ARCTIC: Additional proof against antiplatelet adjusted therapy.
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ABSTRACT:
SUBMITTER: Elmahdy MF
PROVIDER: S-EPMC3963745 | biostudies-literature | 2013
REPOSITORIES: biostudies-literature
Publications
ARCTIC: Additional proof against antiplatelet adjusted therapy.
Elmahdy Mahmoud Farouk MF Antoniucci David D
Global cardiology science & practice 20131101 2
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Project description:Antiplatelet therapy is the most important treatment to reduce the risk of developing recurrent thrombosis, and to prevent progression to a complete occlusion of coronary arterial disease (CAD) patients after percutaneous coronary intervention Aim of study was to investigate the relationship between response to antiplatelet drugs and global mRNA gene expression in peripheral blood cells (PBC) in patients with coronary arterial disease (CAD) All patients were treated crhonically with acetylsalicylic acid (ASA) (100 mg/day) and clopidogrel (75 mg/day). Blood samples were drown before PCI to evaluate platelet reactivity by VerifyNow® ASA and P2Y12 assays and mRNA expression was measured by Affymetrix GeneChip Human Exon 1.0 ST array.
2012-09-15 | E-GEOD-32226 | biostudies-arrayexpress
Project description:Antiplatelet therapy is the most important treatment to reduce the risk of developing recurrent thrombosis, and to prevent progression to a complete occlusion of coronary arterial disease (CAD) patients after percutaneous coronary intervention Aim of study was to investigate the relationship between response to antiplatelet drugs and global mRNA gene expression in peripheral blood cells (PBC) in patients with coronary arterial disease (CAD)
2012-09-15 | GSE32226 | GEO
Project description:The purpose of this study was to identify changes in platelet mRNA that result from exposure to antiplatelet therapy. A total of 84 healthy volunteers were recruited into a longitudinal study of various antiplatelet exposures with 58 completing all study visits. This was a 5 visit study where each visit was separated by ~ 4 weeks. At each Visit purified platelets using a CD45 negative selection protocol was performed in addition to platelet function testing using light transmittance aggregometry (ADP, EPI, and Collagen) and PFA100 (Col/EPI). After the baseline visit (V1), participants were randomized to receive 81mg/day or 325mg/day aspirin x 4 weeks followed by Visit 2. Participants then crossed over to the alternative dose of aspirin for 4 weeks followed by Visit 3. Between Visits 3 and 4 participants washed out their aspirin for 4 weeks. The final exposure was ticagrelor 90mg twice daily x 4 weeks until Visit 5.
2022-03-14 | GSE158765 | GEO
Project description:Antiplatelet therapy is used in the treatment of patients with acute coronary syndromes, stroke, and those undergoing percutaneous coronary intervention. Clopidogrel is the most widely used antiplatelet P2Y12 inhibitor in clinical practice. Genetic variation in CYP2C19 may influence its enzymatic activity, resulting in individuals who are carriers of loss-of-function CYP2C19 alleles and thus have reduced active clopidogrel metabolites, high on-treatment platelet reactivity, and increased ischemic risk. Prospective studies have examined the utility of CYP2C19 genetic testing to guide antiplatelet therapy, and more recently published meta-analyses suggest that pharmacogenetics represents a key treatment strategy to individualize antiplatelet therapy. Rapid genetic tests, including bedside genotyping platforms that are validated and have high reproducibility, are available to guide selection of P2Y12 inhibitors in clinical practice. The aim of this review is to provide an overview of the background and rationale for the role of a guided antiplatelet approach to enhance patient care.
| S-EPMC9868113 | biostudies-literature
Project description:Objectives: Evidence for antithrombotic therapy after endovascular therapy (EVT) is limited. Methods: This retrospective, multicenter, observational study enrolled 732 consecutive patients with lower extremity artery disease who underwent EVT between January 2018 and December 2019. Overall, 570 patients who received single antiplatelet therapy (SAPT) and dual antiplatelet therapy (DAPT) were selected and divided into the SAPT (n = 189) and DAPT (n = 381) groups. The primary outcome was bleeding events at 24 months. The secondary outcomes were bleeding events at 30 days and 24 months after 30 days, ischemic events, and all-cause death at 24 months. Bleeding and ischemic events at 24 months were investigated in subgroups. Results: A propensity score matching yielded 164 patients in both groups. There were no significant differences in bleeding events between the SAPT and DAPT groups (14.2% and 11.3% at 24 months, p = 0.775; 2.5% and 6.1% at 30 days, p = 0.106; 11.7% and 6.7% at 24 months after 30 days, p = 0.162). Additionally, there was no significant difference in ischemic events at 24 months between the two groups (32.7% and 30.6%, p = 0.625). Bleeding and ischemic events at 24 months were similar between subgroups. Conclusions: No significant differences in bleeding or ischemic events between SAPT and DAPT were observed.
| S-EPMC11669015 | biostudies-literature
Project description:Atherosclerotic cardiovascular (CV) disease represents one of leading cause of mortality and morbidity in Western countries. An increased risk of CV events was identified in patients with peripheral arterial diseases (PADs), which include all arterial diseases, other than coronary arteries and the aorta. In particular, lower extremity artery disease (LEAD) and/or carotid artery disease present growing incidence in general population and a consequent increase in mortality and morbidity. Medical treatment, including antiplatelet therapy, is a cornerstone in management of these patients, even when they are treated with endovascular or surgical procedures. Despite their clinical relevance, data on optimal antiplatelet treatment in this clinical setting are lacking and often derived from clinical trials on coronary artery disease and by subgroups analysis. The purpose of this review is to examine the available data from registries, randomized trials and meta-analysis on antiplatelet treatment in patients with LEAD and carotid stenosis with the aim to provide evidence to support clinical decision making.
| S-EPMC6232353 | biostudies-other
Project description:Cardiovascular diseases are the leading cause of death in the Western world. Several factors have led to the increase in vascular disorders, including the aging population, unhealthy lifestyles, increasing rates of diabetes and raised lipids, and further risk factors resulting in inflammation and calcification of the vascular endothelium. Activated platelets in damaged blood vessels can trigger arterial thrombus formation, leading to vascular occlusion with subsequent organ hypoperfusion and clinical manifestation of myocardial infarction, stroke, or peripheral artery disease. Platelet inhibitors such as aspirin and clopidogrel (Plavix(®) and generics) are prescribed as primary or secondary prevention to attenuate chronic platelet activation. However, a significant proportion of patients do not respond adequately to uniform antiplatelet treatment. These 'non-responders' have an increased risk for stent thrombosis, stroke, and other ischemic complications. Platelet function (PF) tests can identify these patients thus enabling physicians to offer personalized and alternative treatment strategies. Recent alternatives to clopidogrel include prasugrel (Efient(®)) and ticagrelor (Brilique(®)) - that are both more potent than clopidogrel but also more expensive and associated with a higher risk of bleeding complications. Given these drawbacks, PF testing might help clinicians to prescribe optimal antiplatelet agent to maximize patient safety and efficacy while minimizing costs. While randomized studies using different test systems have left clinicians puzzled about the medical value of tailored antiplatelet therapy, accumulated evidence from recent studies on tailored antiplatelet therapies and the association with improved outcomes have now resulted in a consensus expert opinion for the specific adoption of PF diagnostics into clinical practice.
| S-EPMC4975182 | biostudies-other
Project description:Activated platelets play a crucial role in the pathogenesis of atherothrombotic disease and its complications. Even under treatment of antiplatelet drugs, such as acetylsalicylic acid and P2Y12 antagonists, morbidity and mortality rates of thromboembolic complications remain high. Hence, the therapeutic inhibition of protease-activated receptor (PAR)-1, which is activated by thrombin, is a novel promising approach in antiplatelet therapy. Recent data suggest that PAR-1 is mainly involved in pathological thrombus formation, but not in physiological hemostasis. Therefore, PAR-1 inhibition offers the possibility to reduce atherothrombotic events without increasing bleeding risk. So far, two emerging PAR-1 antagonists have been tested in clinical trials: vorapaxar (SCH530349; Merck & Co., Whitehouse Station, NJ, USA) and atopaxar (E5555; Eisai, Tokyo, Japan). Although in TRA-CER vorapaxar showed an unfavorable profile for patients with acute coronary syndrome in addition to standard therapy, it revealed promising results for patients with prior myocardial infarction in TRA 2P-TIMI50. Depending on the status of clinical approval, vorapaxar might be an option for patients with peripheral arterial disease to reduce limb ischemia. The second PAR-I antagonist, atopaxar, tended towards reducing major cardiovascular adverse events in acute coronary syndrome patients in a phase II trial. However, although statistically not significant, bleeding events were numerically increased in atopaxar-treated patients compared with placebo. Furthermore, liver enzymes were elevated and the relative corrected QT interval was prolonged in atopaxar-treated patients. Currently, the development of atopaxar by Eisai is discontinued. The future of this novel class of antithrombotic drugs will depend on the identification of patient groups in which the risk-benefit ratio is favorable.
| S-EPMC4107434 | biostudies-literature
Project description:The APPLE COPD-ICON2 trial is a prospective 2×2 factorial, double-blinded proof-of-concept randomised controlled trial targeting patients with chronic obstructive pulmonary disease (COPD) without prior history of cardiovascular disease. The primary goal of this trial is to investigate if treatment with antiplatelet therapy will produce the predefined cut-off of platelet inhibition measured using the Multiplate test in COPD patients. Eligible patients were randomised to aspirin plus placebo, ticagrelor plus placebo, aspirin plus ticagrelor or placebo only for 6 months. The primary outcome comprises inhibition (binary response) of arachidonic acid- (ASPI test, cut-off <40) and adenosine diphosphate- (ADP test, cut-off <46) induced platelet aggregation at 6 months. 543 patients were screened and 120 patients were recruited with mean age of 67.5 years; 47.5% patients were male. The per-protocol ASPI test response rate to aspirin was 68.3% (95% CI 52.3-80.9%). The per-protocol ADP test response rate to ticagrelaor was 68.8% (95% CI 50.4-82.6%). Platelet response to antiplatelet therapy with aspirin and ticagrelor was not observed in nearly one-third of COPD patients without prior history of cardiovascular disease. These findings support the high pro-thrombotic milieu and the need for further research to determine the effect of antiplatelet/antithrombotic therapy on cardiovascular morbidity and mortality in COPD patients.
| S-EPMC6680071 | biostudies-literature
Project description:Platelet mRNA in response to antiplatelet therapy exposure
| PRJNA666442 | ENA