Atherogenesis and Inflammation
Daisuke Shishikura
Search for more papers by this authorYanti Octavia
Search for more papers by this authorUmair Hayat
Search for more papers by this authorVikas Thondapu
Search for more papers by this authorPeter Barlis
Search for more papers by this authorDaisuke Shishikura
Search for more papers by this authorYanti Octavia
Search for more papers by this authorUmair Hayat
Search for more papers by this authorVikas Thondapu
Search for more papers by this authorPeter Barlis
Search for more papers by this authorGeorge D. Dangas MD, MACC, MSCAI, FAHA, FESC
Professor of Medicine (Cardiology) & Surgery (Vascular) Professor of Cardiology Adjunct Professor of Internal Medicine
Icahn School of Medicine at Mount Sinai, Mount Sinai Hospital, New York, NY, USA
National Kapodistrian University of Athens, Greece
Medical University of Vienna, Austria
Search for more papers by this authorCarlo Di Mario MD, PhD, FRCP, FACC, FSCAI, FESC
Professor of Cardiology Director of the Structural Interventional Cardiology Division Honorary Consultant
University of Florence
University Hospital Careggi, Florence, Italy
Cardiologist Royal Brompton Hospital, London, UK
Search for more papers by this authorHolger Thiele MD
Professor of Cardiology at University of Leipzig
Heart Center Leipzig at University of Leipzig, Leipzig, Germany
Search for more papers by this authorPeter Barlis MBBS, MPH, PHD, FACC, FESC, FRACP
Professor of Cardiology Interventional Cardiologist
University of Melbourne, Melbourne, Victoria, Australia
St Vincent's & Northern Hospitals Victoria, Australia
Search for more papers by this authorSummary
This chapter reviews the multifaceted pathology of atherosclerosis leading to plaque progression and destabilisation, with a recent update in coronary imaging modalities and novel developments in computer modelling as promising tools to help improve the understanding of cardiovascular diseases. Acute inflammation involves the rapid recruitment of neutrophils and the stimulation of the endothelium, both type I and type II activation. Enormous researches demonstrated that the oxidisation of low-density lipoprotein particles including reactive oxygen species formation in the intimal wall due to metal ion catalysis could initiate atherogenesis. Anatomical characteristics of vulnerable plaques which are prone to rupture were identified by the histological studies to have fibrous caps that are thin and rich in macrophages overlying a lipid pools. In atherosclerotic plaques, neovascularization proliferates from the adventitia into the arterial wall in order to supply nutrition and inflammatory cell accumulation to the lesion.
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