The effect of a platelet cholesterol modulation on the acetylsalicylic acid-mediated blood platelet inhibition in hypercholesterolemic patients

No effects of atorvastatin (10mg/d or 80mg/d) on nitric oxide, prostacyclin, thromboxane and oxidative stress in type 2 diabetes mellitus patients of the DALI study

“…Nevertheless, the statistically insignificantly changed urinary excretion rates of 2,3-dinor-TxB 2 and 2,3-dinor-6-keto-PGF 1␣ , as well as their molar ratio suggest that the TxA 2 /PGI 2 homeostasis was not altered to a major extent by atorvastatin or placebo in the patients investigated. Literature reports on the effects of atorvastatin on TxA 2 [71][72][73][74][75][76][77][78][79] and PGI 2 [80][81][82][83] synthesis in diabetes are rare and contradictory, presumably because the TxA 2 and PGI 2 synthesis has not been assessed by measuring 2,3-dinor-TxB 2 and 2,3-dinor-6-keto-PGF 1␣ , respectively, as required [41] and has been performed in the present study. It is of particular interest that the urinary excretion of 8-iso-PGF 2␣ correlated considerably with that of 2,3-dinor-TxB 2 but not with the urinary excretion of 2,3-dinor-6-keto-PGF 1␣ , although 2,3-dinor-6-keto-PGF 1␣ correlated with 2,3-dinor-TxB 2 .…”

Effect of coenzyme Q10 andArdisia japonicaBlume on plasma and liver lipids, platelet aggregation, and erythrocyte Na efflux channels in simvastatin-treated guinea pigs

“…Atorvastatin decreases platelet cholesterol content and potentiates the action of aspirin to deactivate platelets in patients with hypercholesterolemia [17]. Fluvastatin dose-dependently inhibits platelet aggregation and decreases platelet-derived nitric oxide release in vitro [37].…”

“…Reduced CoQ10 improves platelet mitochondrial function by protecting platelets from oxidative stress [16]. Statins affect platelet aggregation by modulating platelet cholesterol [17]. Atorvastatin decreases cholesterol content in erythrocyte membranes by decreasing the cholesterol/phospholipid ratio, which provides membrane stability and increased Na-K ATPase activity in guinea pigs [18].…”

Aspirin resistance in adult patients after Fontan surgery

“…Accordingly, long-term antiplatelet therapy for prevention of thrombosis after Fontan operations is a reasonable consideration, even though thrombosis is a common feature (2)(3)(4). However, it is not known whether patients after Fontan operation respond to aspirin and whether aspirin resistance is prevalent in them (11)(12)(13). In reported studies, aspirin resistance has been defined by the presence of incomplete inhibition of ex vivo platelet aggregation induced by arachidonic acid, suboptimal inhibition of platelets in various other ex vivo tests (14)(15)(16), or increased thromboxane B2 (TXB2) metabolites in urine (13).…”