Key result
Coronary stent thrombosis stems from overlapping endothelial dysfunction, inflammation, platelet activation, and hemostatic pathways.
Why the study?
Coronary stent thrombosis remains a major complication with significant impact on mortality and hospital stay despite known clinical, angiographic, and procedural risk factors, and its pathophysiology involves multiple overlapping mechanisms that require further elucidation.
This review provides a comprehensive overview of the pathophysiology, incidence, and predictors of coronary stent thrombosis, a rare but highly fatal complication of percutaneous coronary intervention.
Annually, millions of patients with obstructive coronary artery disease are treated worldwide with a coronary stent. As a result, coronary stent-related complications, even when occurring at a relatively low rate, have a major impact on total mortality and hospital stay. The most dreadful complication after coronary stenting is the abrupt thrombotic closure of the implanted stent: stent thrombosis (ST). Although several studies have already identified clinical, angiographic and procedural determinants of ST, a considerable group of patients develop ST in the absence or paucity of these risk factors. The pathophysiology of ST is generally considered as a culmination of several distinct, but often overlapping candidate pathological pathways including alterations involved in endothelial function, inflammation, platelet function and the hemostatic system. This review covers recent advances in this field of research and discusses the incidence, prognosis, correlates and triggering mechanisms of coronary ST.
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Werkum et al. (2011) conducted a review in Obstructive coronary artery disease. Coronary stenting was evaluated. Coronary stent thrombosis is a severe complication driven by overlapping pathological pathways including alterations in endothelial function, inflammation, platelet function, and the hemostatic system.
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