1,721,347 research outputs found

    Aspirin resistance

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    [No abstract available

    IN VITRO METHOD FOR DETECTING GP91PHOX AS A MARKER OF OXIDATIVE STRESS

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    The invention relates to an in vitro method for detecting the activation of NADPH oxidase by measuring gp91phox protein levels in biological fluids, as a marker of oxidative stress. The method is useful for testing the oxidative stress levels in dysmetabolic pathologies, such as diabetes, hypercholesterolemia and hyperlipidemia, in pathologies of the cardiovascular district, such as hypertension, atherosclerosis, cardiac hypertrophy and stroke, and in clinical conditions comprising sepsis and diseases with a strong inflammatory component

    Aspirin resistance: is this term meaningful?

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    PURPOSE OF REVIEW: To review data for and against the existence of 'aspirin resistance', a term coined to indicate aspirin-treated patients having ex-vivo tests of platelet activation insensitive to aspirin treatment and recurrence of cardiovascular disease. RECENT FINDINGS: 'Aspirin resistance' defined by ex-vivo tests of platelet activation yielded values ranging from 21 to 78%, indicating that such tests do not provide a useful measurement. In long-term aspirin-treated patients, studies demonstrated small but functionally relevant platelet thromboxane A2 formation that was responsible for an enhanced platelet activation in response to platelet agonist. These studies, however, did not fully exclude that aspirin compliance may be implicated in such phenomena. Two trials performed in patients with coronary artery disease demonstrated that laboratory evidence of aspirin resistance was no longer detectable when aspirin compliance was accurately monitored. SUMMARY: Given the multifactorial nature of atherothrombosis, recurrence of cardiovascular events in aspirin-treated patients does not necessarily suggest 'drug failure'. A cause-effect relationship between platelet insensitivity to aspirin and cardiovascular recurrence has not been defined overall because aspirin compliance has been scarcely considered. Until this information is taken into account, the existence of 'clinical resistance' to aspirin should be reconsidered

    Statins as Regulators of Redox Signaling in Platelets

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    Significance: Reactive oxidant species (ROS) are highly reactive molecules produced by several cell lines including platelets and serve as second messenger for intracellular signaling. In recent years it became evident that ROS are also implicated in the thrombotic process. Statins are lipid lowering molecules which reduce serum cholesterol and retard atherosclerotic complication and its clinical sequelae. However there is evidence that statins may exert an antiplatelet effects by interfering with redox signaling. Recent Advances: Experimental and clinical studies provided evidence that intra-platelet ROS formation is implicated in the process of thrombosis, as impaired ROS neutralization is associated with serious thrombotic complication and eventually death. Recent studies demonstrated that statins possess antiplatelet activity via inhibition of platelet NADPH oxidase-derived ROS formation. This effect results in down-regulation of isoprostanes, which are pro-aggregating molecules, and up-regulation of nitric oxide, which is a platelet inhibitor; such changes occurred immediately after statin's administration and were independent from lipid lowering property. Critical Issues: Experimental and clinical studies documented that statins possess an antithrombotic effects which may account for thrombotic-related vascular outcomes. This has been evidenced in clinical settings such as percutaneous coronary intervention, myocardial infarction and venous thrombosis. It is still unclear, however, if the statin's antithrombotic effect is dose-related. Future Directions: Future studies should be addressed to analyze if the antiplatelet effect of statins may preferentially occur at high dosage of statins. Furthermore, the antiplatelet effects of statins could turn useful in clinical settings where the clinical efficacy of aspirin and other antiplatelet drugs are still uncertain. Antioxid. Redox Signal. 20, 1300-1312
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