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DAPT Duration

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Elaborately Engineering a Self-Indicating Dual-Drug Nanoassembly for Site-Specific Photothermal-Potentiated Thrombus Penetration and Thrombolysis Comparison of 1-month Versus 12-month Dual Antiplatelet Therapy after Implantation of Drug-eluting Stents Guided by either Intravascular Ultrasound or Angiography in Patients with Acute Coronary Syndrome: Rationale and Design of Prospective, Multicenter, Randomized, Controlled IVUS-ACS & ULTIMATE-DAPT trial 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines Dual Antiplatelet Therapy Duration in Medically Managed Acute Coronary Syndrome Patients: Sub-Analysis of the OPT-CAD Study Antibody-Based Ticagrelor Reversal Agent in Healthy Volunteers 6-month versus 12-month or longer dual antiplatelet therapy after percutaneous coronary intervention in patients with acute coronary syndrome (SMART-DATE): a randomised, open-label, non-inferiority trial Patient-oriented composite endpoints and net adverse clinical events with ticagrelor monotherapy following percutaneous coronary intervention: Insights from the randomized GLOBAL LEADERS trial Dual Antiplatelet Therapy Duration: Reconciling the Inconsistencies Dual Antiplatelet TherapyIs It Time to Cut the Cord With Aspirin? Prevention of Bleeding in Patients with Atrial Fibrillation Undergoing 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.