Title: A Study of Thyroid Profile and Sick Euthyroid State in Patients with Acute Coronary Syndrome
Authors: Santhi Thoppappatty Sengottaiyan, Dhananjayan Kannan, Sheik sultan Alavudeen Narthakar Dhabre Alam
DOI: https://dx.doi.org/10.18535/jmscr/v5i2.108
Abstract
Back Ground: Acute coronary syndrome (ACS) is still the commonest cause of morbidity and mortality in the cardiovascular disease (CVD) entity worldwide. Studies have shown the effect of thyroid hormones on morbidity and mortality from cardio-vascular events. The sick euthyroid state (SES) has been well associated in ACS affecting the prognosis.
Aim & Objectives: To study the prevalence of SES in patients with ACS, the thyroid profile in ACS and the outcome among the SES patients with ACS. Also to study the distribution of SES according to multiple variables in patients with ACS.
Materials and Methods: The one year study is carried out in our hospital and designed as cross sectional study. Study group included 155 patients diagnosed to have ACS. History, clinical examination and risk stratification is done. Blood samples, thyroid profile, serial ECGs and Echocardiography are done for all patients. Data is analyzed for prevalence by percentage and Chi-square tests used for P-values and significant correlations.
Results: Prevalence of SES in ACS is 25.5%.Statistically Significant P-values for High BMI, CRP positivity, worst outcome in SES group of ACS were observed, correlating well with several studies. Low T3 values and Increased rT3 value (sick euthyroid state) is correlating with the worst outcome in ACS.
Conclusion: Prevalence of sick euthyroid state (SES) is very common in patients with ACS. Almost one quarter of ACS patients had SES. SES significantly associated with high BMI, CRP positivity is associated with worst outcome. So, Sick euthyroid state is a strong prognostic indicator in ACS. The T3 and rT3 levels well correlated with the outcome.
Keywords: Sick euthyroid state, CRP-c reactive protein, Acute coronary syndrome.
References
1. Scirica BM, Cannon CP, McCabe CH, et al: Prognosis in the Thrombolysis in Myocardial Ischemia III Registry according to the Braunwald unstable angina pectoris classification. Am J Cardio 2002; 90:821-826.
2. Braunwald E: Unstable angina: An etiological approach to management. Circulation 1998; 98:2219-2222.
3. Kennon S,Price CP<Mills PG, et al; The central role of plate activation in determining the severity of acute coronary syndromes. Heart 2003; 89:1253-1254.
4. The TIMI IIIA Investigators: Early effects of tissue-type plasminogen activator added to conventional therapy on the culprit lesion in patients presenting with ischemic cardiac pain at rest. Results of the Thrombolysis in Myocardial Ischemia (TIMI IIIA) Trail. Circulation 1998;87:38-52.
5. Ridker PM, Brown NJ, Vaughan DE, Harrison DG, Metha JL. Established and emerging plasma biomarkers in the prediction of first atherothrombotic events. Circulation 2004 ;109:IV6-19.
6. Klein I. Thyroid hormone and the cardiovascular system. Am J Med 1990; 88.631-637.(39)
7. Polikar R, Burgr AG, Shrrer U ,et al. The thyroid and heart. Circulation 1993;87: 1435-41.
8. Friberg L, Drvota V, Bjelak AH, et al. Association between increased levels of reversed triiodothyronin and mortality after acute Myocardial infarction. Am.J. Med 2001;111:699-703.
9. Silva JE, Larsen PR. Contributions of plasma triiodothyronin and local thyroxine monodeiodination to nuclear triiodothy-ronin receptor saturation in pituitary, liver, kidney of hypothyroid rats. Further evidence relating saturation of pituitary nuclear triiodothyronine receptors and the acute inhibition of thyroid stimulating hormone release. J Clinic investigation 1987;61:124 7-59.
10. Chopra I Euthyroid sick syndrome: is it a misnormer? Journal of clinical Endocrin-ology and Metabolism 1997;82:329-334.
11. Kaplan M,Schimmael M& Utiger R. Changes in serum3,30,50-triiodothyronin (reverse T3) concentrations with altered thyroid hormone secretion and metabol-ism. Journal of clinical Endocrinology and Metabolism1977 ;45:447-456.
12. Maury C & Teppo A .Circulating tumor necrosis factor-a (cachectin) in myocardial infarction. Journal of internal Medicine1989;225:333-336.
13. Cruickshank A, Oodroyd K & Cobbe S. Serum interlukin-6 in suspected myoca-rdial infarction. Lancet 1994;343;974.
14. Adams J, Abendschein D & Jaffe A.Biochemical markers of myocardial injury. Is MB creatine kinase the choice for the 1990s? Circulation 1993;88:750-763.
15. Jaume J ,Mndel C, Frost P,Greenspan F &Laughton C. Extremely low doses of heparin release lipase activity into plasma and canthereby cause artifactual elevations in the serum-free thyroxine concentration as measured by equilibrium dialysis. Thyroid 1996;6:79-83.
16. Blum A, Sclarovsky S, Rehavia E & Sho-hat B. Levels of T lymphocyte subpop-ulations, interlukin-I band interlukin-2 receptor in acute myocardial infarction. American Heart journal 1994;127:1226-1230.