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Cardiovascular risk prediction in type 2 diabetes: a comparison of 22 risk scores in primary care settings Flow-Regulated Endothelial S1P Receptor-1 Signaling Sustains Vascular Development Impact of large periprocedural myocardial infarction on mortality after percutaneous coronary intervention and coronary artery bypass grafting for left main disease: an analysis from the EXCEL trial Feasibility and efficacy of the ultrashort side branch dedicated balloon in coronary bifurcation stenting Fractional flow reserve-guided PCI versus medical therapy in stable coronary disease Coronary Optical Coherence Tomography and Cardiac Magnetic Resonance Imaging to Determine Underlying Causes of Myocardial Infarction With Nonobstructive Coronary Arteries in Women Instantaneous Wave-free Ratio versus Fractional Flow Reserve to Guide PCI Left main coronary angioplasty: early and late results of 127 acute and elective procedures Long-term safety and effectiveness of unprotected left main coronary stenting with drug-eluting stents compared with bare-metal stents Outcomes of patients with and without baseline lipid-lowering therapy undergoing revascularization for left main coronary artery disease: analysis from the EXCEL 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.