Therapeutic Hypothermia and Stent Thrombosis: A Nationwide Analysis

This study sought to determine whether "real-world" data supported the hypothesis that therapeutic hypothermia (TH) led to increased rates of stent thrombosis.

TH, which is often instituted after cardiac arrest (CA) to improve neurologic outcomes, alters pharmacokinetics of antiplatelet medications, leading to a theoretical risk of stent thrombosis after percutaneous coronary intervention (PCI).

CA patients with acute myocardial infarction undergoing PCI were identified from the Nationwide Inpatient Sample from 2006 to 2011, with a defined primary outcome of stent thrombosis. The incidence of stent thrombosis in patients undergoing TH versus those not undergoing TH was compared using both logistic regression and propensity score matching.

In this dataset, 49,109 CA patients underwent PCI for acute myocardial infarction from 2006 to 2011, of whom 1,193 (2.4%) underwent TH. The incidence of stent thrombosis in the TH group was 3.9% (43 of 1,193), compared to 4.7% (2,271 of 47,916) in the no TH group (p = 0.61). Logistic regression showed that TH was not a significant predictor of stent thrombosis with an adjusted odds ratio of 0.71 (95% confidence interval: 0.28 to 1.76; p = 0.46). Propensity matching was performed to adjust for baseline differences between the TH and no TH groups, matching 1,155 patients in the TH group with 3,399 patients in the no TH group. No difference was observed in the incidence of stent thrombosis in the TH and the no TH groups after propensity matching (3.5% vs. 6.1%; p = 0.17).

TH does not increase the incidence of stent thrombosis after primary PCI in patients with acute myocardial infarction presenting as CA.