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Spontaneous Coronary Artery Dissection: Pathophysiological Insights From Optical Coherence Tomography Developing a Mobile Application for Global Cardiovascular Education Coronary CT Angiographic and Flow Reserve-Guided Management of Patients With Stable Ischemic Heart Disease Clinical use of intracoronary imaging. Part 1: guidance and optimization of coronary interventions. An expert consensus document of the European Association of Percutaneous Cardiovascular Interventions: Endorsed by the Chinese Society of Cardiology Genetic analyses in a cohort of 191 pulmonary arterial hypertension patients The Impact of Coronary Physiology on Contemporary Clinical Decision Making Physiological Stratification of Patients With Angina Due to Coronary Microvascular Dysfunction Coronary Physiology in the Cardiac Catheterization Laboratory Prognostic Implications of Plaque Characteristics and Stenosis Severity in Patients With Coronary Artery Disease Randomized Comparison of FFR-Guided and Angiography-Guided Provisional Stenting of True Coronary Bifurcation Lesions: The DKCRUSH-VI Trial (Double Kissing Crush Versus Provisional Stenting Technique for Treatment of Coronary Bifurcation Lesions VI)

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.