Background: Fulminant type 1 diabetes (FT1D) is a rare but life-threatening subtype of type 1 diabetes, predominantly reported in East Asian populations and often associated with viral infections. The concurrence of FT1D with myocarditis is uncommon but suggests possible shared pathophysiological mechanisms and attracts further clinical attention.

Case Presentation: A 33-year-old female was transferred to West China Hospital because of altered consciousness, abrupt onset of hyperglycemia with ketoacidosis, significantly increased cardiac biomarkers, and ST-segment elevations. Her plasma glucose on admission was 14.17 mmol/L. HbA1C and glycosylated albumin (GA) were 6.3% and 21.45%, respectively. Her fasting C-peptide level was 0.022 mmol/L. The anti-glutamic acid decarboxylase antibody (GAD-Ab) was 25.06 IU/mL, while insulin autoantibody (IAA), insulinoma-associated antigen-2 antibody (IA-2Ab), islet cell antibody (ICA), and zinc transporter 8 antibody (ZnT8Ab) were negative. All these findings supported the diagnosis of fulminant type 1 diabetes. Electrocardiogram (ECG) showed significant ST-segment elevation in leads II, III, aVF, and V4-V6. Echocardiography revealed a mildly reduced left ventricular ejection fraction (LVEF) of 46%. There was diffuse hypokinesis of the posterior-inferior wall, along with global wall motion incoordination, and left ventricular systolic function was mildly impaired. Coronary angiography revealed no abnormality. Cardiac magnetic resonance imaging (CMR) revealed areas of increased signal intensity in the interventricular septum, free wall, inferior wall, and apical sub-inferior wall and subepicardial late gadolinium enhancement (LGE), particularly in the lateral aspects of the left ventricle on T2-weighted imaging (T2WI). Acute myocarditis was diagnosed based on significantly increased cardiac biomarkers, echocardiography, and cardiovascular magnetic resonance imaging findings. She was treated with insulin, fluid resuscitation, and supportive care, leading to a rapid recovery of cardiac function with an ejection fraction of 51.9%.

At the four-month follow-up, she reported no symptoms suggestive of cardiac dysfunction. She continued insulin therapy with good glycemic control, although her C-peptide levels remained persistently low.

Conclusion: This case report determines the differential diagnosis of acute cardiac involvement in a patient with fulminant type 1 diabetes, highlights the potential shared pathophysiological mechanisms between FT1D and acute myocarditis, and underscores the value of non-invasive techniques, especially cardiac MRI, in diagnosing acute myocarditis. Early recognition and timely intervention are critical to improving clinical outcomes in these rare but severe presentations.