Association of Thyroid Function with Severity of Coronary Artery Disease in Euthyroid Patients OC10-OC13
Dr. Ravi Daswani,
1/12, 2nd Floor, Old Rajinder Nagar, Delhi-110060, India.
Introduction: Thyroid hormone exerts multiple effects on the heart and vascular system. Variations of free T3 have been linked to coronary artery disease. We conducted a study to observe whether there is a relationship between the variation of the serum thyroid hormone levels (TSH, FT3 and FT4) and the presence and severity of CAD in the euthyroid patients. Aim: To study association of serum TSH, FT4 and FT3 levels within the normal range with presence and severity of coronary artery disease. Materials and Methods: A total of 100 euthyroid patients with stable angina, who underwent coronary angiography were enrolled in the study. Coronary artery disease was defined as >50% stenosis in the luminal diameter in at least one major epicardial coronary artery. The Gensini scoring system was used to define the severity of the CAD and serum TSH, FT3 and FT4 levels were measured by the chemiluminescence method. R esults: Single vessel disease was found in 23%, double vessel disease in 15% and triple vessel disease in 17% of patients. TSH and FT4 levels were also comparable between the groups. Normal coronary group had significantly higher mean FT3 values than triple vessel disease (p=0.004) and FT3 levels showed an inverse relation with Gensini score (Pearsonâ€™s correlation =- 0.30) (p =0.002). A level of FT3 = 2.7 predicted the severity of CAD with a 70% sensitivity and 60% specificity (area under curve (AUC): 0.755, p=0.001). C onclusion: In the absence of primary thyroid disease and acute coronary syndrome, the occurrence of CAD is associated with lower serum levels of FT3. FT3 and not the FT4 and TSH levels may be used as an indicator of increased risk for severe CAD. The present study clearly shows the existence of a strong association between the reduction of biologically active T3 and severity of coronary artery disease. However, low T3 state could be at first interpreted as just a biological risk factor of severe coronary artery disease; only the demonstration of beneficial effects on cardiovascular, end points of long term T3 replacement in CAD patients with low T3 state can answer this fundamental issue.