Smoking and lipoprotein abnormalities on platelet aggregation in coronary heart disease

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

scholarly journals Effect of Furostanol Saponins from Allium Macrostemon Bunge Bulbs on Platelet Aggregation Rate and PI3K/Akt Pathway in the Rat Model of Coronary Heart Disease

2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Hui Feng ◽  
Zhipeng Wang ◽  
Changsong Wang ◽  
Xinyi Zhu ◽  
Zhigang Liu ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Platelet Aggregation ◽  
Akt Phosphorylation ◽  
Aggregation Rate ◽  
Furostanol Saponins ◽  
Sd Rats ◽  
Allium Macrostemon

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.

scholarly journals Platelet Aggregation in Heart Disease

1977 ◽  
Author(s):  
K. Oversohl ◽  
W. Theiss ◽  
C.S. So ◽  
K.F. Seidl
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Platelet Aggregation ◽  
Cardiac Catheterization ◽  
Valvular Heart Disease ◽  
Platelet Adhesion ◽  
Control Group ◽  
Vessel Disease ◽  
Platelet Adhesion And Aggregation ◽  
Spontaneous Aggregation

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.

EFFECT OF TIMOLOL ON PLATELET AGGREGATION IN CORONARY HEART DISEASE

2009 ◽  
Vol 210 (S651) ◽  
pp. 101-109 ◽  
Author(s):  
Erik Thaulow ◽  
John Kjekshus ◽  
Jan Erikssen
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Platelet Aggregation

scholarly journals Association of ITGB3, P2RY12, and CYP2C19 gene polymorphisms with platelet functional activity in patients with coronary heart disease during dual antiplatelet therapy

2017 ◽  
Vol 89 (5) ◽  
pp. 74-78 ◽  
Author(s):  
E F Muslimova ◽  
S A Afanasiev ◽  
T Yu Rebrova ◽  
T N Sergienko ◽  
A N Repin
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Platelet Aggregation ◽  
Antiplatelet Therapy ◽  
Gene Polymorphisms ◽  
Receptor Gene ◽  
Platelet Receptor ◽  
Cyp2c19 Gene ◽  
Allele Specific ◽  
Receptor Gene Polymorphisms

Aim. To assess the association of CYP2C19 G681A, P2RY12 H1/H2, and ITGB3 T1565C polymorphisms with the extent of platelet aggregation in patients with coronary heart disease (CHD) during antiplatelet therapy. Subjects and methods. 166 male patients with CHD, living in the Western Siberian Region, were examined. All the patients underwent a test for platelet aggregation induced by ADP (2.5 and 5.0 µm) and epinephrine (0.2 µm). Genotyping was performed using an allele-specific polymerase chain reaction technique. Results. The polymorphic variants of the P2RY12 and ITGB3 genes were ascertained to have no impact on the extent of platelet aggregation in patients receiving clopidogrel and acetylsalicylic acid. An association was found between CYP2C19 681A allele carriage and the increased extent of platelet aggregation induced by ADP. Conclusion. The carriage of the cytochrome P450 CYP2C19 681A allele rather than platelet receptor gene polymorphisms determines a risk for clopidogrel resistance in patients with CHD.

scholarly journals Use of increased concentrations of adenosinediphosphate for high residual platelet reactivity in patients with coronary heart disease

2021 ◽  
Vol 70 (1) ◽  
pp. 129-132
Author(s):  
O.A. Trubacheva ◽  
S.N. Belyaeva ◽  
T.E. Suslova ◽  
I.V. Petrova
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Platelet Aggregation ◽  
Antiplatelet Therapy ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Transmission Curve ◽  
Platelet Suspension

Detection of a tendency to increased thrombosis in patients with coronary heart disease (CHD) is of important prognostic value in the selection of drugs aimed at achieving a persistent antithrombotic effect. The aim of the study was to evaluate the use of elevated ADP inducer concentrations to improve the accuracy of ADP-induced platelet aggregation in patients with coronary heart disease. Material and method. Material and method. We studied 48 patients with CHD who were on continuous double antiplatelet therapy for 6 months (aspirin 75mg and clopidogrel 75mg per day). The aggregation activity of the platelet suspension was studied using the Born method G. in the modification of Gabbasov Z. A. Platelet activity was evaluated by the degree of aggregation of platelet-rich plasma along the light transmission curve under the influence of the inducer adenosine diphosphate (ADP) at a concentration of 2 mmol/l and by its own patented method against the background of additional ADP application. Results. In patients, platelet aggregation decreased to 5-35% (p<0.005) compared to the standard values, which are 50-60%. The values of platelet aggregation with the additional introduction of the inducer of aggregation ADP in a ratio of 2:1 to 2 µmol/l for 1, 2, 3, and 4-minute registration of platelet aggregation, resulted in increased aggregation from 55% to 75% (p<0.001), indicating high residual platelet reactivity on the background of double antiplatelet therapy. Correlations of the degree of aggregation for elevated ADP concentrations with multivessel arterial lesion and dyslipidemia were also found, r=0.86 and r=0.92, respectively. Conclusion. The use of elevated concentrations of adenosine diphosphate in platelet aggregation in patients with ischemic heart disease increases the accuracy of assessing ADP-induced platelet aggregation against the background of dual antiplatelet therapy and contributes to the detection of high residual platelet reactivity.

scholarly journals Resistance to Acetylsalicylic Acid in Patients with Coronary Heart Disease Is the Result of Metabolic Activity of Platelets

2020 ◽  
Vol 13 (8) ◽  
pp. 178
Author(s):  
Yuriy I. Grinshtein ◽  
Andrei A. Savchenko ◽  
Aleksandra A. Kosinova ◽  
Maxim D. Goncharov
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Artery Bypass ◽  
Postoperative Treatment ◽  
Oxygen Species ◽  
Before And After ◽  
Aggregation Activity ◽  
Cabg Patients

Sensitivity to acetylsalicylic acid (ASA) is important in the treatment of patients with coronary heart disease (CHD) after coronary artery bypass grafting (CABG). Patients were divided into ASA sensitive (sASA) and ASA resistant (rASA) by the activity of platelet aggregation induced arachidonic acid (ARA) together with ASA. Induced platelet aggregation activity was studied in sASA and rASA patients with CHD before and after CABG. The level of synthesis of primary and secondary reactive oxygen species (ROS) by platelets was determined using chemiluminescent analysis. The activity of NAD- and NADP-dependent dehydrogenases in platelets was determined by the bioluminescent method. It was found that the aggregation activity of platelets depended on the sensitivity of CHD patients to ASA and decreased during postoperative ASA therapy. The most pronounced differences in metabolic parameters of platelets in sASA and rASA patients were detected by Nox2 activity. The synthesis of secondary ROS by platelets of CHD patients did not depend on the sensitivity of patients to ASA but increased during postoperative treatment with ASA. The activity of NAD(P)-dependent dehydrogenases in platelets did not differ in sASA and rASA patients with CHD.

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