Literature DB >> 12923007

Inflammatory and thrombotic mechanisms in coronary atherosclerosis.

D Tousoulis1, G Davies, C Stefanadis, P Toutouzas, J A Ambrose.   

Abstract

Many molecular and cellular mechanisms link inflammation and haemostatic mechanisms. Inflammation, and perhaps chronic infection, may play important roles in the initiation and progression of atherosclerosis. Atherosclerotic lesions are heavily infiltrated by cellular components associated with inflammation (macrophages and T lymphocytes), and acute plaque rupture is also associated with inflammatory components. Several markers of systemic inflammation may predict future cardiovascular events in apparently healthy subjects as well as in patients with chronic and acute syndromes. There may thus be therapeutic potential in modifying the atherosclerotic, vasomotor, and thrombotic components of ischaemic heart disease.

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Year:  2003        PMID: 12923007      PMCID: PMC1767836          DOI: 10.1136/heart.89.9.993

Source DB:  PubMed          Journal:  Heart        ISSN: 1355-6037            Impact factor:   5.994


  82 in total

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  29 in total

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5.  N-acetyl cysteine suppresses the foam cell formation that is induced by oxidized low density lipoprotein via regulation of gene expression.

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7.  Involvement of Depressive Catecholamines as Thrombosis Risk/Inflammatory Markers in Non-Smoker, Non-Obese Congestive Heart Failure, Linked to Increased Epidermal Growth Factor-Receptor (EGF-R) Production.

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8.  Evaluation of C-Reactive Protein and Fibrinogen in Patients with Chronic and Aggressive Periodontitis: A Clinico-Biochemical Study.

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9.  Deficiency of P-selectin glycoprotein ligand-1 is protective against the prothrombotic effects of interleukin-1β.

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Review 10.  Diabetes and cardiovascular disease: pathophysiology of a life-threatening epidemic.

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