Imaging Techniques for the Study of Fibrosis in Atrial Fibrillation Ablation: From Molecular Mechanisms to Therapeutical Perspectives

Abstract

Atrial fibrillation (AF) is the most prevalent form of cardiac arrhythmia. It is often related to diverse pathological conditions affecting the atria and leading to remodeling processes including collagen accumulation, fatty infiltration, and amyloid deposition. All these events generate atrial fibrosis, which contribute to beget AF. In this scenario, cardiac imaging appears as a promising noninvasive tool for monitoring the presence and degree of LA fibrosis and remodeling. The aim of this review is to comprehensively examine the bench mechanisms of atrial fibrosis moving, then to describe the principal imaging techniques that characterize it, such as cardiac magnetic resonance (CMR) and multidetector cardiac computed tomography (MDCT), in order to tailor atrial fibrillation ablation to each individual.

Keywords: atrial cardiomyopathies; atrial failure; atrial fibrillation; atrial fibrosis; atrial remodeling; cardiac magnetic resonance; left atrial strain; multi detector computed tomography.

Figure 1

Cellular and molecular pathways involved in the structural and electrical remodeling leading to atrial fibrillation. Ang II = Angiotensin II, ATR = Angiotensin receptor, MAPK = mitogen-activated protein kinase, TGF-β = Transforming growth factor-β, PDGF = platelet derived growth factor, CTGF = connective tissue growth factor, SMAD = Small mothers against decapentaplegic, STAT = signal transducer and activator of transcription, ROS = reactive oxygen species, IL-1 = interleukin-1, IL-18 = Interleukin-18, MMPs = matrix metalloproteinases, ECM = extra cellular matrix, miRNAs = microRiboNucleicAcids, EpAT = Epicardial Adipose Tissue, VaT = Visceral adipose Tissue.

Figure 2

Post-processing phase of left atrium detected with cardiac MRI basing on pixel signal intensity. (A): MRI-LGE scan of the left atrium. (B): manual segmentation of the atrial wall with analysis of multiple layers from endocardium to epicardium. (C): pixel intensity map creation along the atrial wall. (D): 3-dimensional shell of the left atrium with pixel intensity map based on different colors; red: dense scar, green/yellow: border zone, purple: healthy tissue. Requested permission from [49].

Figure 3

Usefulness of cardiac MRI in redo procedures of atrial fibrillation and atrial flutter ablation. (A): MRI-LGE of the left atrium in a patient with previous ablation of the roof presenting with atypical flutter. Red areas represent scar due to previous ablation (blue dots = 1). In point 2 (red dot), there is a portion of healthy tissue (purple) between the roof line and the RSPV. (B): Activation mapping during flutter with CARTO system depicts a circuit directed upwards along the posterior wall and crossing the gap identified at the MRI (white arrows). One-shot ablation in point 2 interrupted the roof-dependent atrial flutter. LAA: left atrial appendage, LSPV: left superior pulmonary vein, LIPV: left inferior pulmonary vein, RSPV: right superior pulmonary vein, RIPV: right inferior pulmonary vein. Modified from [49].

Figure 4

Usefulness of cardiac CT in atrial fibrillation ablation. Anterior view of the left atrium after atrial fibrillation ablation around the pulmonary veins. Atrial wall thickness (in mm) is depicted with different colors on the map. Major values in radiofrequency applications (AI) are used in thicker areas. AI = ablation index. LAWT = left atrial wall thickness.