Platelet aggregability to platelet activating factor at rest and after exercise in patients with coronary artery disease

Goudevenos, John; Tselepis, Alexandros D.; Τσουκατοσ, Δημοκριτοσ; Grekas, Georgios; Kritikakos, J.; Sideris, Dimitris A.

doi:10.1093/oxfordjournals.eurheartj.a061044

Cited by 19 publications

(12 citation statements)

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“…This is in contrast with the results of a study by Goudevenos et al (1995) who did not find apparent differences of PAF concentrations in the healthy control group of patients after physical exercise compared with basal values. However, there are important differences between the two studies.…”

Section: Platelet Activating Factorcontrasting

confidence: 99%

Effects of eccentric exercise-induced muscle injury on blood levels of platelet activating factor (PAF) and other inflammatory markers

et al. 2005

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It has been reported that exercise with eccentric contractions can induce damage and inflammation in human muscle tissue, the severity of which depends on the duration and the intensity of exercise. Platelet activating factor (PAF) is a potent inflammatory mediator implicated in a series of pathophysiological conditions. We sought to investigate the relationship between PAF and eccentric exercise induced muscle damage. Thirteen healthy, recreationally active male subjects (27.5+/-3.78 year) performed 36 maximum voluntary eccentric contractions on a motorized muscle dynamometer using the elbow flexor muscles of the non-dominant arm. Venous blood samples were collected immediately before and after exercise at 2, 24, 48, 72 and 96 h. PAF was isolated, purified and determined by a platelet aggregation assay. Serum levels of creatine kinase (CK), lactate dehydrogenase (LDH), C-reactive protein (CRP) and complement C3 (C3), plasma level of fibrinogen and whole blood level of leukocytes (and their subsets) were determined. Established indicators of muscle damage as maximum isometric torque (MIT), range of motion (ROM), relaxed arm angle (RANG), flexed arm angle (FANG), arm circumference (CIRC) and muscle soreness were also measured at the same time points. PAF, leukocytes, CK and LDH were elevated after exercise, while other biochemical parameters such as CRP, C3 and fibrinogen were unchanged. We also observed an inverse association between PAF and MIT and ROM, as well as a positive association with other markers of muscle injury, i.e. CK, LDH, FANG and CIRC (all P's<0.05). Our findings may imply a role for PAF in the mechanism of eccentric exercise induced muscle damage.

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Section: Platelet Activating Factorcontrasting

confidence: 99%

Effects of eccentric exercise-induced muscle injury on blood levels of platelet activating factor (PAF) and other inflammatory markers

et al. 2005

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“…Platelet aggregation to ADP (5 and 10 mM) or to thrombin receptor activating peptide-14 (TRAP-14) (10 mM) was determined in platelet-rich plasma (PRP) as previously described [13]. Platelet aggregation in the presence of ADP or TRAP-14 was measured in aliquots of 0.5 ml PRP, in a platelet aggregometer (model 560, Chronolog Corp.) at 37 C, under continuous stirring (1200 rpm).…”

Section: Platelet Aggregation Studiesmentioning

confidence: 99%

The inhibitory potency of clopidogrel on ADP-induced platelet activation is not attenuated when it is co-administered with atorvastatin (20 mg/day) for 5 weeks in patients with acute coronary syndromes

Mitsios

Παπαθανασίου²,

Elisaf³

et al. 2005

Platelets

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The antiplatelet potency of clopidogrel may be attenuated by short-term co-administration of lipophilic statins metabolized through the cytochrome P-450, isoform 3A4. We investigated whether the co-administration of atorvastatin (20?mg/day) for 5 weeks, in patients with acute coronary syndromes (ACS) could affect the antiplatelet activity of clopidogrel. Fifty-one patients with the first episode of an ACS were included in the study. All patients underwent percutaneous coronary intervention (PCI) and received a loading dose of 375 mg of clopidogrel, followed by 75 mg/day for at least 3 months. Twenty-six of them presented with low density lipoprotein (LDL) cholesterol levels >100?mg/dl (2.6 mmol/l) (measured within 24 h from the onset of symptoms) and received daily 20 mg/day of atorvastatin. The ADP- or TRAP-induced platelet aggregation, as well as P-selectin and CD40L surface expression, were studied at baseline (within 30 min after admission) and 5 weeks afterwards. Atorvastatin did not influence either the clopidogrel-induced inhibition of platelet aggregation initiated by 5 or 10 microM ADP or the clopidogrel-induced reduction of the membrane expression of P-selectin and CD40L induced by ADP. In conclusion, atorvastatin, even at a dose of 20 mg/day does not affect the antiplatelet efficacy of clopidogrel when co-administered for 5 weeks in ACS patients.

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“…Platelet aggregation to ADP (2, 5, and 10 mol/L) or to thrombin receptor activating peptide-14 (TRAP-14; 10 mol/L) was determined in platelet-rich plasma as previously described. 8 The degree of platelet activation was also evaluated by FACScan flow cytometry (Becton-Dickinson), determining the surface expression of P-selectin (CD62p) and CD40L induced by ADP or TRAP-14 (50 mol/L for either agonist) by use of the monoclonal antibodies CD62p and CD154, respectively. Flow cytometry results are presented as the mean fluorescence intensity of the activated sample minus the mean fluorescence intensity of the unactivated sample as previously described.…”

Section: Laboratory Determinationsmentioning

confidence: 99%

Atorvastatin Does Not Affect the Antiplatelet Potency of Clopidogrel When It Is Administered Concomitantly for 5 Weeks in Patients With Acute Coronary Syndromes

et al. 2004

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Background-The antiplatelet effect of clopidogrel may be attenuated by short-term coadministration of lipophilic statins.We investigated whether the coadministration of atorvastatin for 5 weeks in patients with acute coronary syndromes (ACS) could affect the antiplatelet potency of clopidogrel. Methods and Results-Forty-five hypercholesterolemic patients with the first episode of an ACS were included in the study. Patients were randomized to receive daily either 10 mg of atorvastatin (nϭ21) or 40 mg of pravastatin (nϭ24). Thirty patients who underwent percutaneous coronary intervention (PCI) received a loading dose of 375 mg of clopidogrel, followed by 75 mg/d for at least 3 months. In the remaining 15 patients who refused to undergo PCI, clopidogrel therapy was not administered. Eight normolipidemic patients with the first episode of an ACS were also included and received only clopidogrel. The serum levels of soluble CD40L and the adenosine 5Ј-diphosphate-or thrombin receptor activating peptide-14 -induced platelet aggregation, as well as P-selectin and CD40L surface expression, were studied at baseline (within 30 minutes after admission) and 5 weeks later. Neither atorvastatin nor pravastatin significantly influenced the clopidogrel-induced inhibition of platelet activation, nor did clopidogrel influence the therapeutic efficacy of atorvastatin. Conclusions-Atorvastatin does not affect the antiplatelet potency of clopidogrel when coadministered for 5 weeks in ACS patients.

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Platelet aggregability to platelet activating factor at rest and after exercise in patients with coronary artery disease

Cited by 19 publications

References 0 publications

Effects of eccentric exercise-induced muscle injury on blood levels of platelet activating factor (PAF) and other inflammatory markers

Effects of eccentric exercise-induced muscle injury on blood levels of platelet activating factor (PAF) and other inflammatory markers

The inhibitory potency of clopidogrel on ADP-induced platelet activation is not attenuated when it is co-administered with atorvastatin (20 mg/day) for 5 weeks in patients with acute coronary syndromes

Atorvastatin Does Not Affect the Antiplatelet Potency of Clopidogrel When It Is Administered Concomitantly for 5 Weeks in Patients With Acute Coronary Syndromes

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