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1.
Chinese Circulation Journal ; (12): 26-30, 2017.
Article in Chinese | WPRIM | ID: wpr-508046

ABSTRACT

Objective: To explore the impact of different atorvastatin doses on platelet function and highreactivity in patients with acute ST-elevation myocardial infarction (STEMI) after emergent percutaneouscoronary intervention (PCI) therapy. Methods:A total of 120 STEMI patients with emergent PCI therapy were randomly divided into 2 groups:Standard group, the patients received atorvastatin 20 mg/day and Intensive group, the patientsreceived atorvastatin 40 mg/day, all patients were treated for 7 days. n=60 in each group. Blood lipids and biochemistry were examined before PCI and 7 days after atorvastatin treatment respectively;platelet fibrin clot strength induced by ADP (MAADP), AA and ADP induced platelet inhibition rate were measured by thrombelastography (TEG) test. Results: With 7 days treatment, compared with Standard group, Intensive group showed decreased MAADP (38.40±17.40) mm vs (45.70±14.50) mm, P0.05. The patients were followed-up for 3 months and the end point events including unstable angina, non-fatal MI, in-stent restenosis, in-stent thrombosis, and cardiovascular death or target vessel revascularization were similar between 2 groups, P>0.05. Conclusion: Early stage and short term administration of high dose atorvastatin could obviously inhibit platelet activity in STEMI patients after emergent PCI;such intensive atorvastatin treatment had no reduction on end point events in 3 months follow-up period.

2.
Chinese Journal of Internal Medicine ; (12): 932-936, 2016.
Article in Chinese | WPRIM | ID: wpr-505542

ABSTRACT

Objective To investigate the effects of different doses of atorvastatin on plasma endothelin and platelet function in acute ST-segment elevation myocardial infarction (STEMI) patients after emergency percutaneous coronary intervention (PCI).Methods A total of 120 patients with acute STEMI treated with emergency PCI were enrolled and randomly divided into 20 mg of atorvastatin treatment group (standard group,n =60),and 40 mg of atorvastatin treatment group (intensive group,n =60).The blood C reactive protein (CRP),blood lipid profiles,plasma endothelin (ET) were measured before atorvastatin treatment and after 7 days of treatment,respectively.The platelet fibrin clot strength induced by ADP (MAADP) was determined by thrombelastography (TEG).Results Seven days after of atorvastatin treatment,the level of plasma ET in intensive group was significantly lower than that in standard group [(0.49 ± 0.21) pmol/L vs (0.63 ± 0.58) pmol/L,P < 0.05].Moreover,the MAADP in intensive group was significantly decreased compared with the standard group [(38.4 ± 17.4) mm vs (45.7 ± 14.5) mm,P < 0.05].There was a positive correlation between the ET level and MAADP in intensive group after treatment (r =0.378,P < 0.05).However,no significantly differences could be viewed in the CRP and LDL-C levels between the two groups (P > 0.05).Conclusion In patients with acute STEMI,early administration of 40 mg atorvastatin after emergency PCI could significantly reduce the vascular endothelial injury,improve endothelial function,and reduce the residual platelet activity.

3.
Journal of Geriatric Cardiology ; (12): 237-240, 2009.
Article in Chinese | WPRIM | ID: wpr-472820

ABSTRACT

Objective To investigate the effects of insulin-like growth factor-1 (IGF-1) and oxidized low density lipoprotein (oxLDL) on expression of phosphatase PHLPP1 in vascular smooth muscle cells (VSMCs).Methods Rabbit aortic VSMCs were cultured.VSMCs proliferation ability was determined by measuring cell number and mitochondrial dehydrogenase (MD) activity with MTT assay.Western blot was used to detect the protein expression of phosphatase PHLPP 1.Results IGF-1 (100μg/L) increased cell number and MD activity to 3.02 and 3.59 times of that in control group.oxLDL(50μg/ ml) elevated the above two parameters to 2.03 and 2.91 times respectively.Western blot showed that IGF-1 and oxLDL inhibited the expression of PHLPP 1 to 39.27% and 40.26% of the control group (P<0.01).Conclusion IGF-1 and oxLDL may enhance the proliferation of VSMCs by decreasing the expression of phosphatase PHLPP1 .

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