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Query: UMLS:C0162871 (abdominal aortic aneurysm)
 8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The association of statins with markers of inflammation, vasoconstriction, and coagulation was evaluated in 325 patients with abdominal aortic aneurysm with respect to statin treatment or not. Variables evaluated included routine laboratory markers, lipids, homocysteine, endothelin-1, matrix metalloproteinases (MMP)-2 and -9, and activated protein C-protein C inhibitor (APC-PCI) complex. Statin-treated patients were more often male (85% vs 75%; P = .024) and had ischemic heart disease (57% vs 19%; P < .0001). They showed lower levels of cholesterol (P < .0001), homocysteine (P = .027), MMP-9 (P = .038), and endothelin-1 (P = .005), and higher levels of APC-PCI complex (P = .042). Differences persisted in logistic regression for cholesterol (P < .0001), APC-PCI complex (P = .034), and homocysteine (P = .021). Statin-treated patients with abdominal aortic aneurysm show higher APC-PCI complex and lower homocysteine levels. Whether this translates into lower risk for aneurysm expansion or rupture will be evident from further follow-up.
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PMID:Associations between statin treatment and markers of inflammation, vasoconstriction, and coagulation in patients with abdominal aortic aneurysm. 1862 84

Abdominal aortic aneurysm is a vascular disease which, despite the fact that it shares common risk factors with atherosclerosis, develops in parallel but as a partly independent process, through different pathogenic mechanisms. The pathogenic mechanisms involve metalloproteinase and collagenase activation, median and adventitial degradation, elastin lysis, vascular smooth cells transformation and apoptosis, collagen production and lysis imbalance combined with excessive inflammatory infiltration. Endothelial cells respond to a number of stimulating factors, including smoking, hypertension and AT1 receptor stimulation and non-uniform distribution of wall stress. Their ability to produce NO is crucial in order to adapt. Endothelial cells contribute to AAA development due to increased oxidative stress which is partly mediated by impaired NO bioavailability due to endothelial dysfunction and NADPH oxidase overexpression. In addition, they express several molecules among which adherence molecules, selectins, endothelin-1, regulating inflammatory infiltration and oxidative stress. Inflammatory cells consist of monocytes, polymorphonuclear neutrophils and lymphocytes and they are involved in the degrading process in the aortic wall by secreting proteolytic enzymes or by releasing interleukins which mediate the inflammation response. Endothelial dysfunction and arterial stiffness reflect on indices like FMD, carotid-femoral PWV and augmentation index, sometimes with controversial results. At present, surgical treatment is the only option provided in patients with large AAA, in particular. Focusing on the emerging role of endothelial cells in AAA pathology may contribute in creating new therapeutic options in a disease which has not yet a well-accepted, implemented pharmaceutical treatment.
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PMID:The Role of Endothelial Dysfunction in Aortic Aneurysms. 2630 38