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Differential prognostic effect of intravascular ultrasound use according to implanted stent length Nonculprit Lesion Plaque Morphology in Patients With ST-Segment–Elevation Myocardial Infarction: Results From the COMPLETE Trial Optical Coherence Tomography Substudys Differential Impact of Heart Failure With Reduced Ejection Fraction on Men and Women Non-invasive detection of coronary inflammation using computed tomography and prediction of residual cardiovascular risk (the CRISP CT study): a post-hoc analysis of prospective outcome data Association of Coronary Artery Calcium With Long-term, Cause-Specific Mortality Among Young Adults Individualized antiplatelet therapy after drug-eluting stent deployment: Implication of clinical trials of different durations of dual antiplatelet therapy Comprehensive comparative effectiveness and safety of first-line antihypertensive drug classes: a systematic, multinational, large-scale analysis Expansion or contraction of stenting in coronary artery disease? Comparison of Outcomes of Percutaneous Coronary Intervention on Native Coronary Arteries Versus on Saphenous Venous Aorta Coronary Conduits in Patients With Low Left Ventricular Ejection Fraction and Impella Device Implantation Achieved or Attempted (from the PROTECT II Randomized Trial and the cVAD Registry) Stroke Rates Following Surgical Versus Percutaneous Coronary Revascularization

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.