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Published on: August 28, 2018
Association of Thyroid Function with Severity of Coronary Artery Disease in Euthyroid Patients
Ravi Daswani1, B Jayaprakash2, Ranjan Shetty3
1Senior Resident, Department of General Medicine, KMC Manipal , Karnataka, India .
Insights
Lower serum free T3 (FT3) levels are linked to coronary artery disease (CAD) severity in euthyroid patients. FT3, not TSH or FT4, may indicate increased risk for severe CAD.
Area of Science:
- Cardiology
- Endocrinology
- Biochemistry
Background:
- Thyroid hormones significantly impact cardiovascular and vascular systems.
- Variations in free triiodothyronine (FT3) levels are associated with coronary artery disease (CAD).
- This study investigates the relationship between serum thyroid hormone levels (TSH, FT3, FT4) and CAD presence/severity in euthyroid individuals.
Purpose of the Study:
- To examine the association between serum TSH, FT4, and FT3 levels within the normal range and the presence and severity of CAD.
- To determine if FT3 levels correlate with the extent and severity of coronary artery blockages.
Main Methods:
- 100 euthyroid patients with stable angina undergoing coronary angiography were recruited.
- CAD was defined as >50% stenosis in major coronary arteries.
- Gensini scoring system assessed CAD severity; serum TSH, FT3, and FT4 levels were measured using chemiluminescence.
Main Results:
- FT3 levels were significantly higher in patients without CAD compared to those with triple-vessel disease (p=0.004).
- FT3 levels demonstrated an inverse correlation with the Gensini score (r=-0.30, p=0.002).
- An FT3 level ≤ 2.7 predicted severe CAD with 70% sensitivity and 60% specificity (AUC: 0.755, p=0.001).
Conclusions:
- Lower serum FT3 levels are associated with CAD occurrence in euthyroid patients without thyroid disease or acute coronary syndrome.
- FT3 levels, unlike TSH and FT4, may serve as a biomarker for increased risk of severe CAD.
- A reduction in biologically active T3 is strongly linked to CAD severity, warranting further investigation into T3 replacement therapy.
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.
Results:
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 (Pearson'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).
Conclusion:
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.
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