Evidence map›Paper›PMID 11406724›Full record

ReviewJournal of thrombosis and thrombolysis2001

Platelet aggregation inhibition with glycoprotein IIb--IIIa inhibitors.

G Proimos

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of thrombosis and thrombolysis, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Novel agents for anti-platelet therapy.Journal of hematology & oncology · 2011
    Review
  3. Platelet aggregation pathway.Pharmacogenetics and genomics · 2011
    Article
  4. Review
  5. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

G ProimosVictorian Heart Centre, Epsworth Hospital, Consulting Rooms, Richmond, Australia.
Epworth Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhibitors of the platelet receptor glycoprotein (GP) IIb--IIIa are a novel and potent class of antithrombotic drugs for the management of patients with non-ST-segment elevation acute coronary syndromes (ACS) and those undergoing percutaneous coronary intervention (PCI). Pharmacodynamic studies with three currently approved agents in this class (abciximab [ReoPro, Centocor, Inc., Malvern, Pennsylvania, and Eli Lilly & Company, Indianapolis, Indiana]; eptifibatide [INTEGRILIN, COR Therapeutics, Inc., South San Francisco, California, and Key Pharmaceuticals, Inc., Kenilworth, New Jersey]; and tirofiban HCI [Aggrastat, Merck & Co., Inc., Whitehouse Station, New Jersey]) all sought to identify dosing regimens that would establish and maintain >80 % inhibition of ex vivo platelet aggregation throughout the duration of intravenous infusion. Direct comparison of these prior studies is difficult, however, because the assays used different anticoagulants (sodium citrate [abciximab, tirofiban HCI] or D-phenylalanyl-L-prolyl-L-arginine chloromethyl ketone [PPACK] [eptifibatide]) and different concentrations of the platelet agonist adenosine diphosphate (ADP) (5 micromol [tirofiban HCI] or 20 micromol [abciximab, eptifibatide]). More recent work has attempted to overcome these limitations by using similar assay conditions for all GP IIb--IIIa inhibitors. These studies have indicated that the concentrations of all three agents required to provide the targeted effect for platelet inhibition are considerably higher in the presence of an anticoagulant that does not chelate calcium ions (e.g., heparin or PPACK) than in the presence of calcium-chelating anticoagulant (i.e., sodium citrate). Of the three currently approved GP IIb--IIIa inhibitors, eptifibatide is the only agent whose approved dosing is based on an ex vivo platelet aggregation assay that uses such an anticoagulant. Additionally, Kereiakes et al. have recently reported that the high levels of platelet inhibition (>80 %), using PPACK as an anticoagulant and ADP (20 micromol) as an agonist, are more consistently achieved with the approved dosing regimen of eptifibatide. The antiplatelet effect of abciximab showed more interpatient variability, whereas the median inhibition of ex vivo platelet aggregation with the approved dosing regimen for tirofiban HCl was <80 % at almost all time points during drug infusion.

Indexed as

AbciximabAdenosine DiphosphateAmino Acid Chloromethyl KetonesAntibodies, MonoclonalAnticoagulantsClinical Trials as TopicCoronary DiseaseDose-Response Relationship, DrugDrug InteractionsEptifibatideHeparinHumansImmunoglobulin Fab FragmentsOligopeptidesPeptidesPlatelet AggregationAbciximabAdenosine DiphosphateAmino Acid Chloromethyl KetonesAntibodies, MonoclonalAnticoagulantsarginyl-glycyl-aspartic acidEptifibatideHeparinImmunoglobulin Fab FragmentsOligopeptidesPeptidesphenylalanyl-prolyl-arginine-chloromethyl ketonePlatelet Aggregation InhibitorsPlatelet Glycoprotein GPIIb-IIIa ComplexProteinsReceptors, ThrombinThrombinTirofibanTyrosine

Identifiers

PMID11406724
OpenAlexW35709001

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.