Thyroid stimulating hormone elevation as a predictor of long-term mortality in patients with acute myocardial infarction.

Background: Hypothyroidism has been known to be associated with hyperlipidemia, endothelial dysfunction and atherosclerosis. Elevation of thyroid-stimulation hormone (TSH) is a gold standard to detect these conditions. However, no large studies have investigated the association between TSH elevation and long-term clinical outcomes in patients with acute myocardial infarction (AMI).

Hypothesis: Hypothyroidism is associated with higher mortality in patients with AMI.

Methods: A total of 4748 AMI patients undergoing percutaneous coronary intervention (PCI) with drug-eluting stents were consecutively enrolled. We analyzed 1977 patients whose thyroid function data available after the exclusion of hyperthyroidism and possible central hypothyroidism. Patients were divided into two groups; euthyroid group (n = 1846) with normal TSH and normal free thyroxine (FT4); hypothyroidism group (n = 131) with elevated TSH and normal or low FT4. The two groups were subsequently compared with their all-cause and cardiac mortalities.

Results: Median follow-up duration was 3.5 years. Hypothyroidism group were older, included in more females, and had higher incidences of atrial fibrillation, stroke, and renal dysfunction. Elevated TSH was associated with significantly higher all-cause mortality (26.0% vs 11.7%, P < 0.0001) and cardiac mortality (9.2% vs 4.6%, P = 0.014). The multivariate Cox proportional hazards model identified that TSH elevation was a significant predictor of all-cause mortality (adjusted hazard ratio 1.560, 95% confidence interval 1.017 to 2.392, P = 0.041).

Conclusions: Our data suggest that AMI patients with TSH elevation had worse clinical outcome. Moreover, TSH elevation was a predictor of all-cause mortality in patients with AMI.