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Stroke and Transient Ischemic Attacks of the Brain and Eye
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Long-term triflusal, terutroban, VKAs, aspirin plus clopidogrel, and vorapaxar plus standard antiplatelet treatment are not as safe and effective as aspirin or clopidogrel monotherapy or aspirin plus extended-release dipyridamole.
Briefing Therapeutic Approaches in Anticoagulant, Thrombolytic, and Antiplatelet Therapy
Published in Debarshi Kar Mahapatra, Sanjay Kumar Bharti, Medicinal Chemistry with Pharmaceutical Product Development, 2019
Aspirin (Figure 7.11) is a well-established antiplatelet drug regarded as the cornerstone of treatment for patients with any vascular disease. Aspirin irreversibly inhibits cyclooxygenase-1 (COX-1) by its ability to acetylate the hydroxyl group of Ser–529 near the active site. It blocks the binding of COX-1 to its endogenous substrate arachidonic acid. Thus, inhibit the subsequent production of TXA2 via the synthesis of PGH from arachadonic acid. Due to lack of a nucleus, protein synthesis does not occur in platelets. Therefore, cannot replenish the acetylated COX-1 and antithrombotic effect remains for the duration of about 7 to 10 days, which is the normal life span of the platelet. Antithrombotic effects of aspirin include the dose-dependent inhibition of platelet function, boosting the fibrinolysis, and a clampdown of blood coagulation. However, higher dosage of aspirin only adds the side effects like internal bleeding and upper gastrointestinal irritations [80–82]. Triflusal (Figure 7.11) is a platelet aggregation inhibitor. It is found to inhibit COX and cAMP (cyclic adenosine monophosphate) phosphodiesterase. cAMP phosphodiesterase inhibition leads to increased levels of cAMP. Elevated cAMP levels decrease platelet aggregation [83, 84].
Neurobehavioral Syndromes in Patients with Cerebrovascular Pathology
Published in José León-Carrión, Margaret J. Giannini, Behavioral Neurology in the Elderly, 2001
María Dolores Jiménez, Eva Cuartero, Jorge Moreno
The treatment of VaD has an essential preventive nature as treatment can prevent CVA by means of strict control of the vascular risk factors from both a primary and a secondary approach. The treatment includes platelet antiaggregation medication (acetylsalicylic acid, dipyridamole, triflusal, ticlopidine, clopidogrel).48 Depending on the origin of the ischemic condition and the patient’s state, anticoagulation treatments or interventionist therapies to prevent symptomatic carotid stenosis can also be considered. To date, the benefits of endarterectomy on symptomatic carotid stenoses when the VaD has already developed have not been reported. However, some authors suggest that it has some preventive effect on the development of VaD.
Treatment practices and lipid profile of patients with acute coronary syndrome: results from a tertiary care hospital
Published in Acta Cardiologica, 2020
Ioannis Farmakis, Stefanos Zafeiropoulos, Anastasios Kartas, Aristi Boulmpou, Vasileios Nevras, Ioannis Papadimitriou, Athina Tampaki, Anastasia Vlachou, Eleftherios Markidis, Athanasios Koutsakis, Antonios Ziakas, Haralambos Karvounis, George Giannakoulas
Figure 2 presents the medications before admission and upon discharge. Concerning antiplatelet therapy prior to hospitalisation, 8.7% of patients were already under dual antiplatelet therapy, while 24.1% of patients received aspirin, 9% clopidogrel, 1.9% ticagrelor and 0.3% triflusal. At discharge, 93.8% of patients were prescribed aspirin, 47.3% clopidogrel, 44% ticagrelor, 1.4% prasugrel and 0.3% triflusal, while 5.9% were prescribed anticoagulants. In total, 98.3% of patients were prescribed statins and a high-intensity statin was chosen in 89.7% of the cases. An angiotensin-converting-enzyme inhibitor (ACE-i) (or an angiotensin II receptor blocker [ARB]) and a beta-blocker were prescribed to 55.1% (or 12.2%) and 91.8% of patients with LVEF ≤40%, respectively. Patients with preserved systolic function (i.e. LVEF ≥50%) received medication as follows: ACE-i 38.7%, ARB 18.2% and beta-blocker 86.2%. A combination of statin, dual antiplatelet therapy and beta-blockers were prescribed to 79.6% of all patients upon discharge. α combination of statin, dual antiplatelet therapy, beta-blockers and ACE-i/ARB was prescribed to 58.6% of STEMI patients upon discharge.
Management of mild cognitive impairment (MCI): The need for national and international guidelines
Published in The World Journal of Biological Psychiatry, 2020
Siegfried Kasper, Christian Bancher, Anne Eckert, Hans Förstl, Lutz Frölich, Jakub Hort, Amos D Korczyn, Reto W. Kressig, Oleg Levin, María Sagrario Manzano Palomo
Anti-inflammatory agents were investigated for their effectiveness to prevent the onset of Alzheimer’s dementia in patients with MCI. A double-blind, 13-month placebo-controlled trial in 257 MCI subjects was conducted with triflusal, a platelet aggregation inhibitor and non-selective, non-steroidal anti-inflammatory drug (NSAID). According to the authors, compared to placebo, patients in the triflusal group had a significantly lower risk of progression to Alzheimer’s dementia (hazard ratio, 2.10; 95% confidence interval: 1.10–4.01; p = .024). A trend, albeit non-significant, was observed in favour of triflusal regarding cognitive decline (p = .096; as measured by ADAS-cog). However, the trial was interrupted prematurely due to subject recruitment problems (Gomez-Isla et al. 2008).
Indomethacin attenuates neuroinflammation and memory impairment in an STZ-induced model of Alzheimer’s like disease
Published in Immunopharmacology and Immunotoxicology, 2021
Ahmad Karkhah, Mahdiye Saadi, Fereshteh Pourabdolhossein, Kiarash Saleki, Hamid Reza Nouri
Our results demonstrated that escape latency was significantly increased in the STZ-treated animals in all 4 d of acquisition trials compared with the control group; while pre- and post-treatment by IND significantly restored escape latency in STZ-administered rats. In addition, average swimming distance for finding the platform in all trial days was significantly prolonged in STZ group and IND treatment was also able to significantly improve the average swimming distance. The behavioral analysis similarly indicated that, escape latency and traveled distance was significantly reduced on days 3 and 4 compared to the first day of acquisition but this trend was not observed in STZ group. Interestingly, IND treatment restored the decreasing trend of escape latency and traveled distance in STZ-treated group. The obtained results from probe trial showed that there was a significant decrease in the time duration in Q4 in STZ-treated animals compared to control. Also, significant increase of time duration in Q4 in IND-treated animals confirmed that IND administration recover spatial memory impairment in probe test. In line with our behavioral results, it has been proven that treatment by using the COX-1 inhibitor SC-560 significantly improved memory deficits and reduced amyloid deposition and tau phosphorylation in the hippocampus [23]. Coma et al. reported that triflusal, a platelet anti-aggregant and irreversible COX-1 inhibitor, could rescue cognitive deficits by decreasing the dense-core amyloid plaque load, associated glial cell activation, and pro-inflammatory cytokine levels [24]. Similar to the results of a recent study by Coma et al. our results revealed a significant decrease in IL-1β production in the IND treated group compared to other experimental groups. In addition, the higher expression level of ASC in the hippocampus of STZ-administered group was significantly decreased by IND treatment. Investigations regarding the influences of NSAIDs on the inflammatory response in pathogenesis of AD led to two mechanisms by which NSAIDs may protect against AD [25]. One important mechanism is the selective lowering of Aβ42. Similarly, our findings confirmed that IND reduced the amount of p-tau proteins in the lesion area. Another possible mechanism is the reduction of inflammation. According to the proposed mechanism, our results demonstrated that IND treatment significantly reduced the synthesis of IL-1β, ASC, and caspase-1. Kotilinek et al. suggested another mechanism through which NSAIDs may enhance Aβ-induced dysfunctions in the memory and long-term plasticity independent of decreasing inflammation and lowering Aβ42, and the enhanced memory function was inversely related to PGE2 response at synapse [26].