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Background Subclinical hypothyroidism (SCH) is reportedly associated with an increased risk of adverse events in patients undergoing percutaneous coronary intervention (PCI). The prognostic significance of SCH in the elderly was poorly defined. The purpose of this study was to evaluate the association between SCH and long-term outcomes in older patients undergoing PCI. Methods Three thousand one hundred sixty-eight patients aged 65 years or older who underwent PCI from January 2012 to October 2014 were included. Patients were divided into SCH group (n = 320) and euthyroidism (ET) group (n = 2848) based on thyroid function test. Cox proportional hazard regression analyses were used to estimate the relative risks (RRs) of all-cause death and cardiac death for patients with SCH during a 4-year follow-up period. Results There were 227 deaths during the follow-up period including 124 deaths caused by cardiac events. There was no significant difference in mortality rate between the SCH group and the ET group (p > 0.05). After adjustment for covariates, compared with patients with ET, the RRs of death from all-cause and cardiac in patients with SCH were 1.261 (95%CI: 0.802–1.982, p = 0.315) and 1.231 (95%CI: 0.650–2.334, p = 0.524), respectively. When SCH was stratified by age, gender, and degree of thyroid-stimulating hormone elevation, no significant associations were also found in any stratum. Conclusion Our investigation revealed that SCH was negatively associated with the outcome of PCI in older patients.

Macrophages conversion to foam cells strongly promoted atherosclerosis progression by plaque formation and plaque rupture. Macrophages swallow oxidized-low density lipoprotein (ox-LDL) to promote foam cell formation. Protease-activated receptor 2 (PAR2) has been reported to take part in atherosclerotic development. However, the effects of PAR2 in macrophages were rarely investigated. In this study, human monocyte, THP-1 was induced to macrophages by using phorbol 12-myristate 13-acetate (PMA). Subsequently, an in vitro model was arranged by using ox-LDL to treat the macrophages. The data showed that inhibition of PAR2 reduced ox-LDL-induced foam cell formation, inflammation, and apoptosis. Additionally, ox-LDL increased PAR2 and inhibited Dickkopf-related protein 1 (DKK1) expression, which is a Wnt signaling inhibitor. PAR2 knocked-down decreased DKK1 and enhanced expression of Wnt3a, β-catenin. Meanwhile, DKK1 overexpression reversed the effects of PAR2 on foam cell formation, inflammation, and apoptosis. In summary, PAR2 is essential for the formation of foam cells, inflammation, and apoptosis in macrophages which plays a critical role during atherosclerosis. PAR2 plays roles in macrophages treated with ox-LDL via DKK1/Wnt/β-catenin signaling.