Sick Euthyroid Syndrome and Its Association with Cardiogenic Shock in Acute Coronary Syndromes

Abstract Introduction Sick euthyroid syndrome (SES) constitutes an acute response to stress, and patients who develop it usually show more severe illness than those who do not. It could be related to disease severity in acute coronary syndrome (ACS), as assessed with Killip-Kimball class (KK), since cardiomyocytes are specifically sensitive to T3 levels. Objective To determine the prevalence of SES and low T3 in patients with ACS, and to assess its association with disease severity. Methods Prospective, observational and single center study in consecutive patients admitted to the CCU with a diagnosis of ACS. Clinical variables were collected from medical records; blood samples were obtained at admission to measure TSH, T3 and free T4 levels. SES was defined as low T3 with normal TSH and free T4. Maximum KK was determined by treating physicians. Categorical variables were compared with the chi-squared test, and categorical variables with Kruskal-Wallis and Wilcoxon tests. Statistical significance was set at p<0.05. Results There were 149 patients with complete data available for analysis. Their age was 67.8±12.4 years, and 64% were male. A total of 16.3% had SES. There were 7.5% patients with SES and KK-A, 34.8% KK-B, 14.3% KK-C and 70% KK-D (p<0.001). Thus, SES was more frequent in patients with some grade of heart failure, particularly cardiogenic shock. Figure 1 shows the difference in T3 values according to Killip-Kimball class. Conclusion Cardiomyocytes lack deiodinase and only possess T3 receptors, which makes them dependent on circulating T3 levels. T3 directly stimulates calcium channel and contractile protein synthesis in cardiomyocytes, and its deficit could affect cardiac contractility. Future studies should determine if thyroid hormone administration in cardiogenic shock can improve contractility and contribute to hemodynamic stability. T3 values according to Killip-Kimball Funding Acknowledgement Type of funding source: None