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Transcatheter Aortic-Valve Replacement with a Self-Expanding Valve in Low-Risk Patients Transcatheter Aortic-Valve Replacement with a Balloon-Expandable Valve in Low-Risk Patients Early Versus Standard Discharge After Transcatheter Aortic Valve Replacement: A Systematic Review and Meta-Analysis Precision Medicine in TAVR: How to Select the Right Device for the Right Patient A prospective, randomised trial of transapical transcatheter aortic valve implantation vs. surgical aortic valve replacement in operable elderly patients with aortic stenosis: the STACCATO trial Association Between Diastolic Dysfunction and Health Status Outcomes in Patients Undergoing Transcatheter Aortic Valve Replacement Transcatheter or Surgical Aortic-Valve Replacement in Intermediate-Risk Patients Surgical or Transcatheter Aortic-Valve Replacement in Intermediate-Risk Patients Preventing Coronary Obstruction During Transcatheter Aortic Valve Replacement From Computed Tomography to BASILICA Transcatheter Laceration of Aortic Leaflets to Prevent Coronary Obstruction During Transcatheter Aortic Valve Replacement: Concept to First-in-Human
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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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