PubMed · 112424
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G Geissl. 1979-06-29. [Abdominal aortic aneurysms].. https://pubmed.ncbi.nlm.nih.gov/112424/
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The metabolic syndrome is a clustering of low levels of high-density lipoprotein cholesterol, hyperglycemia, high waist circumference, hypertension, and elevated triglycerides, and is associated with cardiovascular disease. Calcified atherosclerotic plaque in the coronary arteries (CAC), measured by cardiac tomographic scans, is a marker for atherosclerosis and relates to mortality. The investigators examined the relation of the metabolic syndrome, and each of its components, to the prevalence of CAC, measured from 2002 to 2004 in 3,166 white and African-American subjects in the National Heart, Lung, & Blood Institute Family Heart Study. Adjusting for age, race, center, smoking, and alcohol consumption, odds ratios and 95% confidence intervals (CI) for a CAC score >100 for subjects with metabolic syndrome were 1.7 (95% CI 1.3 to 2.3) for men and 1.6 (95% CI 1.2 to 2.1) for women. Associations were found for most of the components of the metabolic syndrome with CAC. Associations with the metabolic syndrome were similar for calcified atherosclerotic plaque in the abdominal aorta among 3,173 subjects, with adjusted odds ratios for a score >1,000 of 2.1 (95% CI 1.5 to 3.1) for men and 1.8 (95% CI 1.4 to 2.4) for women. We conclude that the metabolic syndrome and most of its components are associated with a higher prevalence of calcified atherosclerotic plaque in the coronary arteries and abdominal aorta in white and African-American men and women.
OBJECTIVE: It has been suggested that the intraluminal thrombus of abdominal aortic aneurysms (AAAs) predisposes for AAA rupture. Here, we examined the possibility that the intraluminal thrombus influences expression and activity of matrix-degrading proteases in the AAA wall. METHODS AND RESULTS: Twenty patients undergoing elective repair of AAAs were included. From each patient, specimens from both thrombus-covered and thrombus-free wall were taken for analysis. Gene arrays and quantitative real-time polymerase chain reaction showed that matrix metalloproteinase (MMP)-1, -7, -9, and -12 expressions were upregulated in the thrombus-free wall compared with the thrombus-covered wall. Immunohistochemistry confirmed the differential expression of MMP-9 but also localized MMP-9 to the interface between the thrombus and the underlying vessel wall. MMP-9 expression was colocalized with the presence of macrophages. Similar expression patterns were observed for urokinase plasminogen activator (uPA), uPA receptor, and plasminogen activator inhibitor-1. Gelatinase activity was detected in the same regions as MMP-9 protein expression, ie, within the thrombus-free wall and in the interface between the thrombus and the underlying wall. CONCLUSIONS: The present work demonstrates that protease expression and activity differs within the aneurysm wall. The source and activity of the proteases responsible for the degradation of the thrombus-covered wall need to be further determined.
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