The current stratification of arrhythmic risk in dilated cardiomyopathy (DCM) is sub-optimal. Cardiac fibrosis is involved in the pathology of arrhythmias; however, the relationship between cardiovascular magnetic resonance (CMR) derived extracellular volume (ECV) and arrhythmic burden (AB) in DCM is unknown. This study sought to evaluate the presence and extent of replacement and interstitial fibrosis in DCM and to compare the degree of fibrosis between DCM patients with and without AB. This is a prospective, single-center, observational study. Between May 2019 and September 2020, 102 DCM patients underwent CMR T1 mapping. 99 DCM patients (88 male, mean age 45.2 ± 11.8 years, mean EF 29.7 ± 10%) composed study population. AB was defined as the presence of VT or a high burden of PVCs. There were 41 (41.4%) patients with AB and 58 (58.6%) without AB. Replacement fibrosis was assessed with late gadolinium enhancement (LGE), whereas interstitial fibrosis with ECV. Overall, LGE was identified in 41% of patients. There was a similar distribution of LGE (without AB 50% vs. with AB 53.7%; p = 0.8) and LGE extent (without AB 4.36 ± 5.77% vs. with AB 4.68 ± 3.98%; p = 0.27) in both groups. ECV at nearly all myocardial segments and a global ECV were higher in patients with AB (global ECV: 27.9 ± 4.9 vs. 30.3 ± 4.2; p < 0.02). Only indexed left ventricular end-diastolic diameter (HR 1.1, 95%CI 1.0–1.2; p < 0.02) and global ECV (HR 1.12, 95%CI 1.0–1.25; p < 0.02) were independently associated with AB. The global ECV cut-off value of 31.05% differentiated both groups (AUC 0.713; 95%CI 0.598–0.827; p < 0.001). Neither qualitative nor quantitative LGE-based assessment of replacement fibrosis allowed for the stratification of DCM patients into low or high AB. Interstitial fibrosis, expressed as ECV, was an independent predictor of AB in DCM. Incorporation of CMR parametric indices into decision-making processes may improve arrhythmic risk stratification in DCM.

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Background: Cardiac fibrosis is a hallmark of hypertrophic cardiomyopathy (HCM) and has confirmed unfavorable clinical significance. Replacement fibrosis is better known and has already been studied on a larger scale, whereas interstitial fibrosis is less explored. Aims:We aimed to analyze the relationship between serum biomarkers and interstitial fibrosis, as assessed with cardiac magnetic resonance (CMR) in HCM patients. Methods:We performed 3T CMR scans in 50 HCM patients to assess interstitial fibrosis as expressed by extracellular volume (ECV). In all patients, we determined levels of serum cardiac-specific (troponin T [TnT], N-terminal prohormone of brain natriuretic peptide [NT-proBNP]) and fibrosis-specific (procollagen I C-terminal propeptide, procollagen III N-terminal propeptide, transforming growth factor β1, galectin-3) biomarkers. Patients were divided based on their median value of ECV. Results:The final study population included 49 patients. The median value of ECV in our cohort was 28.1%. Patients stratified according to median ECV differed in terms of several variables: body mass index, late gadolinium extent, NT-proBNP, and galectin-3 levels (all P <0.05). Cardiac biomarkers (TnT and NT-proBNP) and galectin-3 were significantly correlated with ECV (r S = 0.34; P = 0.02; r S = 0.39; P = 0.006; r S = 0.43; P = 0.002, respectively). Galectin-3 and body mass index were found to be independent predictors of ECV (odds ratio [OR],; P = 0.03; OR, 0.81 [0.68-0.97]; P = 0.02, respectively).Conclusions: Galectin-3 was an independent predictor of interstitial fibrosis in HCM patients expressed as elevated ECV values. The other measured fibrosis-specific biomarkers were not useful in detecting interstitial fibrosis in HCM. In addition, there was a positive correlation between classical cardiac biomarkers and interstitial fibrosis in HCM patients.