ABSTRACT
Objective To investigate the effect and safety of primary percutaneous coronary intervention (PCI) of acute ST-segment elevation myocardial infarction (STEMI) in elderly patients.Methods 103 consecutive patients with STEMI treated by primary PCI were divided into two groups according to the age:the elderly group [aged≥65 years,with a mean age of (75.7 ±6.2) years(n =49],the non-elderly group [aged＜65 years,with a mean age of (43.0±8.6) years(n =54].Clinical characteristics,complications related to PCI procedure and success rate were analyzed,and major cardiovascular events (MACE) were followed up for(5.7 ± 1.2) months.Results The proportion of female,patients with Killip ≥ Ⅲ,three vessels disease and higher level of serum brain natriuretic peptide were higher in elderly group than in non-elderly group (all P＜0.05).No significant difference was observed between the two groups in success rate and complications of PCI procedure (both P＞0.05).Patients were followed up for (5.7± 1.2) months.The in-hospital and one-month mortalities were higher in elderly group than in non-elderly group [8.2％ (4 cases)vs.0％ (0 case),10.2％(5 cases) vs.0 ％ (0 case),respectively,all P＜0.05].There was no significant difference in six-month mortality and MACE between the two groups.Multivariate logistic regression analysis showed that Killip ≥ Ⅲ was related with the increase of one-month mortality in patients with STEMI undergoing primary PCI,whereas age was not.Conclusions Primary PCI is effective and safe in elderly patients with STEMI.
ABSTRACT
<p><b>BACKGROUND</b>Urotensin II (UII), a potent vasoconstrictive peptide, is able to stimulate phenotypic differentiation of adventitial fibroblasts. This study aimed to determine the effect of UII on monocyte chemoattractant protein-1 (MCP-1) expression in rat aortic adventitial fibroblasts, so as to explore possible mechanisms in the development of vascular inflammation.</p><p><b>METHODS</b>Growth-arrested adventitial fibroblasts were incubated in serum-free medium with UII (10(-10)-10(-7) mol/L) and inhibitors of signal transduction pathways for 1 to 24 hours. MCP-1 mRNA and protein expression and secretion were determined by RT-PCR, Western blotting analysis and enzyme-linked immunosorbent assay (ELISA), respectively.</p><p><b>RESULTS</b>UII dose- and time-dependently promoted MCP-1 mRNA and protein expression and secretion in cells, with maximal effect at 10(-8) mol/L at 3 hours for mRNA expression, 24 hours for protein expression in the cells, and 12 hours for protein secretion from the cells. Furthermore, the UII effects were significantly inhibited by treatment with its receptor antagonist SB710411, Rho kinase inhibitor Y27632, protein kinase C (PKC) inhibitor H7, mitogen-activated protein kinase inhibitor PD98059, calcineurin inhibitor cyclosporine A, and the Ca(2+)channel blocker nicardipine.</p><p><b>CONCLUSION</b>UII may stimulate MCP-1 expression in rat aortic adventitial fibroblasts through its receptor and Rho kinase, PKC, mitogen-activated protein kinase, calcineurin and Ca(2+) channel signal transduction, thus contributing to adventitial inflammation.</p>