Low T3 syndrome improves risk prediction of in-hospital cardiovascular death in patients with acute myocardial infarction.

BACKGROUND

Low triiodothyronine (T3) syndrome (LT3S) is frequently seen in patients with acute myocardial infarction (AMI). We examined the association between LT3S and severity of myocardial injury and determined whether LT3S adds predictive value over thrombolysis in myocardial infarction (TIMI) risk score for in-hospital cardiovascular (CV) death.

METHODS

Of 2459 AMI patients, 529 pairs of euthyroid and LT3S individuals with similar baseline characteristics were identified using 1:1 propensity score matching. LT3S was defined as free T3 (fT3) <2.36pg/mL, normal values of thyroid-stimulating hormone and free thyroxin. Primary outcome was in-hospital CV death. Receiver operating characteristic curves were generated to assess the predictive effects of fT3, TIMI risk score, and TIMI-LT3S risk score on in-hospital CV death.

RESULTS

LT3S was found in 23.3% of patients with AMI. The peak values of cardiac troponin I in ng/mL and N-terminal pro-brain natriuretic peptide in ng/mL were significantly higher in LT3S: 6.6 (1.3-19.6) vs. 3.5 (0.8-12.1), p<0.001 and 3625 (1046-12,776) vs. 2158 (774-6759), p<0.001. Patients with LT3S had significantly higher rate of in-hospital CV death than those without (4.7% vs. 1.7%, p=0.005). Lower levels of fT3 yielded an area under the curve (AUC) of 0.741 for predicting CV death. LT3S, when added to the TIMI risk score, significantly increased AUC for in-hospital CV death than TIMI risk score alone (0.775 vs. 0.738, p=0.005).

CONCLUSIONS

LT3S was associated with more severe myocardial injury and increased in-hospital CV mortality in patients with AMI. Furthermore, it improved risk prediction of in-hospital CV death post-AMI when it was added to the TIMI risk score.