Segmental myocardial tissue remodeling and atrial arrhythmias in hypertrophic cardiomyopathy: Findings from T1-mapping MRI.

Background: Myocardial fibrosis of the left ventricle (LV) has been associated with atrial fibrillation and other arrhythmias in individuals with hypertrophic cardiomyopathy (HCM). However, few studies have quantitatively examined the segmental relationship between diffuse LV fibrosis and atrial arrhythmias in HCM using T1 mapping and extracellular volume fraction (ECV). The aim of this study is to explore this relationship through T1 mapping, offering imaging insights into the pathophysiology of HCM with atrial arrhythmia.

Methods: A total of 38 patients with HCM were classified into two groups-those with atrial arrhythmia and those without-based on electrocardiographic and Holter monitor recordings. A covariance analysis was conducted to compare T1 mapping parameters between the two groups, adjusting for wall thickness (WT) as a covariate. Analysis was performed collectively for all 16 myocardial segments, as well as for each segment individually.

Results: Native T1 values were elevated in the entire LV myocardium and in segments S1-3 in patients with HCM with atrial arrhythmias compared to those without (P < 0.001; P < 0.05, 1316.0 ms ± 15.9 vs 1263.1 ms ± 13.6, 1350.5 ms ± 14.2 vs 1311.9 ms ± 11.7, 1305.7 ms ± 2.5 vs 1271.5 ms ± 10.6, respectively). Notably, the basal anterior segment (S1) and basal inferotseptal segment (S3) exhibited prolonged ECV and elevated native T1 values in patients with HCM and atrial arrhythmia (P < 0.05). Multivariable binary logistic regression analysis identified myocardial native T1 values in the basal anteroseptal segment (S2) as a predictor of atrial arrhythmia presence in HCM, with values exceeding 1350 ms correlating with an increased likelihood of arrhythmia development. No significant difference in WT was observed between the groups in hypertrophic myocardial regions (P > 0.05), while non-hypertrophic myocardium in individuals with HCM and atrial arrhythmias exhibited reduced wall thickness (7.7 mm ± 3.0 vs 9 mm ± 3.0, P < 0.001) compared to those without arrhythmias.

Conclusion: Fibrosis in the basal septal and anterior regions of the left ventricle plays a crucial role in myocardial tissue remodeling, contributing to the development of atrial arrhythmia in HCM. Elevated native T1 values in the basal anteroseptal segment may may serve as a significant marker for the concurrent occurrence of atrial arrhythmias in individuals with HCM.