Inflammation, atherosclerosis, and coronary artery disease.

By G. Hansson. 2005

4,189 citations recorded by the source corpus.

ecent research has shown that inflammation plays a key role in coronary artery disease (CAD) and other manifestations of atherosclerosis. Immune cells dominate early atherosclerotic lesions, their effector molecules accelerate progression of the lesions, and activation of inflammation can elicit acute coronary syndromes. This review highlights the role of inflammation in the pathogenesis of atherosclerotic CAD. It will recount the evidence that atherosclerosis, the main cause of CAD, is an inflammatory disease in which immune mechanisms interact with metabolic risk factors to initiate, propagate, and activate lesions in the arterial tree. A decade ago, the treatment of hypercholesterolemia and hypertension was expected to eliminate CAD by the end of the 20th century. Lately, however, that optimistic prediction has needed revision. Cardiovascular diseases are expected to be the main cause of death globally within the next 15 years owing to a rapidly increasing prevalence in developing countries and eastern Europe and the rising incidence of obesity and diabetes in the Western world. 1 Cardiovascular diseases cause 38 percent of all deaths in North America and are the most common cause of death in European men under 65 years of age and the second most common cause in women. These facts force us to revisit cardiovascular disease and consider new strategies for prediction, prevention, and treatment.

Subfields: Epidemiology, Immunology, Molecular Biology

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Citations in the corpus

Patients with severe psoriasis are at increased risk of cardiovascular mortality: cohort study using the General Practice Research Database. (2010, background): “For example, helper T-cells type 1 (Th-1) chronic inflammation characteristic of psoriasis is also central to the pathophysiology of other conditions such as insulin resistance, atherosclerosis, and plaque rupture leading to thrombotic events.(6,7)”
Burnout and risk of cardiovascular disease: evidence, possible causal paths, and promising research directions. (2006, background): “Recent studies provide evidence indicating a link between inflammation, atherosclerosis, and CVD (Hansson, 2005; Koenig, 2001; Libby, Ridker, & Maseri, 2002; Ross, 1999) and the pathogenesis of Type 2 diabetes (Pickup, 2004).”
Role of platelet-derived growth factors in physiology and medicine. (2008, positive): “Lipoprotein retention and the infiltration and activation of different types of immune cells are believed to play key roles (Figure 10; Hansson 2005).”
The multifaceted contributions of leukocyte subsets to atherosclerosis: lessons from mouse models (2008, background): “This local endothelial-cell defect promotes the adhesion of leukocytes and activated platelets to the damaged endothelium and leads to an increase in the permeability of blood vessels for lipid components in the plasma, such as low-density lipoprotein (LDL”
The Impact of High-Intensity Interval Training Versus Moderate-Intensity Continuous Training on Vascular Function: a Systematic Review and Meta-Analysis (2015, neutral): “turn aggravate vascular dysfunction [74].”
Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel (2020, background): “to the oxidative modification of LDL and thus to the pathogenesis of accelerated atherosclerosis.(285,286) Furthermore, recent data suggest”