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Bleeding-Related Deaths in Relation to the Duration of Dual-Antiplatelet Therapy After Coronary Stenting Left-main restenosis in the DES era-a call for action Aggressive Measures to Decrease Causes of delay and associated mortality in patients transferred with ST-segment-elevation myocardial infarction Nonsystem reasons for delay in door-to-balloon time and associated in-hospital mortality: a report from the National Cardiovascular Data Registry High-Sensitivity Troponins and Outcomes After Myocardial Infarction Comparison of Benefit of Successful Percutaneous Coronary Intervention for Chronic Total Occlusion in Patients With Versus Without Reduced (≤40%) Left Ventricular Ejection Fraction Intravascular ultrasound guidance of percutaneous coronary intervention in ostial chronic total occlusions: a description of the technique and procedural results DK CRUSH系列研究总结 White Blood Cell Count and Major Adverse Cardiovascular Events After Percutaneous Coronary Intervention in the Contemporary Era: Insights From the PARIS Study (Patterns of Non-Adherence to Anti-Platelet Regimens in Stented Patients Registry)

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.