Low T3 Syndrome in Acute Myocardial Infarction: Association With Cardiac Biomarkers and Implications for Myocardial Injury Severity.

Background An acute myocardial infarction (AMI) triggers widespread inflammatory, neuroendocrine, and metabolic shifts across the body. Deviations in thyroid hormone regulation, particularly the development of low triiodothyronine (T3) syndrome, are frequently observed during acute cardiovascular events and may mirror the intensity of the underlying physiological stress. Objective The objective of the study is to evaluate the prevalence of low T3 syndrome in individuals presenting with an initial episode of AMI and to investigate its independent relationship with biochemical indicators of myocardial damage. Methods This prospective observational investigation featured 100 consecutive patients aged 30 to 70 years who were admitted with their first AMI at a tertiary care teaching institution. Cases of AMI were confirmed using clinical presentations, electrocardiographic variations, and elevated troponin I and/or creatine kinase-MB (CK-MB) concentrations. Circulating blood samples collected within roughly six hours of symptom onset were evaluated for free T3 (fT3), free thyroxine (fT4), thyroid-stimulating hormone (TSH), troponin I, and CK-MB using a chemiluminescent microparticle immunoassay. Low T3 syndrome was identified by diminished serum fT3 concentrations alongside relatively steady fT4 and TSH profiles. Skewed biomarker distributions (fT3 and TSH) were reported as median (interquartile range) and subjected to a logarithmic transformation (log10) prior to multivariable analysis. Statistical relationships were evaluated via Pearson correlation analysis and a multivariable linear regression model using log-transformed troponin I as the primary dependent variable. Results The cohort presented a mean age of 56.3 ± 14.3 years, with male patients representing 65% of the total group. Low T3 syndrome was documented in 30% of the study population. In the multivariable linear regression model adjusting for baseline demographic confounders (age and sex), both log-transformed TSH (β = 0.33, p = 0.001) and log-transformed fT3 (β = 0.28, p = 0.003) emerged as significant independent predictors of myocardial injury severity (log-troponin I). Conclusion Low T3 syndrome occurred frequently in patients experiencing a first-episode AMI. Baseline thyroid-axis alterations, specifically log-TSH and log-fT3, are significantly and independently associated with biochemical markers of myocardial injury at admission. However, as these early neuroendocrine shifts represent a cross-sectional baseline snapshot, their direct relationship with structural infarct size, ventricular dysfunction, or long-term clinical prognosis requires further validation in larger trials.