 10,15,16 However, initial data on the accuracy of LGE-MRI-based lesion assessment were somewhat conflicting. 5,7,14 Although the use of LGE-MRI for ventricular ablation lesion assessment is lagging behind compared to the atrium, feasibility has been demonstrated in preclinical and early clinical studies. 5–13 Several groups have reported LGE-MRI-based localisation of functional gaps in atrial ablation lesions with high accuracy, and even LGE-MRI-guided repeat pulmonary vein isolation (PV) has been demonstrated to be efficient and effective as a standalone approach. Of note, by exploiting the slow washout kinetics of gadolinium in extracellular space, LGE-MRI is not only capable of determining native fibrotic tissue, but also of detecting ablation-induced scarring. 1–4 Fibrosis is a hallmark of arrhythmogenic cardiac remodelling and constitutes an important substrate in both atrial and ventricular arrhythmias. Late gadolinium enhancement (LGE) cardiac MRI is increasingly used to detect cardiac fibrosis in the context of arrhythmias. Thus, uniform methodological and analytical standards are warranted to foster a broader implementation in clinical practice. In particular, reproducibility across different centres is impeded by inconsistent thresholds and internal references to define fibrosis. Despite holding great promise, the widespread use of LGE-MRI is still limited by the absence of standardised protocols for image acquisition and post-processing. In this respect, the elimination of LGE-MRI-detected arrhythmogenic substrate may serve as a potential endpoint, but validation in clinical studies is lacking. LGE-MRI-based lesion assessment may also be of value to evaluate the efficacy of ventricular ablation. Even LGE-MRI-guided repeat pulmonary vein isolation has been demonstrated to be feasible as a standalone approach. With a negative predictive value close to 100% it can reliably rule out pulmonary vein reconnection non-invasively and thus may avoid unnecessary invasive repeat procedures where a pulmonary vein isolation only approach is pursued. In the atrium, LGE-MRI has been shown to accurately detect and localise gaps in ablation lines. Thus, it offers the unique opportunity to assess ablation lesions non-invasively. Late gadolinium enhancement (LGE) MRI is capable of detecting not only native cardiac fibrosis, but also ablation-induced scarring.
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