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Transcatheter versus Surgical Aortic Valve Replacement in Patients with Prior Cardiac Surgery in the Randomized PARTNER 2A Trial Predictors of high residual gradient after transcatheter aortic valve replacement in bicuspid aortic valve stenosis Health Status After Transcatheter Versus Surgical Aortic Valve Replacement in Low-Risk Patients With Aortic Stenosis Predictors and Clinical Outcomes of Next-Day Discharge After Minimalist Transfemoral Transcatheter Aortic Valve Replacement Prevalence and Outcomes of Concomitant Aortic Stenosis and Cardiac Amyloidosis Online Quantitative Aortographic Assessment of Aortic Regurgitation After TAVR: Results of the OVAL Study Third-Generation Balloon and Self-Expandable Valves for Aortic Stenosis in Large and Extra-Large Aortic Annuli From the TAVR-LARGE Registry Five-Year Outcomes of Transcatheter or Surgical Aortic-Valve Replacement From organic and inorganic phosphates to valvular and vascular calcifications Discrepancies in Measurement of the Thoracic Aorta: JACC Review Topic of the Week

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.