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- Forsblad, J, et al.
(författare)
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Clinical manifestations of atherosclerosis in an elderly population are related to plasma neopterin, NGAL and endothelin-1, but not to Chlamydia pneumoniae serology.
- 2002
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Ingår i: International Angiology. - 1827-1839. ; 21:2, s. 173-179
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Inflammatory mediators secreted by leukocytes are implicated in atherogenesis. Chlamydia (C.) pneumoniae infection has been suggested as a trigger of this process. We investigated relationships between C. Pneumoniae serology, inflammatory mediators and symptomatic cardiovascular disease in old age. METHODS: In a cross-sectional study at baseline with a prospective 4 year follow-up, intraplatelet cyclic 3'-5'adenosine monophosphate (cAMP) and cyclic 3'-5'guanosine monophosphate (cGMP), plasma neutrophil gelatinase associated lipocalin (NGAL), plasma soluble tumor necrosis factor receptor-1 (TNFR-1) plasma neopterin and plasma endothelin-1 (ET-1) were analysed together with IgG and IgA antibodies for C. Pneumoniae in an elderly reference population (n=140, median age 71 years, 71 females). Twenty-one subjects had clinical manifestations of cardiovascular disease at baseline and another 21 were diagnosed with cardiovascular disease during follow-up. RESULTS: In age adjusted logistic regression, subjects with cardiovascular disease showed higher plasma levels of neopterin (p=0.02), NGAL (p=0.04), and ET-1 (p<0.01). If subjects with cardiovascular disease at baseline were excluded from the analysis, higher plasma neopterin (p=0.01) and lower serum HDL cholesterol (p=0.03) predicted cardiovascular disease during follow-up. The presence of IgG or IgA against C. pneumoniae was not associated with cardiovascular disease. Neither were there any associations between inflammatory or endothelial parameters and C. pneumoniae serology. CONCLUSIONS: The inflammatory mediators neopterin and NGAL and endothelial derived vasoconstrictive ET-1 were increased in elderly subjects with symptomatic cardiovascular disease. Increased plasma neopterin predicted cardiovascular disease during follow-up. No relationships were found between C. Pneumoniae serology and cardiovascular disease.
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- Gottsäter, Anders, et al.
(författare)
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Decreasing plasma endothelin-1 and unchanged plasma neopterin during folate supplementation in hyperhomocysteinemia.
- 2002
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Ingår i: International Angiology. - 1827-1839. ; 21:2, s. 158-164
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Tidskriftsartikel (refereegranskat)abstract
- Hyperhomocysteinemia is a risk factor for atherosclerosis and venous thrombosis, probably exerting its effects through endothelial function. Homocysteine levels are lowered by folate supplementation, and such treatment improves endothelial function. However, whether folate supplementation decreases vascular risk and improves survival is unknown. The aim of this study was to evaluate endothelial function and mononuclear leukocyte inflammatory activity during homocysteine lowering in patients with hyperhomocysteinemia and vascular disease. METHODS: Endothelial function assessed as plasma (p-)endothelin(ET)-1 and intraplatelet cGMP and cAMP, and mononuclear leukocyte inflammatory activity, assessed as p-neopterin were studied during homocysteine lowering in 50 patients with hyperhomocysteinemia and vascular disease, randomized to folate supplementation or no treatment for 3 months. RESULTS: P-homocysteine decreased during the 3 months not only in patients on folate supplementation (from 27 [21-52] to 14 [8-41] &mgr;mol/l; p<0.001), but also in the untreated group (from 23 [20-35] to 19 [4-31] &mgr;mol/l; p<0.001). P-ET-1 decreased during folate supplementation (from 5.7 [2.7-11.6] to 4.1 [1.8-9.0] pg/ml; p<0.01), but was unchanged in the untreated group 4.1 [2.0-9.5] pg/ml and 4.5 [2.7-7.1] pg/ml). P-neopterin was unchanged in patients on folate supplementation (9.7 [5.1-54.4] and 7.6 [5.7-73.0] nmol/l), but increased in the untreated group (from 8.2 [4.7-19.5] to 8.6 [4.6-24.6] nmol/l; p<0.05). Intraplatelet cGMP decrea-sed in patients on folate supplementation (from 0.86 [0.21-2.00] platelets to 0.56 [0.17-1.42] pmol/109 platelets; p<0.05), but was unchanged in the untreated group. No significant differences concerning intraplatelet cAMP occurred in either group. CONCLUSIONS: Folate supplementation in hyperhomocysteinemia is associated with decreasing levels of both ET-1 and intraplatelet cGMP, and the absence of an increase in the levels of the inflammatory mediator neopterin.
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- Mattiasson, Ingrid, et al.
(författare)
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Increased sensitivity to ADP-aggregation in aspirin treated patients with recurrent ischemic stroke?
- 2003
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Ingår i: International Angiology. - 1827-1839. ; 22:3, s. 239-242
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Tidskriftsartikel (refereegranskat)abstract
- AIM: Antiplatelet therapy in order to reduce the platelet aggregability is widely used to prevent recurrent stroke events. Data from several studies indicates that the inter-individual variation concerning the ability of standard doses of aspirin to inhibit platelet aggregation is substantial. The rationale of the present study was to test whether platelet aggregation in whole blood was enhanced in subjects that had suffered an ischemic stroke event under aspirin treatment. METHODS: Two groups of patients were included: 1) patients that have suffered 1 stroke event and were thereafter under continuous treatment with aspirin 75-160 mg once daily (n=17); 2) patients that have suffered at least 2 stroke events, and aspirin 75-160 mg was prescribed after the 1(st) event (n=17). Platelet aggregation was tested in whole blood with collagen (5 microg/mL and 1 microg/mL), ADP (5 microMol/L) and arachidonic acid (0.5 microg/mL). Aggregation was recorded as change in impedance and release of ATP after the addition of a luciferin-luciferase reagent. RESULTS: The inhibitory effect of aspirin tested with arachidonic acid as an agonist was complete in all the tested subjects. Aggregation induced by ADP 5 microMol/L was significantly higher in the subjects with recurrent stroke compared to those with a single stroke, when tested as impedance change. ATP release with ADP as an agonist was the same in both groups. CONCLUSION: The present study gives some indication that differences in ADP-induced aggregation, with a higher remaining aggregating ability after ASA treatment, might be of importance for the risk of stroke recurrence.
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