Hepatic artery thrombosis versus neurological complications – Role of antiplatelet medications in adult living donor liver transplantation
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Aspirin used in the post-operative period as prophylaxis for hepatic artery thrombosis (HAT) increases the risk of neurological complications (NC) in adult living donor liver transplantation (LDLT) recipients was the hypothesis. Case control study was done on 1400 cases operated in our institute. Pediatric transplants, combined liver kidney, cadaver transplants, dual lobe transplants, preexisting organic neurological dysfunction and patients whose records were missing were excluded from the study. There were effectively 880 cases in non-aspirin group (NAG) and 440 cases in aspirin group (AG). The groups were matched for various factors. There were more alcoholics in AG and more ALFs in NAG. On subgroup analysis these two etiological factors were found to be statistically insignificant P > 0.05. So the prophylactic protocol was aspirin 75 mg once daily in all adults (age >12 years) once the platelet counts have reached 50,000 and there is no evidence of bleeding elsewhere. In pediatric population our protocol is use of aspirin 75 mg and clopidogrel 75 mg once daily once the platelet counts have reached 50,000 and there is no evidence of bleeding anywhere else.Keywords:
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Clopidogrel is an antiplatelet drug that irreversibly binds to the platelet purinergic P2Y12 receptor and inhibits ADP-induced stimulation of the GPIIb/IIIa receptor complex. It is widely used for management of atherothrombotic disease in patients who have experienced severe vascular events such as stroke or myocardial infarction or with peripheral artery disease. The current data, however, show that about 5% to 44% of patients treated with conventional doses of clopidogrel do not display adequate antiplatelet response and result in a high risk of recurrent atherothrombotic events. There are several factors that can affect clopidogrel response such as genetic polymorphisms of drug metabolizing enzymes (i.e. CES1, CYP2C19, and PON1), genetic polymorphisms of P2Y12 receptors, drug formulations, and drug-drug interaction. Identification of factors affecting clopidogrel response is needed to improve the antiplatelet effect and reduce risks for cardiovascular events. The purpose of this review is to discuss the contribution of individual factors responsible for variations of action and clopidogrel efficacy. This information will be very useful for physicians, pharmacists, and healthcare personnel for considering and increasing the safety and efficacy of clopidogrel therapy.
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Both aspirin and clopidogrel reduce the rate of cardiovascular events in patients with coronary heart disease. We estimated the cost effectiveness of the increased use of aspirin, clopidogrel, or both for secondary prevention in patients with coronary heart disease.
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Background: Studies regarding the efficacy of Aspirin alone versus combination of Aspirin and Clopidogrel in patients with Unstable Angina are many. But, studies on the comparative role of Aspirin alone versus Aspirin plus Clopidogrel in the background of Acute Coronary Syndrome (ACS) with ST segment elevation myocardial infarction (STEMI) were very few, at the time of starting of this study. Keeping this in mind present study was conducted to compare the efficacy and safety of Aspirin alone with combination of aspirin plus Clopidogrel in prevention of events in Acute Coronary Syndrome with ST segment elevation myocardial infarction.Methods: Patients who are admitted to intensive coronary care unit within 12hrs after the onset of symptoms and whose diagnosis as ACS with ST segment elevation has been established were included in this study. Patients in group 1 received 325 mg of aspirin as loading dose, followed by 150 mg once daily. Patients in group 2 received a combination of aspirin and Clopidogrel 325 and 300 mg, respectively, as loading dose, followed by 150 mg of aspirin and 75 mg of Clopidogrel daily. All the patients received a fibrinolytic agent. Treatment response was weighed against the primary and secondary expected outcomes.Results: Addition of Clopidogrel to Aspirin resulted in significant reduction in severe ischaemia not requiring urgent revascularisation i.e.; 32% in Aspirin alone group versus 10% in Aspirin plus Clopidogrel group and recurrent angina with no ECG changes i.e.; 42% in aspirin alone group versus 20% in Aspirin plus Clopidogrel group. Similarly, there was an improvement in ejection fraction at the end of one month i.e.; 0.3% in Aspirin alone group versus 1.85% in Aspirin plus Clopidogrel group.Conclusions: This study demonstrates the benefit of adding Clopidogrel to Aspirin for myocardial infarction with ST-segment elevation. Treatment with a loading dose of 300mg of Clopidogrel followed by a daily dose of 75mg, in addition to aspirin, resulted in significant improvement in the secondary efficacy related outcomes in patients with acute coronary syndrome with ST-segment elevation.
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Aspirin and clopidogrel resistance: methodological challenges and opportunities Armen Yuri GasparyanClinical Research Unit, Russell's Hall Hospital, Dudley Group of Hospitals NHS Foundation Trust, West Midlands, UKAbstract: Antiplatelet drug resistance is one of the urgent issues in current cardiovascular medicine. Many platelet function tests have been used to define responsiveness of patients with cardiovascular disease to aspirin and clopidogrel. In most studies, cut-off values of platelet function tests for defining responsiveness to antiplatelets were chosen arbitrarily. Different tests provided wide-ranging figures of the prevalence of aspirin and clopidogrel resistance, suggesting poor correlation between currently available platelet function tests. Measurement of platelet size seems to be a promising approach for monitoring antiplatelet drug therapy. This commentary highlights some limitations of studies on aspirin and clopidogrel resistance in patients undergoing coronary interventions.Keywords: aspirin, clopidogrel, resistance, cardiovascular disease, platelet function tests
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Abstract Background The platelet adenosine 5′-diphosphate (ADP) receptor antagonist clopidogrel has proved an effective antiplatelet agent in the prevention of arterial thrombosis. In the vast majority of studies clopidogrel has been used as an alternative to aspirin, but the widespread use of aspirin, and the different modes of actions of the two drugs, makes it important to determine the safety and efficacy of using both drugs in combination. This study reports the effect of this drug combination on bleeding times and platelet function in humans. Methods The study was conducted in normal, healthy subjects to evaluate the effects of different doses of clopidogrel on bleeding time, platelet aggregation and activation, above a baseline of standard aspirin therapy. Seven normal men (mean age 30 years) were given aspirin (150 mg) for 3 days. Subjects received clopidogrel (75 mg) at 24 and 48 h, followed by a third dose of clopidogrel (300 mg) on day 3. Results The combination of aspirin plus clopidogrel leads to a significant reduction in platelet function relative to aspirin alone (P < 0·05), and is associated with a significant increase in the bleeding time (P < 0·05). The response to collagen was similarly affected. Platelet fibrinogen binding in response to both ADP and thrombospondin-related adhesive protein was reduced only partially by aspirin, but significantly reduced by both doses of clopidogrel (P < 0·05 for all). P-selectin expression in response to both agonists was also reduced, but not significantly. Basal levels of fibrinogen binding, P-selectin, glycoprotein (GP) IIb–IIIa and GPIb expression were not affected by treatment. Conclusion Blocking both the cyclo-oxygenase and ADP pathways of platelet activation has a profound effect on platelet response to agonists, which may offer significant potential benefit in preventing thrombotic events relative to aspirin alone. Achieving the correct balance between haemostasis and thrombosis with these useful agents will require further study.
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Ticlopidine
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New antiplatelet drugs are being developed and many clinical trials evaluating the benefits of antiplatelet drugs for the secondary prevention of ischemic events in patients with atherosclerotic vascular disease have been performed.
Ticlopidine
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Stroke
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As we all know,platelets play a key role in the formation of arterial thrombosis and antiplatelet therapy has become the cornerstone for the prevention and treatment of arterial thrombosis in patients with acute coronary syndrome.Clopidogrel is a new antiplatelet drug,which has been confirmed as an important adjuvant therapy of cardiovascular disease.However,Many studies have found that about 11%-44% of patients show low response even non-response to clopidogrel,which is defined as clopidogrel resistance.The causes,which lead to this resistance phenomenon,may be due to inadequate doses of clopidogrel administration,the individual gene polymorphism,drug interactions and so on.The main strategies of clopidogrel resistance include increasing doses of clopidogrel administration,combining with other antiplatelet drugs,reducing adverse drug interactions and using of new drugs.
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Ticlopidine
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Clopidogrel is the most widely used P2Y12 inhibitor, which is administered for secondary prevention of atherothrombotic events in patients with cardiovascular disease after myocardial infarction and coronary stenting. Given the complexity of the clopidogrel metabolism and variety of potential drug-drug interactions, the issue of individual variability of its antiplatelet effects is of paramount concern. Another issue of clinical relevance is related to so-called “smoker’s paradox”. This phenomenon implies that in some patients smoking is associated with increased antiplatelet potency of clopidogrel. In this review, we analyze recent international data on the features of pharmacokinetics and pharmacodynamics of clopidogrel, plausible mechanisms of the “smoker’s paradox” and its clinical significance in patients with coronary artery disease. Comparative efficacy of available P2Y12 inhibitors and possible implications of smoking are considered. Pharmacogenetic aspects and the issues of personalized antiplatelet therapy are discussed.
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