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Dynamic atrioventricular delay programming improves ventricular electrical synchronization as evaluated by 3D vectorcardiography Early Diagnosis of Myocardial Infarction With Point-of-Care High-Sensitivity Cardiac Troponin I Association Between Living in Food Deserts and Cardiovascular Risk Impact of Optimal Medical Therapy on 10-Year Mortality After Coronary Revascularization Heart Failure With Preserved, Borderline, and Reduced Ejection Fraction: 5-Year Outcomes The Astronaut Cardiovascular Health and Risk Modification (Astro-CHARM) Coronary Calcium Atherosclerotic Cardiovascular Disease Risk Calculator Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association Long-Term Outcomes of Biodegradable Versus Second-Generation Durable Polymer Drug-Eluting Stent Implantations for Myocardial Infarction 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC) Canadian Multicenter Chronic Total Occlusion Registry: Ten-Year Follow-Up Results of Chronic Total Occlusion Revascularization

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.