Cardiac and liver MRI characteristics across cumulative alcohol exposure in men with alcohol use disorder before abstinence treatment

Alcohol-associated cardiomyopathy is usually recognized after ventricular dilatation or reduced ejection fraction. Whether myocardial changes occur alongside liver abnormalities during active alcohol use, and how both relate to cumulative exposure, is less clear. In this prospective cross-sectional study, 88 consecutive men with alcohol use disorder (AUD) before inpatient abstinence treatment and 63 healthy male controls underwent cardiac and liver MRI between February 2022 and October 2024. The prespecified primary cardiac outcomes were left ventricular global longitudinal strain (LVGLS) and extracellular volume fraction (ECV). Multivariable linear regression assessed group differences and associations with total lifetime dose of ethanol (TLDE). Cardiac-liver associations were evaluated using Spearman correlation and multivariable regression. The 151 participants had a mean age of 47.4 years. Left ventricular ejection fraction was similar in the AUD and control groups (59.2% ± 8.0 vs. 61.1% ± 6.8; P = 0.11). Participants with AUD had less negative LVGLS (-15.76% ± 2.99 vs. -17.63% ± 1.90; P < 0.001), higher ECV (28.14% ± 1.94 vs. 25.42% ± 2.46; P < 0.001), and higher cardiac and liver proton density fat fractions (PDFF). After adjustment, AUD was associated with 1.49-percentage-point less negative LVGLS (95% CI, 0.49–2.49; P = 0.004) and 2.11-percentage-point higher ECV (95% CI, 1.29–2.93; P < 0.001). Each 5-kg/kg higher TLDE was associated with 0.78-percentage-point less negative LVGLS and 0.75-percentage-point higher ECV (both P < 0.001). After additional adjustment for TLDE, liver PDFF remained associated with cardiac PDFF and ECV. Before abstinence treatment, men with AUD had abnormalities in myocardial deformation and extracellular space despite similar ejection fraction. Cardiac and liver MRI abnormalities increased with cumulative ethanol exposure, and liver fat was related to myocardial fat and ECV. Longitudinal studies are needed to determine reversibility and clinical significance. What is currently known about this topic What is the key research question? What is new? How might this study influence clinical practice? Heavy alcohol exposure can affect the myocardium even in the absence of overt cardiomyopathy. AUD commonly affects the liver, but combined heart-liver MRI data are limited. Do cardiac and liver MRI abnormalities track with cumulative alcohol exposure in AUD? LVGLS was less negative and ECV was higher despite similar LVEF. Cardiac and liver MRI abnormalities increased with cumulative ethanol exposure. Liver PDFF remained related to cardiac PDFF and ECV after TLDE adjustment. Cardiovascular health merits attention in patients with substantial alcohol exposure, while the role of CMR in screening or risk stratification requires further prospective evaluation.