Clinical Impact of Intraprocedural Stent Thrombosis During Percutaneous Coronary Intervention in Patients Treated With Potent P2Y12 inhibitors - a VALIDATE-SWEDEHEART Substudy

Abstract

Background The clinical importance of intraprocedural stent thrombosis (IPST) during percutaneous coronary intervention in the contemporary era of potent oral P2Y12 inhibitors is not established. The aim of this study was to assess IPST and its association with clinical outcome in patients with myocardial infarction undergoing percutaneous coronary intervention with contemporary antithromboticmedications. Methods and Results The VALIDATE-SWEDEHEART study (Bivalirudin Versus Heparin in ST-Segment and Non-ST-Segment Elevation Myocardial Infarction in Patients on Modern Antiplatelet Therapy in the Swedish Web System for Enhancement and Development of Evidence-Based Care in Heart Disease Evaluated According to Recommended Therapies Registry Trial) included 6006 patients with myocardial infarction, treated with potent P2Y12 inhibitors during percutaneous coronary intervention. IPST, defined as a new or worsening thrombus related to a stent deployed during the procedure, was reported by the interventional cardiologist in 55 patients (0.9%) and was significantly associated with ST-segment elevation myocardial infarction presentation, longer stents, bailout glycoprotein IIb/IIIa inhibitors, and final Thrombolysis in Myocardial Infarction flow <3. The primary composite end point included cardiovascular death, myocardial infarction, out-of-laboratory definite stent thrombosis and target vessel revascularization within 30 days. Secondary end points were major bleeding and the individual components of the primary composite end point. Patients with versus without IPST had significantly higher rates of the primary composite end point (20.0% versus 4.4%), including higher rates of cardiovascular death, target vessel revascularization, and definite stent thrombosis, but not myocardial infarction or major bleeding. By multivariable analysis, IPST was independently associated with the primary composite end point (hazard ratio, 3.82; 95% CI, 2.05-7.12; P<0.001). Conclusions IPST is a rare but dangerous complication during percutaneous coronary intervention, independently associated with poor prognosis, even in the current era of potent antiplatelet agents. Future treatment studies are needed to reduce the rate of IPST and to improve the poor outcome among these patients. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT02311231.

Keywords: intraprocedural stent thrombosis; myocardial infarction; oral P2Y12 inhibitors; percutaneous coronary intervention; stent thrombosis.

Conflict of interest statement

Dr Angerås has received consultant fees from Abbott Vascular, AstraZeneca, and Boston Scientific Corporation. Dr James has received institutional research/grant support from AstraZeneca, Bayer, Janssen, and Novartis. Dr Koul has received speaker fees from Pfizer, BMS, and AstraZeneca. The remaining authors have no disclosures to report.

Figures

Figure 1. Clinical impact of intraprocedural stent thrombosis.

Kaplan‐Meier failure functions for the composite primary end point (cardiovascular death, myocardial infarction, target vessel revascularization, and definite stent thrombosis) within 30 days (A) and 180 days (B) in patients with versus without IPST. IPST indicates intraprocedural stent thrombosis.

Figure 2. Clinical impact of intraprocedural stent thrombosis in different subgroups of patients.

The association between IPST and the composite primary end point (cardiovascular death, myocardial infarction, target vessel revascularization, and definite stent thrombosis) within 30 days was consistent among subgroups, with the exception of non‐STEMI. Black lines with boxes represents hazard ratios with 95% CI. IPST indicates intraprocedural stent thrombosis; LTB, large thrombus burden; STEMI, ST‐segment–elevation myocardial infarction; and TIMI, Thrombolysis in Myocardial Infarction. *There were no adverse events among the group of patients with IPST and non‐STEMI.

Figure 3. Clinical impact of final TIMI flow and large thrombus burden.

Kaplan‐Meier failure functions for the composite primary end point (cardiovascular death, myocardial infarction, target vessel revascularization, and definite stent thrombosis) in patients with versus without final TIMI 3 flow (A) and in patients with versus without an initial large thrombus burden (B). TIMI indicates Thrombolysis in Myocardial Infarction.