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Infective Endocarditis After Transcatheter Aortic Valve Replacement Relationship Between Hospital Surgical Aortic Valve Replacement Volume and Transcatheter Aortic Valve Replacement Outcomes Decline in Left Ventricular Ejection Fraction During Follow-Up in Patients With Severe Aortic Stenosis Ascending Aortic Length and Risk of Aortic Adverse Events: The Neglected Dimension Coronary Protection to Prevent Coronary Obstruction During TAVR: A Multicenter International Registry Infective endocarditis after transcatheter aortic valve implantation: a nationwide study Leaflet immobility and thrombosis in transcatheter aortic valve replacement Determinants and Impact of Heart Failure Readmission Following Transcatheter Aortic Valve Replacement Left Ventricular Rapid Pacing Via the Valve Delivery Guidewire in Transcatheter Aortic Valve Replacement Computed tomography angiography-derived extracellular volume fraction predicts early recovery of left ventricular systolic function after transcatheter aortic valve replacement
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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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