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Superficial Calcium Fracture After PCI as Assessed by OCT Long-Term Clinical Outcomes and Optimal Stent Strategy in Left Main Coronary Bifurcation Stenting Transthoracic echocardiography for the evaluation of children and adolescents with suspected or confirmed pulmonary hypertension. Expert consensus statement on the diagnosis and treatment of paediatric pulmonary hypertension. The European Paediatric Pulmonary Vascular Disease Network, endorsed by ISHLT and D6PK Sotatercept for the Treatment of Pulmonary Arterial Hypertension Machine Learning Using CT-FFR Predicts Proximal Atherosclerotic Plaque Formation Associated With LAD Myocardial Bridging Autologous CD34+ Stem Cell Therapy Increases Coronary Flow Reserve and Reduces Angina in Patients With Coronary Microvascular Dysfunction Medical Therapy for CTEPH: Is There Still Space for More? Self-expandable sirolimus-eluting stents compared to second-generation drug-eluting stents for the treatment of the left main: A propensity score analysis from the SPARTA and the FAILS-2 registries Dual Antiplatelet Therapy after PCI in Patients at High Bleeding Risk Pancoronary Plaque Characteristics in STEMI Caused by Culprit Plaque Erosion Versus Rupture: 3-Vessel OCT Study

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.