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Ticagrelor Monotherapy Versus Dual-Antiplatelet Therapy After PCI: An Individual Patient-Level Meta-Analysis Global Approach to High Bleeding Risk Patients With Polymer-Free Drug-Coated Coronary Stents: The LF II Study Safety and efficacy of the bioabsorbable polymer everolimus-eluting stent versus durable polymer drug-eluting stents in high-risk patients undergoing PCI: TWILIGHT-SYNERGY Impact of bleeding during dual antiplatelet therapy in patients with coronary artery disease Optimal duration of dual antiplatelet therapy after drug-eluting stent implantation: a randomized, controlled trial. Ticagrelor Monotherapy Versus Ticagrelor With Aspirin in Patients With ST-Segment Elevation Myocardial Infarction Long-term pharmacodynamic effects of Ticagrelor versus Clopidogrel in fibrinolytic-treated STEMI patients undergoing early PCI Pooled Analysis of Bleeding, Major Adverse Cardiovascular Events, and All-Cause Mortality in Clinical Trials of Time-Constrained Dual-Antiplatelet Therapy After Percutaneous Coronary Intervention Conceptual Framework for Addressing Residual Atherosclerotic Cardiovascular Disease Risk in the Era of Precision Medicine Benefit-risk profile of extended dual antiplatelet therapy beyond 1 year in patients with high risk of ischemic or bleeding events after PCI

Review Article2017 Oct 31;70(18):2278-2289.

JOURNAL:J Am Coll Cardiol. Article Link

Interleukin-1 Beta as a Target for Atherosclerosis Therapy: Biological Basis of CANTOS and Beyond

Libby P Keywords: acute coronary syndromes; high-sensitivity C-reactive protein; interleukin-1; myocardial infarction

ABSTRACT


Inflammatory pathways drive atherogenesis and link conventional risk factors to atherosclerosis and its complications. One inflammatory mediator has come to the fore as a therapeutic target in cardiovascular disease. The experimental and clinical evidence reviewed here support interleukin-1 beta (IL-1β) as both a local vascular and systemic contributor in this regard. Intrinsic vascular wall cells and lesional leukocytes alike can produce this cytokine. Local stimuli in the plaque favor the generation of active IL-1β through the action of a molecular assembly known as the inflammasome. Clinically applicable interventions that interfere with IL-1 action can improve cardiovascular outcomes, ushering in a new era of anti-inflammatory therapies for atherosclerosis. The translational path described here illustrates how advances in basic vascular biology may transform therapy. Biomarker-directed application of anti-inflammatory interventions promises to help us achieve a more precise and personalized allocation of therapy for our cardiovascular patients.