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Extracorporeal Ultrafiltration for Fluid Overload in Heart Failure: Current Status and Prospects for Further Research Colchicine Inhibits Neutrophil Extracellular Trap Formation in Patients With Acute Coronary Syndrome After Percutaneous Coronary Intervention FFR-guided multivessel stenting reduces urgent revascularization compared with infarct-related artery only stenting in ST-elevation myocardial infarction: A meta-analysis of randomized controlled trials Optimal Timing of Intervention in NSTE-ACS Without Pre-Treatment The EARLY Randomized Trial Prognostic and Practical Validation of Current Definitions of Myocardial Infarction Associated With Percutaneous Coronary Intervention Recommendations for Institutions Transitioning to High-Sensitivity Troponin Testing JACC Scientific Expert Panel Galectin-3 Levels and Outcomes After Myocardial Infarction: A Population-Based Study A Novel Algorithm for Treating Chronic Total Coronary Artery Occlusion Characterization of lesions undergoing ischemia-driven revascularization after complete revascularization versus culprit lesion only in patients with STEMI and multivessel disease - A DANAMI-3-PRIMULTI substudy Long-Term Outcomes of Patients With Late Presentation of ST-Segment Elevation Myocardial Infarction

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.