Cobalt-Induced Cardiomyopathy: Mitochondrial Dysfunction, Oxidative Stress, and Reversible Cardiac Toxicity: A Systematic Review

Metal-on-metal (MoM) joint replacements were designed to improve durability in younger, active patients. However, cobalt-induced cardiomyopathy (CIC) has emerged as a rare but serious complication, often misattributed to idiopathic or ischemic causes. We systematically reviewed published case reports, case series, and laboratory studies describing CIC in patients with MoM implants. Data extraction included clinical presentation, diagnostic criteria, treatment, and outcomes. Methodological quality and risk of bias were assessed qualitatively. Eighteen cases were included. Implant wear and corrosion released systemic cobalt, which localised in myocardial tissue. Pathophysiological mechanisms included mitochondrial dysfunction, oxidative stress, impaired calcium handling, and apoptotic injury. Patients commonly presented with non-specific cardiac symptoms such as fatigue, dyspnoea, orthopnoea, arrhythmias, and heart failure, alongside extra-cardiac features including hearing loss, thyroid dysfunction, and neurocognitive changes. Diagnostic confirmation required serum cobalt levels typically exceeding 30-100 µg/L, with cardiac MRI demonstrating non-ischemic fibrosis and oedema. Chelation therapy reduced cobalt burden but was rarely effective alone. Revision of the MoM implant consistently led to clinical improvement when performed early; delayed intervention was associated with irreversible myocardial damage and poorer outcomes. CIC is an under-recognised but potentially reversible form of cardiomyopathy. Routine cobalt screening and early implant revision are essential to prevent progression to heart failure or sudden cardiac death. Multidisciplinary collaboration between cardiology and orthopaedics is critical for the timely diagnosis and management of these conditions.