1. In the present study, we sought to determine whether patients with restenosis after coronary stenting possess increased monocyte reactivity, as manifested by a higher level of adhesion molecule expression and an enhanced propensity to form monocyte-platelet aggregates after activation in vitro. 2. Anti-coagulated peripheral venous blood from 24 patients, 10 with and 14 without angiographically verified restenosis, was obtained. Leucocyte antigen expression and the number of leucocyte-platelet complexes were measured by flow cytometry after activation in whole blood. 3. Surface integrin Mac-1 (CD11b/CD18) and VLA-4 (CD49d/ CD29) expression on monocytes and the relative number of monocyte-platelet complexes after in vitro activation were significantly elevated in patients with restenosis compared with patients without restenosis (fluorescence intensities of 1425 +/- 76 vs 1195 +/- 71, 87 +/- 7 vs 65 +/- 6 and 47 +/- 4 vs 29 +/- 3% for for Mac-1, VLA-4 and monocyte-platelet complexes, respectively; P < 0.05 for each parameter). 4. The results suggest that restenosis is associated with increased monocyte VLA-4 and Mac-1 integrin expression and monocyte-platelet complex formation, which can be revealed after activation in vitro.
The slightly elevated Lp(a) concentration along with changes in the level of T lymphocyte subpopulations was first shown to significantly potentiate the risk of progressive and multiple CA lesion in the examinees. The correlation of IgM anti-Lp(a) autoAb with the lymphocyte activation marker sCD25 and that of IgG anti-Lp(a) autoAb with Th1 have demonstrated that Lp(a) is involved in the autoimmune inflammatory processes in atherosclerosis.
Ingramon treatment was accompanied by less pronounced elevation of hsCRP and fibrinogen levels and decreased MCP-1 concentration in plasma in patients after coronary stenting. Ingramon had no effect on MCP-1 interaction with cell receptors or MCP-1 dimerization, but inhibited MCP-1 binding to heparin. The anti-inflammatory activity of the peptide may be mediated by an impaired chemokine interaction with glycosaminoglycans.
Background. Despite the enormous benefits of radial access, this route is associated with a risk of radial artery occlusion (RAO). Objective. We compared the incidence of RAO in patients undergoing transradial coronary angiography and intervention after short versus prolonged hemostasis protocol. Also we assessed the efficacy of rescue 1-hour ipsilateral ulnar artery compression if RAO was observed after hemostasis. Material and Methods. Patients referred for elective transradial coronary procedures were eligible. After 6 F radial sheath removal, patients were randomized to short (3 hours) (n = 495) or prolonged (8 hours) (n = 503) hemostasis and a simple bandage was placed over the puncture site. After hemostasis was completed, oximetry plethysmography was used to assess the patency of the radial artery. Results. One thousand patients were randomized. Baseline characteristics were similar between both groups with average age 61.4 ± 9.4 years (71% male) and PCI performed on half of the patients. The RAO rate immediately after hemostasis was 3.2% in the short hemostasis group and 10.1% in the prolonged group (
p
<
0.001
). Rescue recanalization was successful only in the short group in 56.2% (11/19); at hospital discharge, RAO rates were 1.4% in the short group and 10.1% in the prolonged group (
p
<
0.001
). Conclusion. Shorter hemostasis was associated with significantly less RAO compared to prolonged hemostasis. Rescue radial artery recanalization was effective in > 50%, but only in the short hemostasis group.
Antioxidant probucol in both high (1000 mg) and low (250 mg) daily doses effectively reduced manifestations of oxidative stress in patients with atherosclerosis (assessed by in vivo accumulation of lipoperoxides in atherogenic LDL). When probucol was administered in a dose of 250 mg/day for 7-10 days before transluminal balloon coronary angioplasty and then for 6 months after surgery, the incidence of restenosis decreased to 25% compared to 45% in the control (without probucol therapy). In the group of operated patients receiving probucol (250 mg/day for 6 months) the minimal artery lumen was significantly higher, and the degree of artery occlusion significantly lower than in the control group not treated with probucol.
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