scholarly journals The Multifaceted Clinical Readouts of Platelet Inhibition by Low-Dose Aspirin

2015 ◽  
Vol 66 (1) ◽  
pp. 74-85 ◽  
Author(s):  
Carlo Patrono
Keyword(s):  
Low Dose ◽  
Platelet Inhibition ◽  
Dose Aspirin ◽  
Low Dose Aspirin

scholarly journals Chronic ischaemic heart disease and rivaroxaban: which patients derive the greatest benefit?

2020 ◽  
Vol 22 (Supplement_L) ◽  
pp. L24-L27
Author(s):  
Leonardo Bolognese ◽  
Massimo Felici
Keyword(s):  
Low Dose ◽  
Stable Coronary Artery Disease ◽  
Composite Endpoint ◽  
Platelet Inhibition ◽  
Everyday Clinical Practice ◽  
Major Cardiovascular Events ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Artery Disease ◽  
Cv Disease

Abstract Patients with established cardiovascular (CV) disease may suffer further CV events, despite receiving optimal medical treatment. Although platelet inhibition plays a central role in the prevention of new events, the use of anticoagulant therapies to reduce events in atheromatous disease has, until recently, been overlooked. The recent Rivaroxaban for the Prevention of Major Cardiovascular Events in Coronary or Peripheral Artery Disease (COMPASS) trial showed that rivaroxaban 2.5 mg twice daily given with low-dose aspirin reduces the incidence of the composite endpoint of stroke, heart attack, and death in patients with stable coronary artery disease. Although there are some limitations to the study, COMPASS offers promising conclusions and may change secondary prevention in patients with stable CV disease. This article reviews the results of the COMPASS study and how these results may affect patient management in everyday clinical practice.

scholarly journals 48: Effect of obesity on platelet inhibition in high-risk pregnant women treated with low dose aspirin

2019 ◽  
Vol 220 (1) ◽  
pp. S38-S39 ◽  
Author(s):  
Matthew M. Finneran ◽  
Veronica M. Gonzalez-Brown ◽  
Devin D. Smith ◽  
Mark B. Landon ◽  
Kara Rood
Keyword(s):  
High Risk ◽  
Pregnant Women ◽  
Low Dose ◽  
Platelet Inhibition ◽  
Dose Aspirin ◽  
Low Dose Aspirin

The effect of chronic platelet inhibition with low-dose aspirin on atherosclerotic progression and acute thrombosis: Clinical evidence from the physicians' health study

1991 ◽  
Vol 122 (6) ◽  
pp. 1588-1592 ◽  
Author(s):  
Paul M. Ridker ◽  
JoAnn E. Manson ◽  
Julie E. Buring ◽  
Samuel Z. Goldhaber ◽  
Charles H. Hennekens
Keyword(s):  
Low Dose ◽  
Clinical Evidence ◽  
Platelet Inhibition ◽  
Health Study ◽  
Acute Thrombosis ◽  
Dose Aspirin ◽  
Low Dose Aspirin

Platelet inhibition by low-dose aspirin but not by clopidogrel reduces the axon-reflex current-induced vasodilation in humans

2008 ◽  
Vol 294 (5) ◽  
pp. R1420-R1426 ◽  
Author(s):  
P. Rousseau ◽  
M. Tartas ◽  
B. Fromy ◽  
A. Godon ◽  
M.-A. Custaud ◽  
...  
Keyword(s):  
Low Dose ◽  
Platelet Inhibition ◽  
High Dose ◽  
Galvanic Current ◽  
Current Application ◽  
Axon Reflex ◽  
Doppler Flowmetry ◽  
Clopidogrel Bisulfate ◽  
Dose Aspirin ◽  
Low Dose Aspirin

We previously showed a prolonged inhibition of current-induced vasodilation (CIV) after a single oral high dose of aspirin. In this study, we tested the hypothesis of platelet involvement in CIV. Nine healthy volunteers took 75 mg aspirin/day, 98 mg of clopidogrel bisulfate/day, or placebo for 4 days. CIV was induced by two consecutive 1-min anodal current applications (0.08 mA/cm2) through deionized water with a 10-min interval. CIV was measured with laser Doppler flowmetry and expressed as a percentage of baseline cutaneous vascular conductance: %Cb. In a second experiment in 10 volunteers, aspirin and placebo were given as in experiment 1, but a 26-h delay from the last aspirin intake elapsed before ACh iontophoresis and postocclusive hyperemia were studied in parallel to CIV. In experiment 1, the means ± SE amplitude of CIV was 822 ± 314, 313 ± 144, and 746 ± 397%Cb with placebo, aspirin ( P < 0.05 from placebo and clopidogrel), and clopidogrel (NS from placebo), respectively. In experiment 2, CIV impairment with aspirin was confirmed: CIV amplitudes were 300 ± 99, and 916 ± 528%Cb under aspirin and placebo, respectively ( P < 0.05), whereas vasodilation to ACh iontophoresis (322 ± 74 and 365 ± 104%Cb) and peak postocclusive hyperemia (491 ± 137 and 661 ± 248%Cb) were not different between aspirin and placebo, respectively. Low-dose aspirin, even 26 h after oral administration, impairs CIV, while ACh-mediated vasodilation and postocclusive hyperemia are preserved. If platelets are involved in the neurovascular mechanism triggered by galvanic current application in humans, it is likely to occur through the cyclooxygenase but not the ADP pathway.

P1716Dual antiplatelet therapy on veno arterial ECMO to bleed or not to bleed?

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Vandenbriele ◽  
A Azzu ◽  
A Gambaro ◽  
M Morosin ◽  
D Arachchillage ◽  
...  
Keyword(s):  
Cardiogenic Shock ◽  
Antiplatelet Therapy ◽  
Major Bleeding ◽  
Low Dose ◽  
Coronary Intervention ◽  
Platelet Inhibition ◽  
Post Surgery ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Va Ecmo

Abstract Background Patients presenting with INTERMACS-1 cardiogenic shock and necessitating VA-ECMO, often undergo coronary angiography and percutaneous coronary intervention (PCI). Therefore, a substantial subset of VA-ECMO patients will have an indication for dual antiplatelet therapy (DAPT) plus unfractionated heparin (UFH). According to atrial fibrillation registry data, bleeding incidence on DAPT combined with oral anticoagulation is significantly higher as compared to anticoagulation alone. Although it has been reported that the addition of low dose aspirin to UFH did not increase bleeding or transfusion in VenoVenous (VV)-ECMO patients, it remains to be elucidated whether the addition of DAPT to UFH on VA-ECMO-therapy enhances bleeding. Methods We report single center data for 100 VA-ECMO patients between 2011 and 2019. VA-ECMO-patients post-surgery were excluded. Patient demographics, blood product transfusions and reported/radiographically diagnosed bleeding or thrombotic complications were analysed. All VA-ECMO patients received UFH, aiming for an anti-Xa levels of at least 0,3 U/ml. Targets were hemoglobin 7 g/dl, fibrinogen 100 mg/dl (or 150 mg/dl when active bleeding) and platelet counts above 50/fL. DAPT-patients were on a low dose aspirin plus a P2Y12-inhibitor (clopidogrel or ticagrelor). Results 51% Of the VA-ECMO-group received DAPT (59% clopidogrel and 41% ticagrelor). UFH-levels were comparable between both groups. Patients on DAPT were significantly older (DAPT 52.8 vs. Control 41.3; p<0.001) and predominantly male (DAPT 76% vs. Control 63%). Total bleedings (DAPT 52% vs. Control 55%; p=0,68) and major bleedings (BARC score of 3 or more; DAPT 41% vs. Control 45%; p=0,71) did not differ significantly. We observed a significant lower number of clinically or radiographically overt arterial/venous thromboses (DAPT 13.7% vs. Control 36.2%; p=0,02) in the DAPT-group. When comparing fresh frozen plasma (FFP), red blood cell and platelet pool transfusions between both groups, only FFP-tranfusion (DAPT 0.47 units/day vs. Control 1.18 units/day; p=0,047) intends to be lower for the DAPT-group. DAPT (plus UFH) vs control (plus UFH) Conclusions Haemorrhage is frequent during extracorporeal support. However, in our cohort, DAPT on top of UFH in the treatment of VA-ECMO-supported ischemic cardiogenic shock does not increase the risk of major bleeding. Therefore, DAPT should not necessarily be witheld in the setting of VA-ECMO. Interestingly, our data support a lower incidence of overt thromboses and a trend towards less FFP-transfusion. These findings suggest DAPT-induced platelet inhibition being protective against both thrombotic events and posibly consumptive coagulopathy without paying a price for major bleeding.

Alert Issued on Low-Dose Aspirin + Ibuprofen

2006 ◽  
Vol 34 (10) ◽  
pp. 8
Author(s):  
ELIZABETH MECHCATIE
Keyword(s):  
Low Dose ◽  
Dose Aspirin ◽  
Low Dose Aspirin

Investigation of the Interaction of Blood Platelets with the Coagulation System at the Site of Plug Formation In Vivo in Man - Effect of Low-Dose Aspirin

1987 ◽  
Vol 57 (01) ◽  
pp. 062-066 ◽  
Author(s):  
P A Kyrle ◽  
J Westwick ◽  
M F Scully ◽  
V V Kakkar ◽  
G P Lewis
Keyword(s):  
Platelet Activation ◽  
Thrombin Generation ◽  
Low Dose ◽  
Bleeding Time ◽  
Blood Platelets ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Plug Formation ◽  
Granule Release

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.

Increased Thromboxane Biosynthesis in Essential Thrombocythemia

1995 ◽  
Vol 74 (05) ◽  
pp. 1225-1230 ◽  
Author(s):  
Bianca Rocca ◽  
Giovanni Ciabattoni ◽  
Raffaele Tartaglione ◽  
Sergio Cortelazzo ◽  
Tiziano Barbui ◽  
...  
Keyword(s):  
Platelet Count ◽  
Platelet Activation ◽  
Essential Thrombocythemia ◽  
Therapeutic Strategy ◽  
Low Dose ◽  
Thrombotic Risk ◽  
Dose Aspirin ◽  
Gender And Age ◽  
Low Dose Aspirin

SummaryIn order to investigate the in vivo thromboxane (TX) biosynthesis in essential thromboeythemia (ET), we measured the urinary exeretion of the major enzymatic metabolites of TXB2, 11-dehydro-TXB2 and 2,3-dinor-TXB2 in 40 ET patients as well as in 26 gender- and age-matched controls. Urinary 11-dehydro-TXB2 was significantly higher (p <0.001) in thrombocythemic patients (4,063 ± 3,408 pg/mg creatinine; mean ± SD) than in controls (504 ± 267 pg/mg creatinine), with 34 patients (85%) having 11-dehydro-TXB2 >2 SD above the control mean. Patients with platelet number <1,000 × 109/1 (n = 25) had significantly higher (p <0.05) 11 -dehydro-TXB2 excretion than patients with higher platelet count (4,765 ± 3,870 pg/mg creatinine, n = 25, versus 2,279 ± 1,874 pg/mg creatinine, n = 15). Average excretion values of patients aging >55 was significantly higher than in the younger group (4,784 ± 3,948 pg/mg creatinine, n = 24, versus 2,405 ± 1,885 pg/mg creatinine, n = 16, p <0.05). Low-dose aspirin (50 mg/d for 7 days) largely suppressed 11-dehydro-TXB2 excretion in 7 thrombocythemic patients, thus suggesting that platelets were the main source of enhanced TXA2 biosynthesis. The platelet count-corrected 11-dehydro-TXB2 excretion was positively correlated with age (r = 0.325, n = 40, p <0.05) and inversely correlated with platelet count (r = -0.381, n = 40, p <0.05). In addition 11 out of 13 (85%) patients having increased count-corrected 11-dehydro-TXB2 excretion, belonged to the subgroup with age >55 and platelet count <1,000 × 1099/1. We conclude that in essential thrombocythemia: 1) enhanced 11-dehydro-TXB2 excretion largely reflects platelet activation in vivo;2) age as well as platelet count appear to influence the determinants of platelet activation in this setting, and can help in assessing the thrombotic risk and therapeutic strategy in individual patients.

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