Extracellular volume is an independent predictor of arrhythmic burden in dilated cardiomyopathy (original) (raw)

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 cutoff 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. Ventricular arrhythmias, including premature ventricular contractions (PVCs) and non-sustained ventricular tachycardia (NSVT), occur in 40% of patients with dilated cardiomyopathy (DCM) 1. The bulk of evidence indicates that runs of NSVT and frequent PVCs, defined as arrhythmic burden (AB), lead to an increased sudden cardiac death (SCD) risk in DCM patients 2. Susceptibility to ventricular arrhythmias in DCM relies on the combined presence of an anatomic substrate (i.e. genetic or acquired abnormalities in the electrical or mechanical properties of the heart) and triggering mechanisms. Profound cardiac remodeling and fibrosis provide ample substrate for the initiation of ventricular arrhythmias. Cardiac fibrosis is typically observed in 40-60% of DCM patients 3,4. Broadly, two types of fibrosis have been identified. Replacement or scarring fibrosis develops as a consequence of local myocytes death and serves to preserve the integrity and function of the heart after injury 5. DCM is typically characterized with widespread interstitial fibrosis given that the need for cardiac repair is minimal and, ultimately, fibrosis is a maladaptive event 5 .