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Association Between Malignant Mitral Valve Prolapse and Sudden Cardiac Death: A Review Italian Society of Interventional Cardiology (GIse) Registry Of Transcatheter Treatment of Mitral Valve RegurgitaTiOn (GIOTTO): Impact of Valve Disease Etiology and Residual Mitral Regurgitation after MitraClip Implantation Initial experience with percutaneous mitral valve repair in patients with cardiac amyloidosis Closure of Iatrogenic Atrial Septal Defect Following Transcatheter Mitral Valve Repair: The Randomized MITHRAS Trial Transcatheter Interventions for Tricuspid Valve Disease: What to Do and Who to Do it On Risk of Atrial Fibrillation According to Cancer Type: A Nationwide Population-Based Study Italian Society of Interventional Cardiology (GIse) Registry Of Transcatheter Treatment of Mitral Valve RegurgitaTiOn (GIOTTO): Impact of Valve Disease Etiology and Residual Mitral Regurgitation after MitraClip Implantation Percutaneous left atrial appendage occlusion: the Munich consensus document on definitions, endpoints, and data collection requirements for clinical studies Novel Transcatheter Mitral Valve Prosthesis for Patients With Severe Mitral Annular Calcification The Tricuspid Annular Plane Systolic Excursion to Systolic Pulmonary Artery Pressure Index: Association With All-Cause Mortality in Patients With Moderate or Severe Tricuspid Regurgitation

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.