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DAPT Duration

Abstract

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Clopidogrel or ticagrelor in acute coronary syndrome patients treated with newer-generation drug-eluting stents: CHANGE DAPT A prospective, randomized, open-label trial of 6-month versus 12-month dual antiplatelet therapy after drug-eluting stent implantation in ST-elevation myocardial infarction: Rationale and design of the State of the art: duration of dual antiplatelet therapy after percutaneous coronary intervention and coronary stent implantation – past, present and future perspectives A Genotype-Guided Strategy for Oral P2Y12 Inhibitors in Primary PCI One-year outcome of a prospective trial stopping dual antiplatelet therapy at 3 months after everolimus-eluting cobalt-chromium stent implantation: ShortT and OPtimal duration of Dual AntiPlatelet Therapy after everolimus-eluting cobalt-chromium stent (STOPDAPT) trial Rationale and design of the comparison between a P2Y12 inhibitor monotherapy versus dual antiplatelet therapy in patients undergoing implantation of coronary drug-eluting stents (SMART-CHOICE): A prospective multicenter randomized trial Derivation, Validation, and Prognostic Utility of a Prediction Rule for Nonresponse to Clopidogrel: The ABCD-GENE Score Impact of age on the comparison between short-term vs 12-month dual antiplatelet therapy in patients with acute coronary syndrome treated with the COMBO dual therapy stent: 2-Year follow-up results of the REDUCE trial
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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.


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