Metabolic and nutritional stress-associated dilated cardiomyopathy in the setting of semaglutide use and long-term nicotine replacement therapy: a case report and literature review

Dilated cardiomyopathy (DCM) is a leading cause of heart failure and cardiac transplantation worldwide. It is a multifactorial condition with diverse aetiologies, in which metabolic and nutritional factors are increasingly recognised, whereas pharmacological contributors remain comparatively underexplored. We describe a 57-year-old man presenting with acute heart failure and cardiogenic shock after a 12-h prodrome of chest pain and dyspnoea. He had intentionally lost 26 kg over 2 months through 0.25 mg semaglutide therapy, and reports >25 years of chronic nicotine replacement therapy (NRT: 30–40 mg/day). Evaluation showed global left ventricular systolic dysfunction with an ejection fraction of 15%, marked dilation, moderate mitral regurgitation and right ventricular insertion-point fibrosis. Coronary angiography and an extensive cardiomyopathy work-up were unremarkable. This case highlights the potential for severe myocardial dysfunction in the setting of profound metabolic and nutritional stress, including rapid weight loss, sustained caloric restriction and high-intensity exercise. Pharmacological exposures, such as glucagon-like peptide-1 agonists and chronic NRT, may have contributed indirectly by facilitating prolonged energy imbalance rather than acting as direct cardiotoxic agents. Evidence directly linking either exposure to DCM remains limited, underscoring the need for further clinical research. This report suggests that the myocardium may be vulnerable to significant energy deficit and nutritional depletion, particularly in the context of pharmacologically facilitated weight-loss behaviours.