Impact of Treatment with Acetylsalicylic Acid on the Proaggregatory Effects of Adrenaline in vitro in Patients with Stable Angina Pectoris: Influence of the Anticoagulant

1993 ◽  
Vol 85 (5) ◽  
pp. 577-583 ◽  
Author(s):  
N. Håkan Wallén ◽  
Claes Held ◽  
Nina Rehnqvist ◽  
Paul Hjemdahl
Keyword(s):  
Angina Pectoris ◽  
Acetylsalicylic Acid ◽  
Stable Angina ◽  
Acid Treatment ◽  
Platelet Rich Plasma ◽  
Extracellular Calcium ◽  
Stable Angina Pectoris ◽  
Enhancing Effect ◽  
The Impact

1. The impact of oral acetylsalicylic acid treatment on the enhancing effect of adrenaline on platelet aggregation in vitro was investigated in patients with stable angina pectoris. In addition, the influence of different anticoagulants (i.e. hirudin and citrate) on platelet aggregation in vitro was compared. 2. Eighty-four patients with stable angina pectoris were studied. Sixteen patients were on acetylsalicylic acid treatment (150-250 mg daily), whereas 68 patients were free from acetylsalicylic acid. Platelet-rich-plasma was prepared from citrate- or hirudin-antkoagulated blood. The EC50 (i.e. the concentration of agonist required to produce half-maximal aggregation) for the ADP-induced extent of aggregation was determined. Thereafter the enhancing effect of adrenaline (10 and 50 nmol/l) on ADP-induced aggregation (at EC50) was investigated. 3. In the patients with angina, acetylsalicylic acid caused the expected effects on ADP-induced platelet responses. Adrenaline significantly enhanced both the extent of aggregation and the initial rate of aggregation (primary aggregation), irrespective of the anticoagulant used. In acetylsalicylic acid-treated patients (citrated platelet-rich plasma) the extent of aggregation was partly inhibited, but no significant effect on the rate of aggregation could be observed. 4. A comparative substudy of the anticoagulants in healthy subjects (n = 8) showed that both the aggregating effect of ADP per se and the enhancing effect of adrenaline on ADP-induced aggregation (at EC50) were less influenced by acetylsalicylic acid when evaluated in hirudinized platelet-rich plasma (i.e. with physiological levels of extracellular calcium) as compared with citrated platelet-rich plasma. 5. It is concluded that acetylsalicylic acid treatment slightly attenuates the proaggregatory effect of high physiological concentrations of adrenaline in vitro. The impact of acetylsalicylic acid in vitro is, however, strongly dependent on the anticoagulant used, and is significantly weaker when evaluated in a medium with normal extracellular calcium levels (i.e. hirudin) than in a medium with low levels of extracellular calcium (citrate). Thus, acetylsalicylic acid may be a weak antagonist of catecholamine-induced platelet activation in vivo.

P13.01 THE IMPACT OF ACUTE SYSTEMIC INFLAMMATION ON ARTERIAL FUNCTION OF PATIENTS WITH STABLE ANGINA PECTORIS: ADDING FUEL TO THE FIRE WITHIN?

2010 ◽  
Vol 4 (4) ◽  
pp. 183
Author(s):  
P. Xaplanteris ◽  
C. Vlachopoulos ◽  
I. Dima ◽  
D. Terentes-Printzios ◽  
N. Alexopoulos ◽  
...  
Keyword(s):  
Angina Pectoris ◽  
Systemic Inflammation ◽  
Stable Angina ◽  
Stable Angina Pectoris ◽  
Arterial Function ◽  
The Impact

Statins in Stable Angina Pectoris

2018 ◽  
Vol 23 (46) ◽  
pp. 7061-7068 ◽  
Author(s):  
Adam Ioannou ◽  
Nikolaos Papageorgiou ◽  
Vincent McCaughan ◽  
Marietta Charakida ◽  
Dimitris Bertsias ◽  
...  
Keyword(s):  
Angina Pectoris ◽  
Stable Angina ◽  
Clinical Symptoms ◽  
Ex Vivo ◽  
Lipid Lowering ◽  
Stable Angina Pectoris ◽  
Excellent Safety Profile ◽  
Established Role

Background: Stable angina is a debilitating and progressive disease caused by narrowing of the coronary arteries, which in turn affects cardiac perfusion. Statins have a well-established role, modifying symptoms and progression of the disease not only through lipid lowering, but also through pleiotropic effects. </P><P> Objective: We sought to evaluate the effect of statins in stable angina pectoris </P><P> Method: We performed a systematic review of the literature searching MEDLINE via Pubmed for all studies which examine the possible effects of statins in stable angina pectoris. </P><P> Results: Statins have demonstrated favourable modification of both biochemical markers (oxidative stress, inflammatory and coagulation markers/factors) and clinical symptoms (anginal and ischemic) of the disease. These effects have been demonstrated in vitro, ex vivo and in vivo in animals and humans, independently of the lipid lowering effects. </P><P> Conclusion: With an excellent safety profile and evidence of efficacy in managing patients with stable angina, statins appear an essential part of the therapeutic armoury against atherosclerotic disease.

scholarly journals In vitro inhibition of platelets aggregation with generic form of clopidogrel versus branded in patients with stable angina pectoris

2017 ◽  
Vol 9 (4) ◽  
pp. 191-195 ◽  
Author(s):  
Rza Hajizadeh ◽  
Samad Ghaffari ◽  
Mojtaba Ziaee ◽  
Behrooz Shokouhi ◽  
Ahmad Separham ◽  
...  
Keyword(s):  
Angina Pectoris ◽  
Stable Angina ◽  
Stable Angina Pectoris ◽  
In Vitro Inhibition

Modulation of Plasma Fibrinogen Levels by Ticlopidine in Healthy Volunteers and Patients with Stable Angina Pectoris

1996 ◽  
Vol 76 (02) ◽  
pp. 166-170 ◽  
Author(s):  
Moniek P M de Maat ◽  
Alf E R Arnold ◽  
Stef van Buuren ◽  
J H Paul Wilson ◽  
Cornells Kluft
Keyword(s):  
Angina Pectoris ◽  
Healthy Volunteers ◽  
Acute Phase ◽  
Stable Angina ◽  
Gene Polymorphisms ◽  
Acute Phase Reaction ◽  
Plasma Fibrinogen ◽  
Phase Reaction ◽  
Stable Angina Pectoris ◽  
Lowering Effect

SummaryElevated plasma fibrinogen levels are associated with an increased risk for cardiac events. Ticlopidine is a drug that inhibits the ADP-induced aggregation of blood platelets and it also has been described that ticlopidine can decrease the plasma fibrinogen level in patients with vascular diseases. The mechanism of this decrease has not yet been elucidated and therefore mechanisms that are known to affect fibrinogen levels were studied, viz. the acute phase reaction, total fibrin plus fibrinogen degradation (TDP) levels and the polymorphisms of the fibrinogen β-gene.The fibrinogen lowering effect of ticlopidine was studied in 26 healthy volunteers, selected on genotype of the BclI polymorphism of the fibrinogen β-gene, and in 26 patients with stable angina pectoris in a double blind, randomized cross-over study. Functional plasma fibrinogen levels were measured with the Clauss assay. Fibrinogen antigen, C-reactive protein (CRP) and TDP levels were measured using an enzyme immuno assay (EIA).In the healthy volunteers the functional fibrinogen levels had decreased by 0.20 g/l (9%, p = 0.005 using the paired Student t-test) after 4 weeks of 250 mg bid ticlopidine administration, whereas fibrinogen antigen, CRP and TDP levels were not significantly changed. In the stable angina pectoris patients the pre-treatment fibrinogen, CRP and TDP levels were significantly higher than in the volunteer group. After four weeks 250 mg bid ticlopidine administration the functional fibrinogen levels had decreased by 0.38 g/l (11%, p < 0.005), whereas the fibrinogen antigen, CRP and TDP levels were not significantly changed. The levels of functional and antigen fibrinogen, CRP and TDP did not change significantly during the placebo period in the volunteers or the patients. Neither in the volunteers nor in the patients was the effect of ticlopidine on the fibrinogen levels associated with the fibrinogen β-gene polymorphisms.Therefore, the fibrinogen lowering effect of ticlopidine is likely to be a modulation of the functionality of the molecule and unlikely to be modulated by the acute phase reaction, TDP-levels or the fibrinogen β-gene polymorphisms.

Treatment of stable angina pectoris. „Mother Courage and her children”

2008 ◽  
Vol 149 (7) ◽  
pp. 291
Author(s):  
Viktor Nagy ◽  
István Czuriga
Keyword(s):  
Angina Pectoris ◽  
Stable Angina ◽  
Stable Angina Pectoris
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