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Radionuclide Image-Guided Repair of the Heart Left Ventricular Assist Devices for Lifelong Support Association of Thrombus Aspiration With Time and Mortality Among Patients With ST-Segment Elevation Myocardial Infarction: A Post Hoc Analysis of the Randomized TOTAL Trial Coronary flow velocity reserve predicts adverse prognosis in women with angina and noobstructive coronary artery disease: resultsfrom the iPOWER study 稳定性冠心病诊断与治疗指南 Cardiovascular Biomarkers and Imaging in Older Adults: JACC Council Perspectives 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Guiding Principles for Chronic Total Occlusion Percutaneous Coronary Intervention Statin Safety and Associated Adverse Events: A Scientific Statement From the American Heart Association Ticagrelor plus aspirin for 1 month, followed by ticagrelor monotherapy for 23 months versus aspirin plus clopidogrel or ticagrelor for 12 months, followed by aspirin monotherapy for 12 months after implantation of a drug-eluting stent: a multicenter, open-label, randomized superiority trial

Review ArticleVolume 74, Issue 12, September 2019

JOURNAL:J Am Coll Cardiol. Article Link

From Focal Lipid Storage to Systemic Inflammation

P Libby, GK Hansson. Keywords: inflammation; LDL cholesterol; smooth muscle cell

ABSTRACT


Concepts of atherogenesis have evolved considerably with time. Early animal experiments showed that a cholesterol-rich diet could induce fatty lesion formation in arteries. The elucidation of lipoprotein metabolism ultimately led to demonstrating the clinical benefits of lipid lowering. The view of atheromata as bland accumulations of smooth muscle cells that elaborated an extracellular matrix that could entrap lipids then expanded to embrace inflammation as providing pathways that could link risk factors to atherogenesis. The characterization of leukocyte adhesion molecules and their control by proinflammatory cytokines, the ability of chemokines to recruit leukocytes, and the identification of inflammatory cell subtypes in lesions spurred the unraveling of innate and adaptive immune pathways that contribute to atherosclerosis and its thrombotic complications. Such pathophysiologic insights have led to the identification of biomarkers that can define categories of risk and direct therapies and to the development of new treatments.