Treatment with Simvastatin and Low-dose Aspirin Depresses Thrombin Generation in Patients with Coronary Heart Disease and Borderline-high Cholesterol Levels

2001 ◽  
Vol 85 (02) ◽  
pp. 221-225 ◽  
Author(s):  
Anetta Undas ◽  
Robert Undas ◽  
Jan Brożek ◽  
Andrzej Szczeklik ◽  
Jacek Musiał

SummaryAspirin and statins are beneficial in coronary heart disease across a broad range of cholesterol levels. We assessed the effects of low-dose aspirin (75 mg daily) on thrombin generation in patients with coronary heart disease and average blood cholesterol levels. We also investigated whether in patients with borderline-high cholesterol level who have been already taking aspirin, additional treatment with simvastatin would affect thrombin generation.Seven-day treatment with low-dose aspirin decreased thrombin generation ex vivo only in patients with total cholesterol 5.2 mmol/L. In patients with higher cholesterol levels aspirin had no effect. In these patients, already taking low-dose aspirin, additional three-month simvastatin treatment resulted in a reduction of thrombin generation. This demonstrates that low-dose aspirin depresses thrombin generation only in subjects with desirable blood cholesterol levels, while in others, with borderline-high cholesterol, thrombin formation is being reduced following the addition of simvastatin.

2020 ◽  
Vol 2 (2) ◽  
pp. 44
Author(s):  
Anak Agung Indah Astrijayanti ◽  
Made Krisna Adi Jaya ◽  
Ida Ayu Manik Partha Sutema ◽  
Ni Putu Wulanda Evayanti ◽  
Ni Ketut Tria Purnamisari

Introduction: Coronary heart disease (CHD) is a disorder of heart function due to a lack of blood in the heart muscle due to narrowing of the coronary arteries. Antiplatelet in patients with CHD is a therapy that must be obtained by patients throughout their lives to prevent recurrent attacks and deaths from CHD. In the Province of Bali, especially in Denpasar, there is a lack of information about the type of side effects that occur on antiplatelet medication, so it is necessary to do a related study. Objective: The aim of this study is to identify the type of side effects that occur on antiplatelet medication in patients with CHD. Methods: A cross-sectional study involving 97 patients was done by observed the CHD patients treated with antiplatelet medication. Side effects were evaluate using Naranjo Algorithm. Patients were divided into three groups, including a low dose aspirin user group, clopidogrel user group, and aspirin-clopidogrel combination user group. Results: Antiplatelet side effects that occur in patients include headache (2.06%), diarrhea (1.03%), cyanosis (1.03%), gastrointestinal bleeding (8.25%), heartburn (11.34%), and nausea (6.19%). These side effects only occurred in 31.96% of the total subjects. The incidence of aspirin side effects was significantly greater than clopidogrel as well as aspirin-clopidogrel in combination (p <0.05). Conclusion: Patients with CHD who use antiplatelet agents in the long term to be more aware of the potential side effects that will occur, especially heartburn in chronic low-dose aspirin users. Keywords: Coronary Heart Disease, Side Effects, Antiplatelet, Aspirin, Clopidogrel


1987 ◽  
Vol 57 (01) ◽  
pp. 062-066 ◽  
Author(s):  
P A Kyrle ◽  
J Westwick ◽  
M F Scully ◽  
V V Kakkar ◽  
G P Lewis

SummaryIn 7 healthy volunteers, formation of thrombin (represented by fibrinopeptide A (FPA) generation, α-granule release (represented by β-thromboglobulin [βTG] release) and the generation of thromboxane B2 (TxB2) were measured in vivo in blood emerging from a template bleeding time incision. At the site of plug formation, considerable platelet activation and thrombin generation were seen within the first minute, as indicated by a 110-fold, 50-fold and 30-fold increase of FPA, TxB2 and PTG over the corresponding plasma values. After a further increase of the markers in the subsequent 3 minutes, they reached a plateau during the fourth and fifth minute. A low-dose aspirin regimen (0.42 mg.kg-1.day-1 for 7 days) caused >90% inhibition of TxB2formation in both bleeding time blood and clotted blood. At the site of plug formation, a-granule release was substantially reduced within the first three minutes and thrombin generation was similarly inhibited. We conclude that (a) marked platelet activation and considerable thrombin generation occur in the early stages.of haemostasis, (b) α-granule release in vivo is partially dependent upon cyclo-oxygenase-controlled mechanisms and (c) thrombin generation at the site of plug formation is promoted by the activation of platelets.


2009 ◽  
Vol 101 (04) ◽  
pp. 687-690 ◽  
Author(s):  
Caterina Pettinella ◽  
Mario Romano ◽  
Liborio Stuppia ◽  
Francesca Santilli ◽  
Rossella Liani ◽  
...  

SummaryCOX-1 polymorphism C50T, in complete linkage disequilibrium with the other polymorphism A-842G, has been depicted as a determinant of pharmacological response to aspirin treatment. Whether these polymorphisms exert an effect on response to aspirin both in vitro and ex vivo is still controversial. We geno-typed a population of 148 healthy individuals for the C50T/A-842G haplotype. Thirty of them underwent low-dose aspirin (100 mg daily) treatment for four weeks and were followed up for seven days after withdrawal. In this subgroup, we evaluated the thromboxane-dependence of biochemical and functional indexes used to monitor the antiplatelet effect of low-dose aspirin. Among the 148 subjects studied, 10 were heterozygous for the C50T/A-842G haplotype (6.7%) and only one was homozygous for the 50T/-842G haplotype (0.67%). In the group on low-dose aspirin, serum thromboxane (TX) B2 as well as urinary 11-dehydro-TXB2 and arachidonic acid (AA)-induced aggregation were similarly suppressed in carriers and non-carriers of the 50T/-842G haplotype, with an increase until basal levels of all the parameters within seven days after withdrawal. We found no relationship between the 50T/-842G haplotype and the so-called phenomenon of aspirin resistance. Platelet cyclooxygenase activity, as reflected by serum TXB2, was uniformly and persistently suppressed by low-dose aspirin in both carriers and non carriers of these polymorphisms.


1994 ◽  
Vol 71 (03) ◽  
pp. 284-285 ◽  
Author(s):  
T W Meade ◽  
D J Howarth ◽  
P J Brennan

SummaryThe effects on the haemoglobin level of low dose aspirin and of low intensity oral anticoagulation with warfarin separately and in combination have been established in men aged between 45 and 69 at high risk of ischaemic heart disease. The findings confirm that combined treatment with warfarin and aspirin (WA) leads to a clear excess of minor bleeding episodes over warfarin alone (W) or aspirin alone (A). Each separate treatment on its own (either W or A) leads to an increase in these episodes compared with those on placebo (P) treatment. However, neither combined treatment (WA) nor the separate treatments (W or A) cause a fall in haemoglobin levels over a period of up to two years.


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