Key result
Alcoholic cardiomyopathy is linked to ~3-fold higher odds of LGE versus idiopathic DCM.
Why the study?
Alcoholic cardiomyopathy is a major preventable cause of non-ischemic DCM, but its specific CMR features remain incompletely defined.
Does alcoholic cardiomyopathy present with distinct CMR features compared to idiopathic dilated cardiomyopathy?
Cohort (n=148)
No
Does alcoholic cardiomyopathy present with distinct CMR features compared to idiopathic dilated cardiomyopathy?
Alcoholic cardiomyopathy has a distinct CMR phenotype characterized by midwall linear LGE fibrosis and more severe RV involvement compared to idiopathic DCM, independent of LV systolic function.
Answers are grounded in this paper and cite their sources.
May support distinct CMR phenotype in ACM; hypothesis-generating and requires prospective validation before clinical adoption.
Background/Objectives: Alcoholic cardiomyopathy (ACM) is a major preventable cause of non-ischemic dilated cardiomyopathy (DCM), yet its specific cardiac magnetic resonance (CMR) remains incompletely defined. We aimed to characterize the CMR features of ACM, focusing on late gadolinium enhancement (LGE) subpatterns and biventricular function and to compare them with idiopathic DCM. Methods: In total, 148 consecutive patients (ACM n = 20, idiopathic DCM n = 128) referred for CMR at a single center were retrospectively analyzed. Sequential logistic regression adjusted for age, sex, left ventricular ejection fraction (LVEF), and right ventricular ejection fraction (RVEF) was used to identify independent association with LGE presence. Results: LVEF did not differ between groups (32.5% vs. 35.0%, p = 0.293). ACM patients showed significantly worse RVEF (40.5% vs. 52.0%, p = 0.010) and larger indexed right ventricle (RV) volumes. Any LGE was present in 70% vs. 40% (p = 0.015); when the non-specific RV insertion point pattern (non-RV-IP) was excluded, non-RV-IP LGE was 45% vs. 22.7% (p = 0.051), with a specific midwall linear pattern (25% vs. 8%, p = 0.033). ACM was independently associated with LGE across all models with an adjusted odds ratio (OR) of 3.06 [95% CI 1.05–8.95], p = 0.041, and RV dysfunction (RVEF < 45%) (OR 4.79 [95% CI 1.60–14.32], p = 0.005). No differences in major adverse cardiovascular events (MACEs) were observed at 24 months (log-rank p = 0.697). Conclusions: ACM has a distinct CMR phenotype characterized by midwall linear LGE fibrosis and more severe RV involvement, independent of left ventricle (LV) systolic function. These exploratory findings suggest that CMR may provide clinically relevant phenotypic information in ACM beyond LVEF, warranting confirmation in prospective studies.
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Vallejo-Garcia et al. (2026) conducted a cohort in Alcoholic cardiomyopathy and idiopathic dilated cardiomyopathy (n=148). Alcoholic cardiomyopathy vs. Idiopathic dilated cardiomyopathy was evaluated on Presence of any late gadolinium enhancement (LGE) (OR 3.06, 95% CI 1.05-8.95, p=0.041). Alcoholic cardiomyopathy was associated with greater presence of late gadolinium enhancement compared to idiopathic dilated cardiomyopathy (70% vs 40%; OR 3.06; 95% CI 1.05-8.95; p=0.041).
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