scholarly journals Effect of Oral Anti-platelet Regimens on Platelet Aggregation using Chronolog Light Transmittance Aggregometry in Coronary Heart Disease Patients: An Observational Study

Author(s):  
Usharani P.
2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Hui Feng ◽  
Zhipeng Wang ◽  
Changsong Wang ◽  
Xinyi Zhu ◽  
Zhigang Liu ◽  
...  

Aim. To investigate the effect of Furostanol Saponins from Allium Macrostemon Bunge Bulbs (FSAMB) on platelet aggregation rate of rats with coronary heart disease and discuss the mechanism of FSAMB affecting the platelet aggregation rate through PI3K/Akt pathway. We established the rat models with coronary heart disease (CHD) and prepared the platelet-rich plasma. The effect of different concentrations of FSAMB on platelet aggregation in SD rats induced by ADP was observed in vitro and in vivo. And Lactate Dehydrogenase (LDH), Creatine Kinase-MB Form (CK-MB), and Cardiac Troponin I (cTnI) are detected in the blood to know the level of damage to heart cells. The expansion of platelets in the immobilized fibrinogen in different concentrations of FSAMB was observed. Western blot was conducted to detect the phosphorylation level of protein kinase B (also known as Akt) and the expression level of phosphoinositide 3-kinase (PI3K). We found that FSAMB had a significant inhibitory effect on the ADP-induced platelet aggregation in vitro. Intragastric administration of FSAMB also inhibited platelet aggregation induced by ADP in rats. LDH, CK-MB, and cTnI levels in serum of rats in FSAMB (672 mg/kg) group were lower than those in the model control group after the intervention (P<0.01 or P<0.05). FSAMB inhibited the expansion of platelets on immobilized fibrinogen. Also, FSAMB inhibited ADP-induced platelet PI3K expression and Akt phosphorylation. The inhibition of Akt phosphorylation by FSAMB was more obvious after the inhibition of the expression of PI3K. This study demonstrated that FSAMB can reduce the degree of myocardial cell damage and inhibit ADP-induced platelet aggregation in SD rats, possibly by inhibiting platelet PI3K/Akt signaling pathway in vitro and in vivo.


1977 ◽  
Author(s):  
K. Oversohl ◽  
W. Theiss ◽  
C.S. So ◽  
K.F. Seidl

Increased platelet adhesion and aggregation has been reported in patients suffering from rheumatic valvular heart disease and from atherosclerotic heart disease. We therefore measured spontaneous aggregation “PAT III” (Breddin) and ADP-induced platelet aggregation (Born) in 141 patients who underwent cardiac catheterization. There were 50 patients with coronary heart disease, 41 with valvular heart disease, 18 with cardiomyopathy; 32 with normal findings at catheterization served as control group.In comparison to controls, patients with coronary heart disease had significantly increased aggregation. Subdivision into 1, 2, or 3 vessel disease revealed no significant differences. Patients with valvular heart disease also had significantly increased aggregation. This appears to be particularly the case after valvular grafting. Cardiomyopathies were not associated with increased platelet aggregation.


2009 ◽  
Vol 210 (S651) ◽  
pp. 101-109 ◽  
Author(s):  
Erik Thaulow ◽  
John Kjekshus ◽  
Jan Erikssen

1997 ◽  
Vol 62 (2) ◽  
pp. 151-154 ◽  
Author(s):  
Antonio de Padua Mansur ◽  
Bruno Caramelli ◽  
Caio Brito Vianna ◽  
Dalton Chamone ◽  
José Antonio F Ramires

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