Thyroid Function Abnormalities in Acute Coronary Syndrome: Current Evidence and Clinical Implications – A Narrative Review

Abstract Thyroid hormones influence several cardiovascular functions, including myocardial contractility, vascular tone, and lipid metabolism. Abnormal thyroid activity – ranging from overt hypo- or hyperthyroidism to transient low T3 syndrome – has been linked to the onset, severity, and prognosis of acute coronary syndrome (ACS). Hospital-based studies report thyroid function abnormalities in approximately 15%–30% of patients presenting with ACS, most commonly low T3 syndrome and subclinical hypothyroidism. This narrative review summarizes current evidence on how thyroid dysfunction affects cardiovascular physiology and clinical outcomes in ACS. Proposed mechanistic links include effects on myocardial contractility, vascular tone, endothelial function, inflammation, and arrhythmogenesis. Hypothyroidism promotes atherogenesis through dyslipidemia and endothelial dysfunction, while hyperthyroidism increases myocardial oxygen demand and arrhythmic risk. Low T3 syndrome, frequently observed during ACS hospitalization, correlates with larger infarct size, left ventricular dysfunction, and increased mortality. Although these hormonal alterations may partly reflect adaptive responses to acute illness, they carry important prognostic implications. Evidence from Indian and global studies indicates that thyroid abnormalities are common among ACS patients, yet routine screening remains limited. Understanding these interactions may help clinicians identify high-risk individuals, refine risk stratification, and optimize post-ACS management, particularly in settings where cardiovascular and endocrine disorders frequently coexist.