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Figure 1: (a‑c) Cardiac magnetic resonance imaging examination while patient exposed to alcohol. (a) Cine steady state free precession showing a globally dilated LV; (b) T2‑short tau inversion recovery black blood imaging showing localized increased T2 signal (arrow) affecting the basal inferolateral wall suggestive of myocardial edema (166.9 ± 15 in area of interest vs. 94.2 ± 7.8 in remote myocardium); (c) Late gadolinium enhancement imaging showing no enhancement in the area of edema; (d‑f) Cardiac magnetic resonance imaging examination following a period of abstinence from alcohol; (d) Repeated cine SSFP showing a still globally dilated left ventricle; (e) T2‑STIR black blood revealing complete resolution of increased T2 signal at the inferolateral wall; (f) Late gadolinium enhancement imaging again revealing no enhancement in the basal inferolateral wall, confirming the absence of permanent injury (scarring)

Figure 1: (a‑c) Cardiac magnetic resonance imaging examination while patient exposed to alcohol. (a) Cine steady state free precession showing a globally dilated LV; (b) T2‑short tau inversion recovery black blood imaging showing localized increased T2 signal (arrow) affecting the basal inferolateral wall suggestive of myocardial edema (166.9 ± 15 in area of interest vs. 94.2 ± 7.8 in remote myocardium); (c) Late gadolinium enhancement imaging showing no enhancement in the area of edema; (d‑f) Cardiac magnetic resonance imaging examination following a period of abstinence from alcohol; (d) Repeated cine SSFP showing a still globally dilated left ventricle; (e) T2‑STIR black blood revealing complete resolution of increased T2 signal at the inferolateral wall; (f) Late gadolinium enhancement imaging again revealing no enhancement in the basal inferolateral wall, confirming the absence of permanent injury (scarring)