Investigating Strain as a Biomarker for Atrial Fibrosis Quantified by Patient Cine MRI Data

Ahmed Qureshi, Henry Chubb, Adelaide de Vecchi, Oleg Aslanidi
King's College London


Introduction: Atrial fibrillation (AF) is a widespread cardiac arrythmia responsible for deterioration of left atrial (LA) mechanical function. Catheter ablation (CA) terminates AF through radiofrequency heating to create regions of scar (fibrosis) which electrically isolate ectopic foci associated with arrhythmogenesis. This study aims to i) determine whether there is correlation between regions of low strain (reduced mechanical function) and atrial fibrosis, and ii) assess whether addition of scar through CA to improve LA electrical function may detriment its’ contractile ability. Methods: Patient-specific 3D LA surface models were reconstructed from Cine and Late Gadolinium Enhanced (LGE) MRI in two groups; AF: AF during pre-CA and regular sinus rhythm (SR) post-CA, and SR: SR during both. Standardised LGE signal intensities were mapped to represent atrial fibrosis. Motion-tracking applied on the time-dependant Cine images produced a series of 3D deforming LA meshes for calculation of maximum absolute strain (MAS) which characterises regional contractile ability. The resulting 3D LA models were divided into 24 regions of clinical interest for quantitative inter- and intra-patient comparisons on the effects of CA and fibrosis on LA mechanical function. Results: A Spearman’s rank coefficient of r_s=-0.99 showed statistically significant correlation between low strain and fibrosis in the AF group, and r_s=-0.74 for the combined patient groups, both in the LA posterior wall region. Strain measurements showed an average increase of 8.9% in MAS after CA in the AF group but a decrease of 10% over the LA in the SR group, attributed to improvement in mechanical function due to restoration of SR by CA, and diminishment of contractile ability through addition of scar, respectively. Conclusion: This study suggests i) myocardial strain may be used as a reliable biomarker for atrial fibrosis and ii) intentional damage to the LA through CA to terminate AF can weaken its’ mechanical function.