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Angiotensin–Neprilysin Inhibition in Heart Failure with Preserved Ejection Fraction Timing of Intervention in Aortic Stenosis Minimizing Permanent Pacemaker Following Repositionable Self-Expanding Transcatheter Aortic Valve Replacement From Focal Lipid Storage to Systemic Inflammation Bioprosthetic valve oversizing is associated with increased risk of valve thrombosis following TAVR Aliskiren, Enalapril, or Aliskiren and Enalapril in Heart Failure Coronary plaque redistribution after stent implantation is determined by lipid composition: A NIRS-IVUS analysis Sex- and Race-Related Differences in Characteristics and Outcomes of Hospitalizations for Heart Failure With Preserved Ejection Fraction Suture- or Plug-Based Large-Bore Arteriotomy Closure: A Pilot Randomized Controlled Trial The Prevalence of Myocardial Bridging Associated with Coronary Endothelial Dysfunction in Patients with Chest Pain and Non-Obstructive Coronary Artery Disease
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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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