scholarly journals MMP-2, MMP-9, and TIMP-4 and Response to Aspirin in Diabetic and Nondiabetic Patients with Stable Coronary Artery Disease: A Pilot Study

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Wiktor Kuliczkowski ◽  
Marek Radomski ◽  
Mariusz Gąsior ◽  
Joanna Urbaniak ◽  
Jacek Kaczmarski ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Pilot Study ◽  
Platelet Rich Plasma ◽  
Stable Coronary Artery Disease ◽  
Impedance Aggregometry ◽  
Artery Disease ◽  
Induced Aggregation

Background. High on-aspirin treatment platelets reactivity (HPR) is a significant problem in long-term secondary prevention of cardiovascular events. We hypothesize that imbalance between platelets MMPs/TIMPs results in cardiovascular disorders. We also explored whether chronically elevated blood glucose affects MMP-2/TIMP-4 release from platelets. Materials and Methods. Seventy patients with stable coronary artery disease, supplemented with aspirin, participated in this pilot study. The presence of HPR and/or diabetes mellitus was considered as the differentiating factor. Light aggregometry, impedance aggregometry, and ELISA tests for TXB2, MMP-2, MMP-9, and TIMP-4 were performed in serum, plasma, platelet-rich plasma, and platelets-poor plasma, as appropriate. Results. Aspirin-HPR did not affect plasma MMP-2, MMP-9, and TIMP-4. Arachidonic acid-induced aggregation of platelets from aspirin-HPR patients did not lead to increased release of MMP-2, MMP-9, and TIMP-4. Studying patients at the lowest TXB2 serum concentration quartile revealed that high concentration of plasma TIMP-4 and TIMP-4 negatively correlated with TXB2 and platelet aggregation. Diabetics showed an increased plasma MMP-2 as well as an increased MMP-2 in supernatants after platelet aggregation. However, diabetes mellitus did not affect MMP-9 and TIMP-4. Conclusion. Aspirin-HPR did not affect the translocation and release of MMPs and TIMP-4 from platelets. TIMP-4 may serve as a marker of TXA2-mediated platelet aggregation. Chronically elevated plasma glucose increases plasma MMP-2, and HPR potentiates this phenomenon.

Thrombopoietin and platelet aggregation in patients with stable coronary artery disease

Platelets ◽  
2017 ◽  
Vol 28 (8) ◽  
pp. 822-824
Author(s):  
Sanne Bøjet Larsen ◽  
Erik Lerkevang Grove ◽  
Søs Neergaard-Petersen ◽  
Morten Würtz ◽  
Anne-Mette Hvas ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Stable Coronary Artery Disease ◽  
Artery Disease

scholarly journals The Effect of Low-Dose Ticagrelor on Platelet Function Profiles in Patients With Stable Coronary Artery Disease in Trinidad: The TWIST Pilot Study

2020 ◽  
Vol 9 (2) ◽  
pp. 493-503 ◽  
Author(s):  
Naveen Seecheran ◽  
Brent Boodhai ◽  
Aarti Maharaj ◽  
Arvinash Ramdeen ◽  
Niranjan Debideen ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Pilot Study ◽  
Platelet Function ◽  
Low Dose ◽  
Stable Coronary Artery Disease ◽  
Artery Disease

Greater reduction of platelet activation markers and platelet-monocyte aggregates by prasugrel compared to clopidogrel in stable coronary artery disease

2008 ◽  
Vol 100 (10) ◽  
pp. 626-633 ◽  
Author(s):  
Christoph arenhorst ◽  
Stefan James ◽  
John T. Brandt ◽  
Joseph A. Jakubowski ◽  
Kenneth J. Winters ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Platelet Activation ◽  
Maintenance Dose ◽  
Stable Coronary Artery Disease ◽  
Loading Dose ◽  
Activation Markers ◽  
Fluorescent Intensity ◽  
Artery Disease

SummaryPrasugrel, a novel P2Y12 ADP-receptor antagonist, has been reported to achieve greater inhibition of platelet aggregation compared to clopidogrel as assessed by light transmission aggregometry. It was the objective of this study to investigate the effect of prasugrel on alternative markers of platelet activation in comparison to a high loading dose and the approved maintenance dose of clopidogrel. One hundred ten aspirintreated patients with stable coronary artery disease were randomized to a loading dose (LD, day 1)/ maintenance dose (MD, days 2–29) of prasugrel 60 mg/10 mg or clopidogrel 600 mg/75 mg. Platelet activation markers were analyzed by whole blood flow cytometry pre-dose and at 2 and 24 hours after LD and pre-dose at 14 and 29 days. After stimulation with 20 µM ADP, 2 hours after LD, significantly lower expression of activated GPIIb/IIIa (4.3 vs. 21.8 [mean fluorescent intensity (MFI)], p < 0.001) and P-selectin (2.0 vs. 11.7 MFI, p < 0.001) along with decreased formation of platelet-monocyte aggregates (16.4% vs.29.6% positive cells, p < 0.001) was observed with prasugrel versus clopidogrel. All these effects were maintained through 24 hours and during the MD period. In conclusion, prasugrel 60 mg LD and 10 mg MD inhibit several markers of platelet activation and the formation of platelet-monocyte aggregates more effectively than a 600 mg LD and 75 mg MD of clopidogrel. Attenuated platelet aggregation and reduced expression of platelet procoagulant and pro-inflammatory markers with prasugrel suggest the potential to reduce cardiovascular events both in the acute setting and in longterm treatment.

scholarly journals Relationship Between the Serum sCD40L Level and Aspirin-Resistant Platelet Aggregation in Patients With Stable Coronary Artery Disease

2008 ◽  
Vol 72 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Burak Pamukcu ◽  
Huseyin Oflaz ◽  
Imran Onur ◽  
Kenan Midilli ◽  
Gulden Yilmaz ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Stable Coronary Artery Disease ◽  
Artery Disease ◽  
Scd40l Level

Abstract 4448: Clopidogrel Effect Depends on Body Weight and Abolishes Platelet Leukocyte Interaction in Patients with Coronary Artery Disease Treated by Stenting

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Philipp Diehl ◽  
Christoph Olivier ◽  
Christoph Halscheid ◽  
Thomas Helbing ◽  
Christoph Bode ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Body Weight ◽  
Coronary Artery ◽  
Stable Coronary Artery Disease ◽  
Obese Patients ◽  
Platelet Activity ◽  
Impedance Aggregometry ◽  
Increased Risk ◽  
Leukocyte Counts ◽  
Artery Disease

Background: Poor response to aspirin and clopidogrel has been associated with an increased risk for thrombotic events after PCI. The optimal dose of clopidogrel is unknown as platelet aggregability (PA) is not routinely measured in clopidogrel treated patients. Methods and Results : In order to assess potential mechanisms of clopidogrel responsiveness we have performed bedside platelet impedance aggregometry in patients with stable coronary artery disease (group CAD; n=62) and patients who underwent elective PCI (group PCI; n=90) compared to control individuals in whom coronary artery disease was excluded by coronary angiography (group control; n=28). Control patients did not receive antiplatelet therapy, CAD patients were treated with aspirin 100mg/d, and PCI patients with aspirin 100mg/d and clopidogrel 75mg/d. Impedance aggregometry was performed using arachidonic acid [AA] (final conc [fc]: 0.5mM) or ADP (fc: 6.5μM) and the area under the curve (AUC) was quantified to detect the effect of aspirin or clopidogrel, respectively. Indeed, PA was specifically reduced by either drug (AA: [control vs. CAD vs. PCI] 877±300 vs. 183±134 vs. 111±90; ADP: [control vs. PCI] 725±275 vs. 288±174 AUC). We detected a negative correlation between body weight and clopidogrel response (r=0.28; p=0.008), suggesting that clopidogrel may have been underdosed in obese patients. Furthermore, we found a positive correlation between leukocyte counts and PA (r=0.4, p=0.028) confirming that platelets and leucocytes interact functionally. Administration of clopidogrel abolished this interaction as detected by comparison of control individuals with PCI patients but also in intra-individual follow-up tests before and after introduction of clopidogrel. Conclusion: Impedance aggregometry is useful to assess PA routinely. Dosage of clopidogrel may need to be adjusted in obese patients. PA depends on leukocyte counts confirming that platelet activity is modulated by leukocytes; this interaction is effectively inhibited by clopidogrel.

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