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Published on: February 16, 2011
Free triiodothyronine level correlates with statin responsiveness in acute myocardial infarction
Wen-Yao Wang1, Kuo Zhang1, Wei Zhao2
1Departments of Cardiology, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Insights
Thyroid hormone levels, specifically free triiodothyronine (FT3), influence statin effectiveness in acute myocardial infarction (AMI) patients. Lower FT3 levels are linked to reduced cholesterol-lowering response to statins.
Area of Science:
- Cardiology
- Endocrinology
- Lipid Metabolism
Background:
- Thyroid hormone (TH) significantly impacts lipid metabolism.
- The relationship between TH and statin responsiveness remains under-investigated.
- This study hypothesizes TH influences statin effectiveness in acute myocardial infarction (AMI) patients.
Purpose of the Study:
- To investigate the association between thyroid hormone levels and statin responsiveness in AMI patients.
- To explore the correlation between free triiodothyronine (FT3) and lipid profile changes, including LDL-C, following statin therapy.
Main Methods:
- 1091 hospitalized AMI patients were categorized into low, moderate, and high-intensity statin treatment groups.
- Lipid levels, including LDL-C and total cholesterol (TC), were measured 10-14 days post-statin initiation.
- Statistical analyses explored the association between FT3 levels and achievement of lipid-lowering goals.
Main Results:
- A significant inverse linear trend between FT3 and LDL-C/TC levels was observed in moderate and high-intensity statin groups.
- No significant correlation was found in the low-intensity statin group.
- Higher FT3 levels were associated with a greater likelihood of achieving LDL-C goals (<3.0 mmol/L and <1.8 mmol/L).
Conclusions:
- FT3 levels are related to statin-induced cholesterol-lowering responsiveness in AMI patients.
- Low FT3 may contribute to poor statin response and failure to reach LDL-C targets.
- These findings highlight FT3 as a potential factor influencing statin efficacy in cardiovascular patients.
Background:
Although thyroid hormone (TH) has important effects on lipid metabolism, the relationship between TH and statin responsiveness has never been investigated. We hypothesize that TH plays an important role in statin responsiveness in patients with acute myocardial infarction (AMI).
Methods:
Consecutive 1091 hospitalized AMI patients in Fuwai hospital (Beijing, China) were enrolled into this current study. The study population was divided into three groups based on the intensity of statin treatment: low-intensity (n = 221), moderate-intensity (n = 712) and high-intensity (n = 158). Lipid levels were measured after statin therapy lasting for 10-14 days. The association between TH, lipid profile levels and achievement of low-density lipoprotein cholesterol (LDL-C) lowering goals was explored in patients with AMI on statin therapy.
Results:
By general linear analysis, a significant linear trend between free triiodothyronine (FT3) and LDL-C level (linear coefficient r = -0.082, P = 0.001) and FT3 and total cholesterol (TC) level (r = -0.105, P = 0.031) was observed in the moderate-intensity statin group. A more apparent linear trend was detected in the high-intensity statin group (for LDL-C: r = -0.113, P = 0.005; for TC: r = -0.172, P = 0.029, respectively). However, no significant correlation was observed in the low-intensity statin group. Compared with the low-FT3 group (defined as FT3 < 1.79 pg/mL), the OR (95% CI) for attaining a LDL-C < 3.0mmol/L was found to be 2.217 (1.001-4.839) in the higher FT3 group (> 2.95 pg/mL). The OR (95% CI) for attaining the more intensive goal (LDL-C < 1.8mmol/L) was 2.836 (1.014-5.182).
Conclusions:
Our study reveals that variation in FT3 levels is related to the cholesterol-lowering responsiveness of statins in AMI patients. These findings suggest that low FT3 may be a factor responsible for lack of LDL-C goal attainment and patients' poor responsiveness to statin treatment.
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