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Coronary fractional flow reserve in bifurcation stenoses: what have we learned? Coronary Artery Intraplaque Microvessels by Optical Coherence Tomography Correlate With Vulnerable Plaque and Predict Clinical Outcomes in Patients With Ischemic Angina Joint consensus on the use of OCT in coronary bifurcation lesions by the European and Japanese bifurcation clubs Management of pulmonary hypertension from left heart disease in candidates for orthotopic heart transplantation Local Low Shear Stress and Endothelial Dysfunction in Patients With Nonobstructive Coronary Atherosclerosis Classification and treatment of coronary artery bifurcation lesions: putting the Medina classification to the test Left ventricular remodelling and changes in functional measurements in patients undergoing transcatheter vs surgical aortic valve replacement: a head-to-head comparison Diagnostic accuracy of intracoronary optical coherence tomography-derived fractional flow reserve for assessment of coronary stenosis severity T and small protrusion (TAP) vs double kissing crush technique: Insights from in-vitro models Optimal Fluoroscopic Projections of Coronary Ostia and Bifurcations Defined by Computed Tomographic Coronary Angiography
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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.


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