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Management of two major complications in the cardiac catheterisation laboratory: the no-reflow phenomenon and coronary perforations Advances in Coronary No-Reflow Phenomenon-a Contemporary Review Optimal Stenting Technique for Complex Coronary Lesions Intracoronary Imaging-Guided Pre-Dilation, Stent Sizing, and Post-Dilation A Randomized Trial to Assess Regional Left Ventricular Function After Stent Implantation in Chronic Total Occlusion The REVASC Trial Homeostatic Chemokines and Prognosis in Patients With Acute Coronary Syndromes A Randomized Trial Comparing the NeoVas Sirolimus-Eluting Bioresorbable Scaffold and Metallic Everolimus-Eluting Stents Better Prognosis After Complete Revascularization Using Contemporary Coronary Stents in Patients With Chronic Kidney Disease Management of Patients With NSTE-ACS: A Comparison of the Recent AHA/ACC and ESC Guidelines Long-Term Effect of Ultrathin-Strut Versus Thin-Strut Drug-Eluting Stents in Patients With Small Vessel Coronary Artery Disease Undergoing Percutaneous Coronary Intervention: A Subgroup Analysis of the BIOSCIENCE Randomized Trial Percutaneous Support Devices for Percutaneous Coronary Intervention

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.