PubMed · 15505863
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
David R Holmes. 2004. A view from within.. https://doi.org/10.1002/ccd.20208
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
The pathological remodeling of the arterial wall in atherosclerosis involves protease activities, which play a major role in complications, through plaque rupture. Here, we investigated the release of active proteases by human carotid plaques in relation to (1) the degree of lesion complexity and (2) their compartmentalization between cap, core and media. Eighty human carotid endarterectomy specimens were dissected into culprit stenosing (CPs) and adjacent non-complicated/non-stenosing plaques (NPs). Thirty-five additional CPs were microdissected into cap, core and media. All specimens were compared to control non-atherosclerotic endarteries for the release of components of the plasminogen/plasmin system and matrix metalloproteinases (MMPs). Results show a greater release of the plasminogen activators (PAs), plasmin and active MMPs by CPs compared to NPs, whereas healthy arteries released even lower levels. Furthermore, we highlight a functional interaction between these proteases in human atherosclerotic tissues and more importantly, we demonstrate that the core constitutes the main source of protease activities within CPs. Together, these results suggest that CPs generate plasmin, mainly in the core, which could in turn participate in MMP activation and the onset of complications.
Explore the source record for details and available documents.
BACKGROUND: Although the metabolic syndrome can predict cardiovascular events in middle-aged individuals, data on its association with the progression of subclinical atherosclerosis, particularly in elderly women, are limited. We investigated the association of the metabolic syndrome with the progression of carotid intima-media thickness (IMT) in elderly women. METHODS: We performed a 12-year follow-up study in a population-based sample of 101 women (age range at baseline, 60-70 years). All study variables were measured at baseline and 12 years later. We used the National Cholesterol Education Program definition for metabolic syndrome (> or =3 of 5 risk factors) and quantified carotid IMT noninvasively by ultrasonography. RESULTS: The prevalence of metabolic syndrome increased from 13% at baseline to 46% after 12 years of follow-up (P<.001). The mean +/- SD IMT increased by 21% (from 1.05 +/- 0.31 mm to 1.27 +/- 0.38 mm) during 12 years (P<.001). Among the individuals without metabolic syndrome at baseline, the increase in carotid IMT was greater in 34 women who developed metabolic syndrome during 12 years (0.31 +/- 0.37 mm) than in 54 women who did not (0.16 +/- 0.25 mm) after adjustment for age, prevalent cardiovascular diseases, physical activity, smoking, alcohol intake, serum low-density lipoprotein cholesterol level, use of cholesterol-lowering medication, carotid IMT, and National Cholesterol Education Program metabolic risk score at baseline (P = .04 for difference). CONCLUSION: Incident metabolic syndrome is associated with accelerated progression of carotid IMT in elderly women.