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Distinct CMR Phenotype in Alcoholic Cardiomyopathy: Greater Myocardial Fibrosis and Right Ventricular Dysfunction
Víctor Vallejo-García1,2, Manuel Barreiro-Pérez3, David González-Calle4
1Servicio de Cardiología, Hospital IMED Valencia, 46100 Burjassot, Spain.
Insights
Alcoholic cardiomyopathy (ACM) shows distinct cardiac magnetic resonance (CMR) features, including midwall linear late gadolinium enhancement (LGE) and worse right ventricular (RV) function, differentiating it from idiopathic dilated cardiomyopathy (DCM). These findings suggest CMR provides valuable phenotypic information beyond ejection fraction in ACM.
Area of Science:
- Cardiology
- Radiology
- Medical Imaging
Background:
- Alcoholic cardiomyopathy (ACM) is a significant, preventable cause of non-ischemic dilated cardiomyopathy (DCM).
- Specific cardiac magnetic resonance (CMR) characteristics of ACM are not fully understood.
- Defining these features is crucial for accurate diagnosis and management.
Purpose of the Study:
- To characterize the CMR features of ACM, focusing on late gadolinium enhancement (LGE) patterns and biventricular function.
- To compare these CMR findings with those in idiopathic DCM.
- To identify independent predictors of LGE in ACM.
Main Methods:
- Retrospective analysis of 148 patients (20 ACM, 128 idiopathic DCM) undergoing CMR.
- Assessment of biventricular function (LVEF, RVEF) and LGE patterns.
- Logistic regression analysis adjusted for clinical and functional parameters to identify associations with LGE.
Main Results:
- ACM patients exhibited significantly worse right ventricular ejection fraction (RVEF) and larger RV volumes compared to idiopathic DCM.
- A higher prevalence of LGE was observed in ACM, particularly a midwall linear pattern when excluding RV insertion points.
- ACM was independently associated with LGE and RV dysfunction (RVEF < 45%).
Conclusions:
- Alcoholic cardiomyopathy presents a distinct CMR phenotype characterized by midwall linear LGE fibrosis and more severe RV involvement.
- CMR findings are independent of left ventricular (LV) systolic function.
- Cardiac magnetic resonance imaging offers clinically relevant phenotypic information in ACM, potentially aiding diagnosis and guiding future research.
Abstract:
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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