Platelets and Atherothrombosis: An Essential Role for Inflammation in Vascular Disease — A Review |
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Authors: | Steven R Steinhubl MD L Kristin Newby MD MHS Marc Sabatine MD MPH Shinichiro Uchiyama MD Myles Connor MBBCh FCP FCNeurol Matthias Endres MD Alvaro Avezum MD PhD Eric Wahlberg MD |
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Institution: | 1. Division of Cardiology, University of Kentucky, 900 S. Limestone Avenue, 326 Charles T. Wethington Bldg., Lexington, KY 2. Duke University Medical Center, Durham, NC 3. Division of Cardiovascular Medicine, Brigham and Women’s Hospital, Boston, MA 4. Tokyo Women’s Medical University, School of Medicine, Tokyo, Japan 5. Department of Neurosciences, University of the Witwatersrand, South Africa 6. Klinik und Poliklinik für Neurologie, Charité – Universit?tsmedizin Berlin, Berlin, Germany 7. Dante Pazzanese Institute of Cardiology, S?o Paulo, Brazil 8. Dept of Vascular Surgery, Karolinska University Hospital, Stockholm, Sweden
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Abstract: | Atherothrombosis is the common link between clinical manifestations of arterial vascular disease including ischemic stroke
and acute coronary syndromes, such as unstable angina and acute myocardial infarction. Our understanding of the common pathologic
mechanisms underlying these conditions has significantly increased during the past ten years, yet atherothrombosis as the
“root cause” of a large proportion of cardiovascular and cerebrovascular diseases is largely underappreciated. Although the
classical risk factors of dyslipidemia, smoking, diabetes, hypertension, obesity, and sedentary lifestyle are widely recognized
as being associated with a heightened risk of vascular disease, inflammation of the vascular system during the past decade
has become increasingly regarded as the principal underlying mechanism in the development of clinical atherothrombotic disease.
In addition, platelet-derived inflammatory mediators play an essential role in the pathogenesis of cardiovascular disease,
being involved at all stages of plaque development until their eventual rupture and subsequent formation of a platelet-rich
thrombus. Mounting evidence supports the role of both localized and systemic inflammation in these events. Platelets are central
to vascular inflammatory processes. Thus, inflammation can stimulate local thrombosis and thrombosis can amplify inflammation.
Consequently, antiplatelet therapy for the prevention of serious vascular events may provide a double benefit via an anti-inflammatory
action of the antiplatelet agent in modifying plaque formation and stability and antiplatelet activity that inhibits platelet
aggregation and thrombus formation from occurring following plaque rupture. |
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