Endothelium : journal of endothelial cell research
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Meta Analysis Comparative Study
Meta-analysis shows similar risk of thrombosis after drug-eluting stent, bare-metal stent, or angioplasty.
Coronary stent thrombosis remains an important problem after the implantation of different stent types. This study investigates the risk of stent thrombosis associated with the use of drug-eluting stents (DESs), bare-metal stents (BMSs) compared to balloon angioplasty. A meta-analysis of 28 randomized trials involving 5612 versus 7639 versus 2994 patients with coronary heart disease treated with DES, BMS, or balloon angioplasty was therefore performed. ⋯ Comparing incidences of stent thromboses in patients receiving balloon angioplasty or implantation of BMS, the rate of SAT in the balloon angioplasty group (1.7% SAT) versus BMS group (1.8% SAT) was also similar (OR = 0.93, 95% CI 0.61 to 1.4, p < .71). Finally, there was no significant difference in the occurrence of stent thrombosis for the different coatings of DESs. In conclusion, the use of DES was not observed to have a significant effect on stent thrombosis events, compared with the implantation of BMS or balloon angioplasty.
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Plasma levels of endothelin-1 (ET-1) and adrenomedullin (ADM), two opposingly acting peptides, correlate with mortality in endotoxemia, but their measurement is cumbersome. New sandwich assays have been introduced that measure more stable precursor fragments. The objective of this study was to investigate the counterplay of their precursor peptides in septic patients and to compare them with disease severity and other biomarkers. ⋯ Receiver operating characteristics (ROC) curve analysis showed a higher prognostic accuracy of the calculated ratio of both counteracting substances as compared to CT-proET-1 (p = 0.001) and C-reactive protein (CRP) (p = .001) and in the range of MR-proADM (p = .51), procalcitonin (p = 0.22), and the APACHE II score (p = .61). Endothelin-1 and adrenomedullin precursor peptides gradually increase with increasing severities of infection in critically ill patients. The ratio of the two counteracting peptides correlates with mortality and shows a prognostic accuracy to predict adverse outcome comparable to the APACHE II score.
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Endothelial nitric oxide synthase (eNOS) is regulated by phosphorylation of Ser(1177) and Thr(495), which affects NO bioavailability. Cigarette smoke disturbs the eNOS-cGMP-NO pathway and causes decreased NO production. Here the authors investigated the acute effects of cigarette smoke on eNOS phosphorylation, focusing on protein kinases (PKs). ⋯ Cigarette smoke causes a disruption of the enzymatically active eNOS dimers and shifts the eNOS phosphorylation to an inhibitory state. Both effects might lead to reduced NO bioavailability. The shift of the eNOS phosphorylation pattern to an inhibitory state seems to be independent of the PKA and phosphoinositol 3-kinase (PI3-K)/Akt pathways, whereas PKC appears to play a key role.
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Vascular network formation requires several endothelial cell growth factors. These factors have a potent angiogenic effect, and their precise coordination is essential for vascular development. Among them, angiopoietins function through the Tie2 receptor, whose signaling is critical to regulate vascular stabilization and remodeling. ⋯ Interestingly, Angptls also function in angiogenesis through regulating survival and migration of endothelial cells, although Angptls do not bind the angiopoietin receptor Tie2. Currently, Angptls are orphan ligands, but they have been reported to have pleiotropic effects not only on vascular cells but also on metabolism and tumor biology. Here, the authors review current findings relating to the roles of angiopoietins and Angptls in vascular biology and discuss molecular mechanisms relevant to these factors and angiogenesis.
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Although impaired endothelial function is well known in patients with diabetes mellitus (DM), the precise mechanism and the factors that contribute to this dysfunction remain to be clarified. The authors examined the effect of acute hyperglycemia on endothelium-dependent vasodilation in patients with DM or impaired glucose metabolism in vivo by plethysmography. In eight patients with diabetes mellitus or impaired glucose metabolism, the vasodilatory response to acetylcholine at infusion rates of 7.5, 15, and 30 microg/min was studied in the fasting state and at two levels of hyperglycemia, which were achieved by the infusion of glucose, insulin, and somatostatin. ⋯ The FBFR at an acetylcholine infusion rate of 7.5 microg/min was 1.13 +/- 0.07 and 1.19 +/- 0.06 for stages 1 and 2, respectively, compared with 1.36 +/- 0.08 for stage 3 (p < .05). In addition, at an acetylcholine infusion rate of 30 microg/min, the reduction in FBFR was associated with the degree of hyperglycemia (3.72 +/- 0.51, 2.98 +/- 0.42, 2.42 +/- 0.32 for stages 1, 2, and 3 glucose levels, respectively, at an acetylcholine infusion rate of 30 microg/min, p < .05 by analysis of variance [ANOVA]). The results show that the induction of hyperglycemia results in a significant attenuation of endothelial function, and suggests the importance of hyperglycemia in the development of endothelial dysfunction observed in patients with DM or impaired glucose metabolism.