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Platelet‐associated and secreted PAF‐acetylhydrolase activity in patients with stable angina: sequential changes of the enzyme activity after angioplasty
Author(s) -
Goudevenos J.,
Tselepis A. D.,
Vini M. P.,
Michalis L.,
Tsoukatos D. C.,
Elisaf M.,
Ninio E.,
Sideris D. A.
Publication year - 2001
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.2001.00782.x
Subject(s) - platelet , thrombin , platelet activating factor , medicine , platelet activation , endocrinology , agonist , receptor
Background Platelet‐activating factor (PAF), the lipid mediator of inflammation and potent platelet agonist, can be hydrolysed and inactivated by PAF‐acetylhydrolase (PAF‐AH). We investigated the PAF‐AH activity in relation to PAF formation in platelets from patients with stable angina undergoing elective percutaneous transluminal coronary angioplasty (PTCA). Twenty‐seven patients with stable angina, undergoing PTCA, and 30 age‐ and sex‐matched controls were studied. The platelet‐associated and secreted PAF‐AH activity was measured, before PTCA, as well as at 4 h, 48 h and 6 months afterwards. PAF formation by thrombin‐stimulated platelets and the platelet aggregation responses to PAF and ADP were also determined. Results The PAF‐AH activity secreted by thrombin‐stimulated platelets before PTCA (in pmol/10 9 cells/h) was significantly higher compared to controls (892 ± 222 vs. 624 ± 144, P < 0·001). The enzyme activity was not altered at 4 h after PTCA, but was significantly increased at 48 h (1284 ± 312, P < 0·005) to return to the levels observed in the control group 6 months afterwards. Detectable levels of PAF in thrombin‐stimulated platelets were found only at 6 months after PTCA. Furthermore, the cell‐associated enzyme activity in resting platelets before PTCA was significantly lower compared with controls. Unlike in controls, the platelet‐associated enzyme activity in the patient group was not increased after stimulation with thrombin and it was associated by a platelet hyperaggregability to PAF. Both the intact cell‐associated activity and the platelet hyper‐reactivity to PAF were restored at 6 months after PTCA. Conclusions Alterations in the platelet PAF‐AH activity, which affect the PAF formation in thrombin‐stimulated platelets and are associated by an increased aggregatory response to PAF, are observed in patients with stable angina and are completely restored after PTCA.