Cardiometabolic risk profiles in subclinical hypothyroidism, and the potential impact of statin therapy: A cross-sectional and longitudinal study

Background

Subclinical hypothyroidism (SH) has been linked to an increased cardiovascular risk, though the specific contributing factors remain unclear.

Methods

We studied 120 consecutive adults with SH and 120 euthyroid controls matched for age, gender, and date of blood draw. Smoking status did not differ between groups. Groups were compared on clinical and laboratory data, lipid, insulin resistance (IR), glycemic, and liver steatosis/fibrosis indices, 10-year and lifetime cardiovascular risk (SCORE2, LIFE-CVD), as well as atherogenic and additional markers (lipoprotein(a), homocysteine, fibrinogen, highly sensitive C-reactive protein, apolipoproteins A1/B). A subset of individuals with SH and ≥TSH ≥10 mIU/L (n = 16) was followed up after L-thyroxine supplementation.

Results

SH subjects had a more adverse cardiovascular profile, with worse lipid, glycemic, IR, and hepatic markers, and higher 10-year (5.3 % vs. 4.1 % and 3.8 % vs. 2.8 %) and lifetime (28.5 % vs. 23.0 %) cardiovascular risk (all p < 0.05). Complementary markers were also elevated in SH (p < 0.01). Estimated absolute risk reductions from atorvastatin 20 mg were greater in SH (1.3 % vs. 0.9 % p = 0.008 and 7.7 % vs. 6.2 %, p < 0.001). The differences were more pronounced in severe SH (TSH ≥10). L-thyroxine led to modest risk amelioration (−0.21 % and −1.18 %), primarily owing to total/LDL cholesterol reductions.

Conclusions

SH is linked to a more adverse cardiovascular, metabolic and hepatic profile, indicating its potential as a candidate risk modifier. Intensive risk factor management is warranted, along with L-thyroxine supplementation in selected cases.