A Narrative Review of Cardiac Troponin Elevation in Acute Ischemic Stroke: Clinical Implications, Differential Diagnosis, and Mechanistic Pathways

Patients with acute ischemic stroke (AIS) frequently present with elevated cardiac troponin levels, but interpreting this biomarker in the hyperacute setting remains a clinical challenge. This narrative review synthesizes current evidence on the prognostic implications, differential diagnostic criteria, and underlying mechanisms of cardiac troponin elevation in AIS. We integrate modern guideline frameworks, specifically the Fourth Universal Definition of Myocardial Infarction, to distinguish between acute nonischemic myocardial injury, chronic myocardial injury, and type 1 or type 2 myocardial infarction. Importantly, while serial testing differentiates acute from chronic myocardial injury, recent prospective multicenter trial evidence demonstrates that dynamic biomarker kinetics alone do not reliably discriminate acute myocardial infarction or establish injury etiology in stroke patients. Instead, markedly elevated absolute baseline troponin concentrations carry a substantially stronger association with type 1 acute coronary syndromes. The underlying etiologies are multifactorial, spanning pre-existing structural heart disease, oxygen supply–demand mismatch (type 2 myocardial infarction), acute nonischemic myocardial strain, and stroke-heart syndrome mediated by central autonomic dysregulation. Interdisciplinary management algorithms incorporating clinical symptoms, serial electrocardiograms, absolute troponin thresholds, and selective cardiac imaging are essential to optimize diagnostic accuracy while ensuring that emergency stroke reperfusion therapies are never delayed.