Clin Cardiol. 2026 Apr;49(4):e70286. doi: 10.1002/clc.70286.
ABSTRACT
BACKGROUND: Stent thrombosis (ST) remains a rare but potentially life-threatening complication of percutaneous coronary intervention (PCI), associated with high rates of myocardial infarction and mortality. Despite advances in stent technology and antithrombotic therapy, its multifactorial pathophysiology and optimal management remain challenging.
METHODS: We performed a narrative review of the current literature focusing on the pathophysiological mechanisms, clinical predictors, and contemporary management strategies of ST. Particular attention was given to stent-related, pharmacological, and patient-related factors, as well as emerging therapeutic approaches and preventive strategies.
RESULTS: ST arises from the complex interplay between mechanical factors (e.g., stent malapposition, underexpansion, and neoatherosclerosis), pharmacological aspects (e.g., premature discontinuation or inadequate response to dual antiplatelet therapy), and patient-related conditions, including hypercoagulability and systemic inflammation. In the acute setting, prompt PCI with restoration of coronary flow remains the cornerstone of treatment, while intravascular imaging plays a key role in identifying underlying mechanisms and optimizing outcomes. Preventive strategies rely on procedural optimization, appropriate antithrombotic therapy, and careful patient selection. New-generation drug-eluting stents and imaging-guided PCI have reduced ST incidence, whereas emerging approaches-including drug-coated balloons, subcutaneous antiplatelet agents, and anti-inflammatory therapies-represent promising adjunctive strategies, although ST-specific benefits are not yet fully established.
CONCLUSIONS: ST is a multifactorial complication requiring an integrated approach combining optimized PCI techniques, tailored antithrombotic therapy, and careful risk stratification. Ongoing advances in device technology and pharmacological treatments, along with a growing understanding of inflammatory pathways, may further improve prevention and clinical outcomes.
PMID:41910580 | DOI:10.1002/clc.70286