CBS 2019
CBSMD教育中心
中 文

DAPT Duration

Abstract

Recommended Article

Six Versus 12 Months of Dual Antiplatelet Therapy After Implantation of Biodegradable Polymer Sirolimus-Eluting Stent: Randomized Substudy of the I-LOVE-IT 2 Trial Gut microbiota induces high platelet response in patients with ST segment elevation myocardial infarction after ticagrelor treatment Mortality Following Cardiovascular and Bleeding Events Occurring Beyond 1 Year After Coronary Stenting - A Secondary Analysis of the Dual Antiplatelet Therapy (DAPT) Study Inhibition of Platelet Aggregation After Coronary Stenting in Patients Receiving Oral Anticoagulation 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

Review ArticleVolume 74, Issue 12, September 2019

JOURNAL:J Am Coll Cardiol. Article Link

From Detecting the Vulnerable Plaque to Managing the Vulnerable Patient

A Arbab-Zadeh, V Fuster. Keywords: atherosclerosis; coronary artery disease; coronary heart disease; coronary stenosis; myocardial ischemia

ABSTRACT


The past decades have seen tremendous progress on elucidating mechanisms leading to acute coronary syndrome and sudden cardiac death. Pathology and imaging studies have identified features of coronary atherosclerosis that precede acute coronary events. However, many factors influence the risk of adverse events from coronary atherosclerotic disease and available data support our transition from focusing on individual “vulnerable plaque,” coronary arterial stenosis, and inducible myocardial ischemia to understanding coronary heart disease as multifactorial, chronic disease. The concept of the vulnerable patient has evolved, with the atheroma burden, its metabolic activity, and the disposition to vascular thrombosis building a platform for assessing central aspects of coronary heart disease. In turn, this model has directed us to a focus on controlling the activity of atherosclerotic disease and on modifying the susceptibility of vascular thrombosis which has led to reduced morbidity and mortality from coronary heart disease.