Готові списки джерел за темами / Triple antithrombotic therapy

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Добірка наукової літератури з теми "Triple antithrombotic therapy"

Автор: Grafiati

Опубліковано: 10 березня 2023

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Статті в журналах з теми "Triple antithrombotic therapy"

Mega, Jessica, and Edward T. Carreras. "Antithrombotic therapy: triple therapy or triple threat?" Hematology 2012, no. 1 (December 8, 2012): 547–52. http://dx.doi.org/10.1182/asheducation.v2012.1.547.3798919.

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Abstract Antithrombotic therapy plays an essential role in the management of some of the most common and morbid medical conditions. Triple oral antithrombotic therapy (TOAT) is defined as the administration of both therapeutic oral anticoagulation (OAC) and dual antiplatelet therapy (DAPT) to patients with indications for both treatments. The current societal guidelines regarding TOAT are derived from observational studies and some trials of the use of warfarin in addition to antiplatelet therapy in patients with atrial fibrillation and a recent acute coronary syndrome or percutaneous coronary intervention. The general apprehension to administer TOAT is due to the heightened concern for bleeding, rendering warfarin's pharmacokinetic properties concerning. Newer anticoagulant agents may serve as appealing alternatives, and further investigations are warranted. The results of the recent trials that have studied the use of these agents in atrial fibrillation and acute coronary syndrome offer some useful applications to TOAT. Ultimately, selecting the most favorable antithrombotic strategy is going to involve weighing the risks and benefits for each patient.

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Nouri, Shayan Nabavi, and Brian L. Block. "Triple Oral Antithrombotic Therapy." JAMA Internal Medicine 176, no. 10 (October 1, 2016): 1433. http://dx.doi.org/10.1001/jamainternmed.2016.4415.

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Verheugt, Freek W. A. "Triple Antithrombotic Therapy After Coronary Stenting." Circulation: Cardiovascular Interventions 4, no. 5 (October 2011): 410–12. http://dx.doi.org/10.1161/circinterventions.111.965210.

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Han, Seongwook, Sola Han, Sung-Won Jang, Myung-Yong Lee, Young-Keun On, Oh Young Bang, Ji-Min Lee, et al. "Treatment Pattern of Antithrombotic Therapy over Time after Percutaneous Coronary Intervention in Patients with Atrial Fibrillation in Real-World Practice in Korea." Healthcare 9, no. 9 (September 9, 2021): 1185. http://dx.doi.org/10.3390/healthcare9091185.

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We examined antithrombotic treatment patterns with clinical characteristics and therapy changes over time in patients with atrial fibrillation (AF) after percutaneous coronary intervention (PCI). Using the Health Insurance Review and Assessment service claims database (01JAN2007-30NOV2016) in Korea, we included adult patients with AF and PCI: (1) who underwent PCI with stenting between 01JAN2008 and 30NOV2016; (2) with ≥1 claim for AF (ICD code: I48) (3) with antithrombotics 1 day prior to or at the date of PCI; and (4) with CHADS2-VASc of ≥2. In this study, 7749 patients with AF who underwent PCI, triple therapy, dual therapy, dual antiplatelet therapy (DAPT), and single antiplatelet therapy were prescribed to 24.6%, 3.4%, 60.8%, and 11.0%, respectively. In the triple therapy group, 23.1% persisted with triple therapy for 12 months, whereas the remaining patients switched to a different therapy. In the entire cohort and several subgroups, the median treatment duration of triple therapy was 55–87 days. DAPT use for 12 months was the most common treatment pattern (62.6%) in the DAPT group (median treatment duration, 324–345 days). A significant discrepancy exists between the current guidelines and real-world practice regarding antithrombotic treatment with PCI for patients with AF. Appropriate use of anticoagulants should be emphasized.

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Aloia, Elio, Paolo Orselli, and Carlotta Sciaccaluga. "Triple Antithrombotic Therapy vs. Double Antithrombotic Therapy: One Scenario, 8 Questions, Many Conclusions." Current Cardiology Reviews 15, no. 3 (May 6, 2019): 219–23. http://dx.doi.org/10.2174/1573403x15666190111095438.

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In patients with atrial fibrillation undergoing percutaneous coronary intervention with the placement of stents, a triple antithrombotic therapy is empirically established, which consists of a combination of dual antithrombotic therapy (aspirin plus a P2Y12 inhibitor) and an oral anticoagulant agent. This choice is guided by the desirable result of reducing cerebrovascular and coronary ischemic events. However, there is an unwelcome outcome: an increased incidence of bleeding. On this matter, in 2018, a North American Perspective Update was published, about a year later it was followed by the publication of the European focus update on the dual antiplatelet therapy. After analysing the main differences between these two consensus documents, this review aims at examining the major studies on which they are based on, as a starting point to define the foundation of new trials that can help shed light on this prominent topic.

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Sulaica, Elisabeth M., Matthew A. Wanat, and Tracy E. Macaulay. "Clinical Considerations Prior to Transition From Triple Antithrombotic Therapy to Dual Antithrombotic Therapy." JAMA Cardiology 5, no. 1 (January 1, 2020): 111. http://dx.doi.org/10.1001/jamacardio.2019.4542.

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Turaga, Naga Sai Shravan, Danish Abbasi, Tanya Sharma, and Barry Uretsky. "DOUBLE TROUBLE MANAGED WITH TRIPLE ANTITHROMBOTIC THERAPY." Journal of the American College of Cardiology 77, no. 18 (May 2021): 2420. http://dx.doi.org/10.1016/s0735-1097(21)03775-x.

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Fukaya, Hidehira, and Junya Ako. "Triple Antithrombotic Therapy – Always One Too Many? –." Circulation Journal 80, no. 2 (2016): 316–17. http://dx.doi.org/10.1253/circj.cj-15-1360.

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Sørensen, Rikke, and Gunnar Gislason. "Triple Antithrombotic Therapy: Risky but Sometimes Necessary." Revista Española de Cardiología (English Edition) 67, no. 3 (March 2014): 171–75. http://dx.doi.org/10.1016/j.rec.2013.08.010.

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Aytürk, Mehmet, Hamza Sunman, and Ekrem Yeter. "A Persisting Dilemma for Triple Antithrombotic Therapy." Journal of the American College of Cardiology 64, no. 2 (July 2014): 231. http://dx.doi.org/10.1016/j.jacc.2013.10.089.

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Дисертації з теми "Triple antithrombotic therapy"

Hung, Chih-Chung, and 洪智中. "Efficacy and Safety of Triple Oral Antithrombotic Therapy in Atrial Fibrillation and Coronary Artery Stenting." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/9kg579.

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碩士
高雄醫學大學
藥學系碩士在職專班
103
Background: Atrial fibrillation is a very common and severe cardiac arrhythmia which easily lead to heart blood clots to the brain ischemic stroke leading to death. Treatments of atrial fibrillation are not only to reduce cardiac symptoms, but also to prevent blood clots caused by cardiac ischemic stroke. According to ACCF/AHA/HRS therapeutic guideline, patient with high-risk (CHADS2 score≧1) can have anticoagulants to prevent stroke. Besides traditional oral Vitamin K Antagonists (Warfarin), In recent years, the development of new oral anticoagulant treatment which recommended in therapeutic guideline. Acute myocardial infarction (AMI) is a common reason for sudden cardiac death or heart failure, and the most common symptom is chest pain. When patient has MI’s symptom, he or she need to be sent to a emergency department (ED). Doctor from ED has to evaluate the reason for chest pain as soon as possible, and gives appropriate treatment in time. So far, the recommended treatments are percutaneous coronary intervention (PCI) or giving tissue plasminogen activator (tPA). Purpose: The study is base on to understand efficacy and safety with different treatments of antithrombotic agents selections that patient with atrial fibrillation and using anticoagulants has treatment after AMI occurred. Method: The study is using retrospective cohort study which included patient from 2004 to 2012 year. All patients in this study has atrial fibrillation and using anticoagulants, and they all had triple or non-triple antithrombotic agents therapy after Percutaneous coronary intervention (PCI) treatment in this hospital. Patients will use antithrombotic drugs are divided into two groups, namely the Triple oral antithrombotic therapy (TOAT group)and non- Triple oral antithrombotic therapy(NTOAT group). efficacy and safety clinical outcomes six months after the period of use of different combinations of antithrombotic drugs, such as: cerebrovascular relations events, cardiovascular events, bleeding events and time, patient mortality ,etc, whether or not a statistical difference. Results: In a retrospective study of medical records included a total of 332 patients met the criteria. And then based on the first day after admission, the clinical use of antithrombotic drugs for type divided into two groups, triple antithrombotic therapy group (TOAT group) A total of 57 patients; non-triple antithrombotic therapy group (NTOAT group) A total of 275 patients. Cardiovascular, cerebrovascular events and death as the efficacy of the two groups of patients presenting results. The case of total cardiovascular events were observed, triple therapy group 27 (47%) patients, non-triple therapy group 144 (52%) patients, the relative risk is 0.84 (95% CI 0.52-1.36), there was no statistically significant difference (p = 0.624> 0.05), in the case of cerebrovascular events were observed, the triple therapy group 7 (12%) patients, non-triple therapy group 91 (33%) patients, the relative risk is 0.33 (95% CI 0.15-0.71), the two group are statistically significant differences (P = 0.002 <0.05), and finally to the situation observed deaths, triple therapy group 12 (21 %) patients, non-triple therapy group, 103 (372%) patients, the relative risk is 0.50 (95% CI 0.27-0.91), the two are statistically significant differences (P = 0.018 <0.05), bleeding of patients as a vascular event to present safety. In the case of total bleeding events were observed, triple therapy group, 35 (62%) patients, non-triple therapy group had 123 (44%) patients, the relative risk is 1.75 (95% CI 1.75-2.85), There are statistically significant differences between the two group (P = 0.022 <0.05). Conclusion: According to the results from this study with atrial fibrillation after coronary artery stenting in these patients using oral medication triple antithrombotic effect is indeed effective in the prevention of ischemic stroke or death, but the opposite is caused by bleeding events also raised a lot, so how to increase both accurate and safe and effective use of antithrombotic drugs are currently used to assess more carefully.

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Berteotti, Martina, Anna Maria Gori, Betti Giusti, Renato Valenti, Carlo Di Mario, Niccolò Marchionni, and Rossella Marcucci. "Improving the net clinical benefit of dual/triple antithrombotic therapy in patients with atrial fibrillation and acute coronary syndrome: discovery and validation of prognostic factors for a tailored therapy." Doctoral thesis, 2022. http://hdl.handle.net/2158/1264944.

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We sought to identify possible clinical and laboratory predictors of bleeding and ischaemic risk in a real-world population with concomitant atrial fibrillation and PCI, discharged from our cardiology ward with double antithrombotic therapy (DAT) or triple antithrombotic therapy (TAT). Nell'ambito della tesi sono stati ricercati predittori clinici o laboratoristi di eventi ischemici o emorragici in una popolazione di pazienti con storia di fibrillazione atriale, sottoposti ad angioplastica, e dimessi in duplice o triplice terapia antitrombotica.

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Частини книг з теми "Triple antithrombotic therapy"

"Triple antithrombotic therapy after coronary stenting for chronically anticoagulated patients: too much of a good thing?" In Challenging Concepts in Cardiovascular Medicine, edited by Aung Myat, Shouvik Haldar, and Simon Redwood, 33–44. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199695546.003.0030.

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Becker, Richard C., and Frederick A. Spencer. "Cardiac Chamber, Aortic, and Valvular Thromboembolism." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0009.

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The left-sided cardiac chambers (left atrium, left ventricle) and heart valves (mitral valve, aortic valve) (native, prosthetic) serve as potential niduses for systemic thromboembolism, including fatal or debilitating stroke. The ascending aortic is also recognized as a source for embolism (aortoembolism) and should be considered when a comprehensive patient evaluation is being undertaken. The pathogenesis of intracavitary mural thrombosis, much like venous thromboembolism, follows the construct of Virchow’s triad. The area of stasis is often provoked by chamber dilation, reduced performance, or impaired flow across an existing heart valve (e.g., left atrial dilation from mitral stenosis). Endothelial injury may follow either an acute (e.g., myocardial infarction) or chronic (e.g., dilated cardiomyopathy) cardiac process. In the case of aortoembolism, plaque rupture in areas of advanced atherosclerosis serves as the primary site for thrombus development. The third component, prothrombotic state, may be focal (areas of inflammation and necrosis) and/or systemic. Left ventricular mural thrombosis is diagnosed either echocardiographically or at the time of autopsy among patients with myocardial infarction (MI), especially in those with anterior infarction involving the ventricular apex. In large, nonrandomized clinical trials of anticoagulant therapy, researchers have reported an incidence of cerebral embolism of 2% to 4% among nontreated patients, frequently causing either severe neurologic deficits or death. Of these trials, two showed a statistically significant reduction in stroke with early anticoagulation, whereas the third trial demonstrated a positive trend (Davis and Irelant, 1986). A meta-analysis performed by Vaitkus and Barnathan (1993) supports the findings of three previous studies published in the early 1980s. The odds ratio for systemic embolism in the presence of echocardiographically demonstrated mural thrombus was 5.45 (95% confidence interval [CI] 3.02–9.83). The odds ratio of anticoagulation versus no anticoagulation in preventing embolism was 0.14 (95% CI 0.04–0.52) with an event rate difference of –0.33 (95% CI –0.50 to –0.16). The odds ratio of anticoagulation versus control in preventing mural thrombus formation was 0.32 (95% CI 0.20–0.52) and the event difference was –0.19 (95% CI 0.09–0.28).

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Becker, Richard C., and Frederick A. Spencer. "Plaque-Stabilizing Therapies." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0028.

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The association between elevated low density lipoprotein (LDL) cholesterol and atherothrombotic vascular disease is well established. Lipid-lowering therapies reduce cardiovascular events; however, the mechanism of benefit attributable to HMG CoA reductase inhibitors likely transcends lipids alone by directly or indirectly affecting inflammatory response, endothelial cell resistance, apoptosis, and progenitor cell behavior. Although collectively in the same class of drugs, statins have unique pharmacokinetic profiles. They may also differ in their ability to impact inflammatory responses, endothelial performance including enhanced thromboresistance capability, plaque vulnerability, and vascular thrombosis. Unlike the LDL cholesterol–lowering effect, the “nonlipid”-related properties of statins are less closely tied to dose (Undas et al., 2005). Support for a multifactorial benefit from statin therapy has been derived from a number of clinical trials revealing a nonlinear correlation between LDL cholesterol reduction and protection from clinical events. In the Anglo-Scandinavian Cardiac Outcomes Trial–Lipid Lowering Arm (ASCOT-LLA), 1,934 hypertensive patients (ages 40–75) with at least three other cardiovascular risk factors and either average or below average total cholesterol levels received either atorvastatin (10 mg) or placebo. By 3.3 years of follow-up, there was a marked reduction in cardiovascular death, nonfatal myocardial infarction (MI), and stroke (fatal and nonfatal) in patients receiving low-dose atorvastatin (Sever et al., 2003). Several studies and registries have also shown a benefit attributable to statin use among patients with acute coronary syndromes. Many, with the exception of the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL), have been post hoc, retrospective analyses or observational studies (Arntz et al., 2000; Aronow et al., 2001; Bybee et al., 2001; Schwartz et al., 2001). However, in the PROVE-IT (Pravastatin or Atorvastatin Evaluation and Infection Therapy) trial (Cannon et al., 2004), 4,162 patients treated with either pravastatin (40 mg daily—moderate-intensity statin therapy) or atorvastatin (80 mg daily—intensive therapy) within 10 days of an acute coronary syndrome (ACS) had a 16% reduction in the likelihood of death (any cause), MI, ACS requiring hospitalization, revascularization, or stroke with more intensive treatment.

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Becker, Richard C., and Frederick A. Spencer. "Venous Thromboembolism Prophylaxis." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0030.

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Venous thromboembolism represents a true worldwide medical problem that is encountered within all realms of practice. Venous thromboembolism (VTE) occurs in approximately 100 patients per 100,000 population yearly in the United States and increases exponentially with each decade of life (White, 2003). Approximately one-third of patients with symptomatic deep vein thrombosis (DVT) experience a pulmonary embolism (PE). Death occurs within 1 month in 6% of patients with DVT and 12% of those with PE. Early mortality is associated strongly with presentation as PE, advanced age, malignancy, and underlying cardiovascular disease. An experience dating back several decades has provided a better understanding of disease states and conditions associated with VTE (Anderson and Spencer, 2003). Given the potential morbidity and mortality associated with VTE, it is apparent that prophylaxis represents an important goal in clinical practice. A variety of anticoagulants including unfractionated heparin, low-molecular-weight heparin (LMWH), and warfarin have been studied. More recently, two new agents have been developed that warrant discussion. Fondaparinux underwent a worldwide development program in orthopedic surgery for the prophylaxis of VTE. The program consisted mainly of four large, randomized, double-blind phase II studies comparing fondaparinux (SC), at a dose of 2.5 mg starting 6 hours postoperatively, with the two enoxaparin regimens approved for VTE prophylaxis—40 mg qd or 30 mg twice daily beginning 12 hours postoperatively. The results support a greater protective effect with fondaparinux, yielding a 55.2% relative risk reduction of VTE (Bauer et al., 2001; Eriksson et al., 2001; Lassen et al., 2002; Turpie et al., 2001, 2002; ). A European program of three large-scale clinical trials (MElagatran for THRombin inhibition in Orthopedic surgery [METHRO] I, II, and III, and EXpanded PRophylaxis Evaluation Surgery Study [EXPRESS]) (Eriksson et al., 2002a, b, 2003a, b) evaluated the safety and efficacy of subcutaneous melagatran followed by oral ximelagatran compared with LMWH for thromboprophylaxis following total hip replacement (THR) and total knee replacement (TKR) surgery.

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Becker, Richard C., and Frederick A. Spencer. "Platelet Antagonists." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0035.

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Platelet antagonists play an important role in both primary and secondary prevention of atherothrombotic events. Despite their proven benefit, individual response (and protection) varies considerably, emphasizing the importance of developing monitoring tools (tested prospectively in clinical trials) that can better determine the degree of platelet inhibition that is both safe and effective. Platelet function studies were developed originally for the evaluation of patients with unexplained bleeding and have contributed greatly to the understanding, diagnosis, and management of hereditary abnormalities such as von Willebrand disease and Glanzmann’s thrombasthenia (platelet glycoprotein [GP] IIb/IIIa receptor deficiency). Although conventional platelet function studies (turbidimetric aggregometry) have technical limitations that preclude their routine use for gauging antithrombotic therapy, they may provide guidance when hemorrhagic complications arise and in determining pretreatment risk in individuals suspected of having an intrinsic platelet abnormality. The bleeding time, considered an indicator of primary hemostasis (platelet plug formation), is defined as the time between making a small standardized skin incision and the precise moment when bleeding stops. The test is performed with a template, through which the medial surface of the forearm is incised under 40 mmHg standard pressure. A normal bleeding time is between 6 and 10 minutes. Although considered a “standardized” test of platelet function, the bleeding time can be influenced by a variety of factors, including platelet count, qualitative abnormalities, and features intrinsic to the blood vessel wall (George and Shattil, 1991). Platelet adhesion is the initiating step in primary hemostasis. Although platelet binding is an important component of this process, there are many others, including blood flow rate, endothelial cell function, adhesive proteins, and the subendothelial matrix. The original test used for assessing adhesion, platelet retention, was based on adherence to glass bead columns. The current laboratory evaluation of platelet function is based predominantly on turbidimetric platelet aggregometry (also known as light transmission aggregometry). This test is performed by preparing platelet-rich plasma (with platelet-poor plasma as a control) and eliciting an aggregation response with adenosine diphosphate, epinephrine, collagen, arachidonic acid, and ristocetin (Born, 1962).

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Becker, Richard C., and Frederick A. Spencer. "Clopidogrel." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0013.

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Clopidogrel, a thienopyridine derivative, is a novel platelet antagonist that is several times more potent than ticlopidine but associated with fewer adverse effects. After repeated 75-mg oral doses of clopidogrel, plasma concentrations of the parent compound, which has no platelet-inhibiting effect, are very low. Clopidogrel is extensively metabolized in the liver. The main circulating metabolite is a carboxylic acid derivative with a plasma elimination half-life of 7.7 ± 2.3 hours. Approximately 50% of an oral dose is excreted in the urine and the remaining 50% in feces over the following 5 days. Dose-dependent inhibition of platelet aggregation is observed 2 hours after a single oral dose of clopidogrel, with a more significant inhibition achieved with loading doses (≥300 mg) by approximately 6 hours. Repeated doses of 75 mg of clopidogrel per day inhibit adenosine diphosphate (ADP)-mediated aggregation, with steady state being reached between day 3 and day 7. At steady state, the average inhibition to ADP is between 40% and 60%. Based on ex vivo studies, clopidogrel is approximately 100-fold more potent than ticlopidine. There are no cumulative antiplatelet effects with prolonged oral administration. The combined administration of clopidogrel (300 mg loading dose) and aspirin yields a readily discernible platelet-inhibiting effect within 90 to 120 minutes. Clopidogrel selectively inhibits the binding of ADP to its platelet receptor (P2Y12) and the subsequent G-protein–linked mobilization of intracellular calcium and activation of the glycoprotein (GP)IIb/IIIa complex (Gachet et al., 1992). The specific receptor has been cloned and is abundantly present on the platelet surface (Hollopter et al., 2001). Clopidogrel has no direct effect on cyclooxygenase, phosphodiesterase, or adenosine uptake. Clopidogrel is rapidly absorbed following oral administration with peak plasma levels of the predominant circulating metabolite occurring approximately 60 minutes later. Administration with meals does not significantly modify the bioavailability of clopidogrel. The available information suggests that clopidogrel offers safety advantages over ticlopidine, particularly with regard to bone marrow suppression and other hematologic abnormalities. Although thrombotic thrombocytopenic purpura (TTP) has been reported with clopidogrel (Bennett et al., 2000), its occurrence (11 cases per 3 million patients treated) is rare, and has not been reported in randomized clinical trials performed to date.

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Becker, Richard C., and Frederick A. Spencer. "Acute Coronary Syndromes." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0025.

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For over a century astute clinicians have recognized that prodromal symptoms often precede acute myocardial infarction (MI). The evolution of symptoms was subsequently found to correlate with changes in atherosclerotic plaque composition, morphology, and thrombogenicity, leading to the classification of symptoms that are currently categorized to better delineate diagnostic and management strategies. Acute coronary syndromes (ACSs) are traditionally divided into two separate categories—ST-segment elevation and non–ST-segment elevation ACS—based on the presenting electrocardiogram. The latter category is then subdivided into unstable angina and non–ST-segment elevation MI, based on the absence or presence of elevated cardiac biomarkers, respectively. This chapter considers ST-segment elevation MI and non–ST-segment elevation ACS based on pharmacologic and clinical (diagnostics and routine management) constructs. ST-segment elevation MI (STEMI), in a vast majority of cases, is caused by occlusive thrombosis at a site of plaque rupture. In others, particularly when the stimulus for thrombosis is strong, occlusion may follow minor disruption of the plaque surface (erosion) or occur in areas of endothelial cell injury (activation with inflammatory features and concomitantly impaired vascular thromboresistance). Coronary arterial spasm, in the absence of intrinsic vascular disease (as may be seen with cocaine use), can also impair restrictive blood flow to the myocardium, resulting in cellular death. The goal of pharmacology-based therapy (and mechanical intervention) is to restore myocardial blood flow as quickly and completely as possible. The “open vessel hypotheses” predicts that rapid, complete, and sustained myocardial perfusion through the prompt restoration of physiologic blood flow will minimize (salvage) myocardium, promote ventricular performance, and reduce mortality. Strong support for the open-vessel hypothesis can be traced to the Thrombolysis and Myocardial Infarction (TIMI) trial performed in the 1980s (Dalen et al., 1988; TIMI Study Group, 1985). Patients with patent infarct-related coronary arteries 90 minutes after the initiation of fibrinolytic therapy had an 8.1% mortality at 1 year, compared to a 14.8% mortality among those with an occluded vessel. Since that time, several large-scale clinical trials have confirmed the importance of an open infarct-related coronary artery for early, intermediate, and long-term outcome.

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"Thrombolytic/antithrombotic clinical trials in cardiology: an overview." In Thrombolytic and Antithrombotic Therapy for Stroke, 74–89. CRC Press, 2004. http://dx.doi.org/10.1201/b14309-8.

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"Study design for thrombolytic and antithrombotic treatment trials in acute stroke: mistakes and lessons." In Thrombolytic and Antithrombotic Therapy for Stroke, 90–103. CRC Press, 2004. http://dx.doi.org/10.1201/b14309-9.

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Minhas, Jatinder S., Amit K. Mistri, and Thompson G. Robinson. "Secondary prevention and revascularization in the older person." In Stroke in the Older Person, 353–64. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198747499.003.0023.

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‘Secondary prevention and revascularization in the older person’ examines the proven and contentious issues of secondary prevention strategies following stroke or transient ischaemic attack; however, the majority of large randomized clinical trials supporting individual interventions are in a younger population than real-life, older, stroke survivors. Various strategies for secondary prevention, lifestyle approaches, research trials of antithrombotic therapy and blood pressure reduction, lipid modification, atrial fibrillation, glycaemia, surgical interventions, and intracerebral haemorrhage are dealt with in detail. The older population has greater disability and dependency from stroke and other comorbidities, and the benefits and risks of secondary prevention therapy may therefore differ from their younger counterparts. While there is a need for further research on secondary prevention strategies in older populations, the current management involves incorporation of evidence-based approaches into a pragmatic individualized approach, with careful consideration of risks and benefits.

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Тези доповідей конференцій з теми "Triple antithrombotic therapy"

Assaf, Omar, Sabeeh Shams, Aysha Basir, Tawfiq Choudhury, and Kenneth Wong. "41 Meta-analysis of clinical trials comparing triple versus dual antithrombotic therapy in patients with atrial fibrillation and acute coronary syndromes or coronary artery disease requiring percutaneous intervention." In British Cardiovascular Society Virtual Annual Conference, ‘Cardiology and the Environment’, 7–10 June 2021. BMJ Publishing Group Ltd and British Cardiovascular Society, 2021. http://dx.doi.org/10.1136/heartjnl-2021-bcs.41.

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Ferreira, Hanna dos Santos, Agata Layanne Soares da Silva, and João Lucas de Sousa Peres. "Fibrinolytic therapy in the treatment of pediatric ischemic stroke." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.033.

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Анотація:

Introduction: Pediatric stroke is a disorder that can result in morbidity and mortality. The ischemic type is the most common and has thrombolytics as the preferred therapy. Objective: To evaluate the therapeutic management and efficacy of fibrinolytics in pediatric patients with ischemic stroke. Methodology: The literature review was carried out in PUBMED, MEDLINE, Embase databases, with the descriptors “Fibrinolytic Agents”, “Thrombolytic Therapy”, “Ischemic Stroke”, “Stroke”, “Pediatrics” and “Treatment”. Included were clinical trials, randomized controlled trials, cohort, case- control, and case series in English or Portuguese published in the last 5 years. It gathered 8 articles. Results: Treatment in the acute phase and for secondary prevention in the chronic phase of pediatric stroke are antithrombotic therapies and platelet antiaggregants, commonly aspirin. Comparing the latter and low molecular weight heparin, neither has shown superiority in preventing stroke recurrence. Without good evidence, however, aspirin is indicated for idiopathic stroke and anticoagulants in cardioembolic stroke by some guidelines. In recombinant tissue plasminogen activator therapy in one paper it was suggested there is more risk for conversion to hemorrhagic events compared to untreated, but in another paper hemorrhage was not seen. There was high mortality with this therapy and higher chances of being discharged to short term hospital, skilled nursing facility or intermediate care facility. In endovascular therapy, delay in diagnosis limits its use and stroke complications did not differ between patients who did or did not undergo this therapy. Conclusion: Further studies are needed to evaluate the efficacy of fibrinolytics.

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Colleran, R., RA Byrne, H. Rai, A. Kastrati, and S. Cassese. "14 Antithrombotic therapy with or without aspirin after percutaneous coronary intervention or acute coronary syndrome in patients taking oral anticoagulation: a meta-analysis and network analysis of randomised controlled trials." In Irish Cardiac Society Annual Scientific Meeting & AGM (Virtual), October 1st – 3rd 2020. BMJ Publishing Group Ltd and British Cardiovascular Society, 2020. http://dx.doi.org/10.1136/heartjnl-2020-ics.14.

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