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Patient Selection and Clinical Outcomes in the STOPDAPT-2 Trial: An All-Comer Single-Center Registry During the Enrollment Period of the STOPDAPT-2 Randomized Controlled Trial A randomized comparison of Coronary Stents according to Short or Prolonged durations of Dual Antiplatelet Therapy in patients with Acute Coronary Syndromes: a pre-specified analysis of the SMART-DATE trial Major Bleeding Rates in Atrial Fibrillation Patients on Single, Dual, or Triple Antithrombotic Therapy Trial Design Principles for Patients at High Bleeding Risk Undergoing PCI: JACC Scientific Expert Panel Dual-Antiplatelet Therapy Cessation and Cardiovascular Risk in Relation to Age: Analysis From the PARIS Registry Rivaroxaban Plus Aspirin Versus Aspirin in Relation to Vascular Risk in the COMPASS Trial The optimal duration of dual antiplatelet therapy after coronary stent implantation: to go too far is as bad as to fall short Twelve or 30 months of dual antiplatelet therapy after drug-eluting stents Efficacy and Safety of Ticagrelor Monotherapy in Patients Undergoing Multivessel PCI A risk score to predict postdischarge bleeding among acute coronary syndrome patients undergoing percutaneous coronary intervention: BRIC-ACS study
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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.

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