Impact of diabetes on immature platelets fraction and its relationship with platelet reactivity in patients receiving dual antiplatelet therapy

2016 ◽  
Vol 42 (2) ◽  
pp. 245-253 ◽  
Author(s):  
Monica Verdoia ◽  
Patrizia Pergolini ◽  
Matteo Nardin ◽  
Roberta Rolla ◽  
Lucia Barbieri ◽  
...  
Platelets ◽  
2014 ◽  
Vol 26 (6) ◽  
pp. 593-597 ◽  
Author(s):  
Bernadeta Chyrchel ◽  
Justyna Totoń-Żurańska ◽  
Olga Kruszelnicka ◽  
Michał Chyrchel ◽  
Waldemar Mielecki ◽  
...  

2012 ◽  
Vol 23 (8) ◽  
pp. 723-728 ◽  
Author(s):  
Peter Bobbert ◽  
Caroline Stellbaum ◽  
Daniel Steffens ◽  
Claudia Schütte ◽  
Thomas Bobbert ◽  
...  

2021 ◽  
Vol 22 (6) ◽  
pp. 3180
Author(s):  
Nina Đukanović ◽  
Slobodan Obradović ◽  
Marija Zdravković ◽  
Siniša Đurašević ◽  
Maja Stojković ◽  
...  

Lipids play an essential role in platelet functions. It is known that polyunsaturated fatty acids play a role in increasing platelet reactivity and that the prothrombotic phenotype plays a crucial role in the occurrence of major adverse cardiovascular events. The ongoing increase in cardiovascular diseases’ incidence emphasizes the importance of research linking lipids and platelet function. In particular, the rebound phenomenon that accompanies discontinuation of clopidogrel in patients receiving dual antiplatelet therapy has been associated with changes in the lipid profile. Our many years of research underline the importance of reduced HDL values for the risk of such a rebound effect and the occurrence of thromboembolic events. Lipids are otherwise a heterogeneous group of molecules, and their signaling molecules are not deposited but formed “on-demand” in the cell. On the other hand, exosomes transmit lipid signals between cells, and the profile of such changes can be monitored by lipidomics. Changes in the lipid profile are organ-specific and may indicate new drug action targets.


2016 ◽  
Vol 6 (1) ◽  
pp. 38-46
Author(s):  
NS Neki

Antiplatelet agents are mainly used in the prevention and management of atherothrombotic complications. Dual antiplatelet therapy, combining aspirin and clopidogrel, is the standard care for patients having acute coronary syndromes or undergoing percutaneous coronary intervention according to the current ACC/AHA and ESC guidelines. But in spite of administration of dual antiplatelet therapy, some patients develop recurrent cardiovascular ischemic events especially stent thrombosis which is a serious clinical problem. Antiplatelet response to clopidogrel varies widely among patients based on ex vivo platelet function measurements. Clopidogrel is an effective inhibitor of platelet activation and aggregation due to its selective and irreversible blockade of the P2Y12 receptor. Patients who display little attenuation of platelet reactivity with clopidogrel therapy are labeled as low or nonresponders or clopidogrel resistant. The mechanism of clopidogrel resistance remains incompletely defined but there are certain clinical, cellular and genetic factors including polymorphisms responsible for therapeutic failure. Currently there is no standardized or widely accepted definition of clopidogrel resistance. The future may soon be realised in the routine measurement of platelet activity in the same way that blood pressure, cholesterol and blood sugar are followed to help guide the therapy, thus improving the care for millions of people. This review focuses on the methods used to identify patients with clopidogrel resistance, the underlying mechanisms, metabolism, clinical significance and current therapeutic strategies to overcome clopidogrel resistance.J Enam Med Col 2016; 6(1): 38-46


2019 ◽  
Vol 120 ◽  
pp. 106564 ◽  
Author(s):  
Monica Verdoia ◽  
Patrizia Pergolini ◽  
Matteo Nardin ◽  
Roberta Rolla ◽  
Federica Negro ◽  
...  

2008 ◽  
Vol 99 (03) ◽  
pp. 637-639 ◽  
Author(s):  
Sonja Postma ◽  
Johannes Kelder ◽  
Christian Hackeng ◽  
Jurrien ten Berg ◽  
Freek Verheugt ◽  
...  

2010 ◽  
Vol 103 (04) ◽  
pp. 774-779 ◽  
Author(s):  
Thomas Cuisset ◽  
Michalis Hamilos ◽  
Leen Delrue ◽  
Corinne Frere ◽  
Katia Verhamme ◽  
...  

SummaryPlatelet response to clopidogrel shows inter-individual variability that is partially explained by genetic polymorphisms. This variability affects clinical outcome when clopidogrel is administered in patients with acute coronary syndrome (ACS). Catecholamines, released during ACS, contribute to platelet aggregation through platelet α2A- (α2A-AR) and β2-adrenergic receptor (β2-AR) stimulation. It was the objective of this study to assess the potential influence of α2A-AR and β2-AR gene polymorphisms on platelet reactivity after dual antiplatelet therapy with aspirin and clopidogrel in ACS. We screened 641 ACS patients for 6.3/6.7 kb α2A-AR polymorphism, and for Arg16Gly and Gln27Glu β2-AR polymorphism. After 600 mg clopidogrel, we assessed ADP 10 μmol-induced platelet aggregation (ADP-Ag) and vasoactive stimulated phosphoprotein (VASP). All single nucleotide polymorphisms were in Hardy-Weinberg equilibrium. A slight though negligible association was found between 6.3 kb allele of α2A-AR with platelet reactivity ADPAg induced (beta: –2.91 [-5.68;-0.14], p=0.04). A borderline not significant reduction in PRI VASP was observed in 6.3 kb α2A-AR carriers (beta: –3.81 [-0.09;7.72], p=0.06). No significant effect on platelet parameters was observed for the other tested polymorphisms. Common α2A- and β2-adrenergic receptor polymorphisms do not show any major impact on residual platelet reactivity in non-ST-elevation ACS when a dual antiplatelet therapy with 250 mg aspirin and 600 mg clopidogrel is administered.


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