Effect of statins on platelet function in patients with hyperlipidemia

Abstract

IntroductionIt is generally assumed that cholesterol reduction by statins is the predominant therapeutic result underlying their beneficial effects in cardiovascular disease. However, the action of statins may be partially independent of their effects on plasma cholesterol levels, as they combine lipid lowering with positive effects on hemorheological conditions and endothelial function. We evaluated the impact of statin treatment on platelet adhesion to fibrinogen (spontaneous and ADP-activated), along with ADP, collagen or ristocetin-induced aggregation in type II hyperlipidemic patients.Material and methodsThe study group included 70 persons: 50 patients affected by type II hyperlipidemia without concomitant diseases and 20 healthy volunteers. The effects of 8-week statin treatment (atorvastatin 10 mg/day, simvastatin 20 mg/day, or pravastatin 20 mg/day) on platelet activation were evaluated.ResultsRegardless of the type of statin, a significant decrease in ADP-induced platelet aggregation was observed: for atorvastatin 50.6 ±12.8% vs. 41.1 ±15.8% (p < 0.05), for simvastatin 57.2 ±18.0% vs. 44.7 ±22.1% (p = 0.05), and for pravastatin 55.8 ±19.5% vs. 38.8 ±23.3% (p < 0.05). There was no significant effect of statins on collagen or ristocetin-induced platelet aggregation and adhesion.ConclusionsTherapy with statins beneficially modifies ADP-induced platelet aggregation in patients with hyperlipidemia and does not affect spontaneous or ADP-induced platelet adhesion to fibrinogen and platelet aggregation induced by collagen or ristocetin.

Extract of Aronia melanocarpa-modified hemostasis: in vitro studies

“…Our studies have shown that 2 months of regular supplementation with polyphenols results in normalization of hemostatic parameters in patients with metabolic syndrome and favorably modifies platelet aggregation, albeit to a smaller extent [4]. Similar beneficial decrease in the platelet aggregation was observed in people in whom newly diagnosed hyperlipidemia was treated with statins, which are known for their numerous pleiotropic effects [5]. …”

Platelet‐Rich Fibrin Combined With 1.2% Atorvastatin for Treatment of Intrabony Defects in Chronic Periodontitis: A Randomized Controlled Clinical Trial

“…[22][23][24] Apart from lipid-lowering ability, ATV has been found to beneficially modify adenosine diphosphate-induced platelet aggregation in patients with hyperlipidemia. 25 Recently, local delivery of 1.2% ATV was found to stimulate a significant increase in: 1) probing depth (PD) reduction; 2) relative clinical attachment level (rCAL) gain; and 3) improved radiographic defect depth reduction compared with placebo gel as adjunct to scaling and root planing (SRP) in the treatment of CP, and in individuals with type 2 diabetes mellitus and CP. 26,27 Considering the various regenerative materials available and the fact that combined properties of these materials could prove beneficial in regeneration of periodontal defects by a synergistic action, combinations of regenerative materials like platelet concentrates and bone grafts, with and without statins, have been successfully used in periodontal regeneration.…”

“…Among members of the statin group, atorvastatin (ATV) has been shown to have: 1) higher lipid‐lowering action; and 2) greater antiatherogenic; 3) anti‐inflammatory; and 4) antioxidant actions compared with other statins 22–24 . Apart from lipid‐lowering ability, ATV has been found to beneficially modify adenosine diphosphate‐induced platelet aggregation in patients with hyperlipidemia 25 …”

Pharmacological Effects of Atorvastatin in Platelet Function and Plaque Rupture

“…Therapy with statins successfully modifies ADP-induced platelet aggregation in hyperlipidemic patients and does not affect ADP-induced platelet adhesion to fibrinogen as well as platelet aggregation induced by collagen or ristocetin (Sikora et al, 2013). Moscardo et al (2013), reported the direct downregulation with atorvastatin and simvastatin of platelet cPLA2 activity through effects on calcium, Mitogen-activated protein kinases (MAPK) and decrease TXA2 synthesis, which induced by collagen.…”