Malondialdehyde Assay in the Evaluation of Aspirin Antiplatelet Effects

Abstract

Aspirin is essential in secondary prevention of patients after myocardial infarction and with coronary artery disease. However, impaired pharmacodynamic response to aspirin is frequent (high on-treatment platelet reactivity [HTPR]). This leads to an enhanced prevalence of cardiovascular events and to an impaired clinical outcome. The current specific assays to evaluate aspirin antiplatelet effects are complex, time-consuming and demand for a high laboratory expertise. Therefore, we developed a potentially bedside assay based on the determination of malondialdehyde (MDA). MDA is a by-product of the thromboxane (TX) formation, which is synthesized in equimolar concentrations. In this study, we compared this MDA assay to the conventional assays in determination of pharmacodynamic aspirin response. For this, aspirin antiplatelet effects were measured in 22 healthy individuals and 63 aspirin treated patients using TX B2 formation enzyme-linked antibody assay, arachidonic acid induced light transmission aggregometry (LTA) and the new fluorometric MDA assay. In patients, MDA levels correlated well with TX formation (R = 0.81; 95% CI 0.69–0.88; p < 0.001) and LTA (R = 0.84; CI 0.74–0.91; p < 0.001). Receiver operating characteristic analyses revealed that the MDA assay does detect HTPR to aspirin sufficiently (area under the curve: 0.965; p < 0.001). The optimal cut-off was > 128 nmol/L (sensitivity of 100%, specificity of 91%). The new MDA assay is reliable in detecting HTPR. It is highly specific in the evaluation of antiplatelet effects by aspirin. This promising and potential bedside assay needs to be evaluated in clinical practice.

Mean platelet volume-to-platelet count ratio after elective cardiac surgical procedures is superior in reflecting platelets metabolic hyperactivity compared to other routine morphological platelet indices: A preliminary report

“…Oxidative stress altering platelets redox state may lead to their activation and eventually thrombus formation. It was previously observed that increased intraplatelet MDA content was also shown to be related to higher platelet activity, including aggregation [ 14 , 29 ]. This association was confirmed by the other studies that found suppression of platelet MDA levels resulted in inhibition of arachidonate- and collagen-induced aggregation [ 30 ].…”

“…However, its measurement is laborious and time-consuming, also when using commercially available colorimetric assays. On the other hand, malondialdehyde (MDA), a broadly and easily assayed marker of lipid peroxidation and oxidative stress [ 13 ], is also known to be produced by the platelet’s thromboxane synthase in amounts that are equimolar to TXA 2 [ 14 ]. Therefore, the aforementioned methods may not be considered as routine studies done in all patients in the early postoperative period.…”

Synthesis, Antioxidant, Cytotoxicity, Induce Apoptosis Investigation and Docking Study of New Halogenated Dihydropyrano[3,2-b]Chromene-3-Carbonitrile Derivatives on MCF-7 Breast Cancer Cell Line

“…The absorbance of the samples was determined at 570 nm by a microplate reader, and the quantification of nitrite in the sample was standardized with 0 - 100 mmol/L of nitrite concentration (NaNO 2 ) ( 19 ). Also, lipid peroxidation was determined on the exposed cells to the HDCCD (6a-j) ( 20 ). In this part, the MDA content of the cell supernatant and culture media on the cells was measured using TBA reaction.…”