Abstract
BackgroundAlthough 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).MethodsConsecutive 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.ResultsBy 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).ConclusionsOur 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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