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Assessment of coronary atherosclerosis by IVUS and IVUS-based imaging modalities: progression and regression studies, tissue composition and beyond Frailty Is Intertwined With Heart Failure: Mechanisms, Prevalence, Prognosis, Assessment, and Management Comparison of intravascular ultrasound guided versus angiography guided drug eluting stent implantation: a systematic review and meta-analysis Phenomapping for Novel Classification of Heart Failure With Preserved Ejection Fraction Surgery Does Not Improve Survival in Patients With Isolated Severe Tricuspid Regurgitation Temporal Trends in Inpatient Use of Intravascular Imaging Among Patients Undergoing Percutaneous Coronary Intervention in the United States Positive recommendation for angiotensin receptor/neprilysin inhibitor: First medication approval for heart failure without "reduced ejection fraction" Derivation, Validation, and Prognostic Utility of a Prediction Rule for Nonresponse to Clopidogrel: The ABCD-GENE Score 6-Month Versus 12-Month Dual-Antiplatelet Therapy Following Long Everolimus-Eluting Stent Implantation: The IVUS-XPL Randomized Clinical Trial Cardiovascular biomarkers in patients with acute decompensated heart failure randomized to sacubitril-valsartan or enalapril in the PIONEER-HF trial

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.