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Lege Artis Medicinae

DECEMBER 15, 2015

[The positive additive effect of rosuvastatin on platelet aggregation parameters in patients with cerebrovascular disease]

FEHÉR Gergely

[Statin therapy is the cornerstone of anti-atherosclerotic treatment, and it considered obligatory in the secondary prevention of atherosclerotic diseases. Rosuvastatin is well-known and efficacious lipid-lowering agent and seems to have benefitial antiplatelet efficacy and anti-inflammatory profile. The aim of our study was to determined the antiplatelet effect of 20 mg rosuvastatin (Xeter®, Richter Gedeon Nyrt.) in clopidogrel treated cerebrovascular patients. 20 patients with documented ischaemic cerebrovascular events and on 75 mg clopidogrel daily treatment were included in our study. 20 mg generic rosuvastatin significantly decreased total cholesterol (5.67 vs. 3.99 mmol/l, p<0.05), low-density lipoprotein (3.11 vs. 1.92 mmol/l, p<0.05) and trigliceride levels (1.75 vs. 1.29 mmol/l, p<0.05), and there was a non-significant high-density lipoprotein increasing (1.28 vs. 1.36 mmol/l, p=0.09) and high-sensitive C-reactive protein level decreasing tendency (3.35 vs. 2.99 mg/l, p=0.07). Rosu­vastatin treatment significantly decreased ADP 5 µM (46.15 vs. 31.35%) and collagen 2 mg/ml (68.62 vs. 52.22%) induced platelet aggregation (p<0.05). 20 mg rosuvastatin has a robust antilipaemic profile with benefitial additive effect on agonist induced platelet aggregation.]

Clinical Neuroscience

JANUARY 25, 2013

[Aspirin and clopidogrel resistance: possible mechanisms and clinical relevance. Part II: Potential causes and laboratory tests]

VADÁSZ Dávid, SZTRIHA K. László, SAS Katalin, VÉCSEI László

[Recent meta-analyses have indicated that patients with vascular disease demonstrated by laboratory tests to be aspirin or clopidogrel-resistant are at an increased risk of major vascular events. The suggested mechanisms of aspirin resistance include genetic polymorphism, alternative pathways of platelet activation, aspirin-insensitive thromboxane biosynthesis, drug interactions, or a low aspirin dose. Clopidogrel resistance is likely to develop as a result of a decreased bioavailability of the active metabolite, due to genetic variation or concomitant drug treatment. Additional work is required to improve and validate laboratory tests of platelet function, so that they may become useful tools for selection of the most appropriate antiplatelet therapy for an individual patient. Improvements in antiplatelet treatment strategies in the future should lead to a reduction in premature vascular events.]

Clinical Neuroscience

NOVEMBER 20, 2012

[Aspirin and clopidogrel resistance: possible mechanisms and clinical relevance. Part I: Concept of resistance]

VADÁSZ Dávid, SZTRIHA K László, SAS Katalin, VÉCSEI László

[Aspirin and clopidogrel are well established as antiplatelet medication in the treatment of atherothrombotic vascular disease. However, despite treatment, a substantial number of patients experience recurrent ischemic episodes, referred to as aspirin or clopidogrel treatment failure. Various laboratory techniques are available with which to evaluate the effectiveness of antiplatelet drugs. Interestingly, the agreement between the results of the different tests may be poor. The term aspirin or clopidogrel resistance denotes those conditions in which an inadequate inhibitory efficacy of the given antiplatelet agent is detected by an in vitro assay of platelet function. It has been estimated that on average some 30% of patients treated with aspirin, and 20% on clopidogrel, do not achieve an appropriate level of efficacy as concerns platelet activity.]

Lege Artis Medicinae

OCTOBER 20, 2011

[Examination of the efficacy of clopidogrel-hydrogen-sulphate in patients with cerebrovascular disease]

SZAPÁRY László, FEHÉR Gergely

[INTRODUCTION - On the basis of current guidelines, acetylsalicylic acid plus dipyridamole or clopidogrel monotherapy should be used for the long-term treatment of patients with cerebrovascular disease, whereas acetylsalicylic acid monotherapy is not recommended. The efficiency of recently introduced generic clopidogrels has not been assessed in patients with a history of acute stroke. PATIENTS AND METHODS - 100 patients with a history of acute stroke or transient ischaemic attack were involved in our study. The patients received acetylsalicylic acid monotherapy in the first 48 hours, followed by clopidogrel-hydrogen sulphate (Egitromb®) monotherapy. The efficiency of the therapy was assessed on day 7 and 28 of medical therapy. RESULTS - At the first measurement (day 7) after clopidrogel-hydrogen sulphate treatment, the therapy seemed to be inefficient in 11 patients (11%). A strong, clinically significant correlation was found between blood pressure values, blood glucose and lipid parameters, hsCRP levels and platelet aggregation values. At the second measurement (day 28), an aggressive secondary preventive threapy resulted in the normalisation of the above mentioned parameters, and the efficiency of platelet aggregation inhibtion therapy was also improed, whereas no patients proved to be resistant. No unwanted events or haemorrhagic complications were registered. CONCLUSIONS - On the basis of the result of our study, treatment with clopidogrel- hydrogen sulphate is safe and efficient both clinically and on the basis of optical aggregometry. The significance of an aggressive secondary preventive therapy should be considered as a factor that might influence the efficiency of thrombocyte aggregation inhibitory therapy.]

Lege Artis Medicinae

APRIL 20, 2003

[Benefit of combined clopidogrel-aspirin platelet aggregation inhibition in acute coronary syndrome and after percutaneous coronary angioplasty]


[Platelet aggregation inhibition is equally important both in conservative and interventional cardiological treatment of acute coronary syndrome. Recently, results from three important trial were published. All three proved the efficacy of the combined aspirin + clopidogrel treatment. The basic results of the three clinical trials (CURE, PCI-CURE, CREDO) are summarized in the article. In the CURE trial the combined primary endpoint was reached in 11.4% of the patients in the control group and in 9.3% in the clopidogrel group. The relative risk reduction was 20%. The combined primary endpoint included CV mortality, MI and stroke. The treatment effect was mostly detectable in the prevention of MI and stroke. In the PCI-CURE trial 2658 patients of the CURE trial were analysed. All of them were treated by coronary angioplasty. In this group the primary endpoint (CV death, nonfatal MI, urgent revascularisation) was reached in 6.4% of the aspirin treated and in 4.5% of the aspirin + clopidogrel treated patients. The relative risk reduction was 30%. The CREDO trial investigated patients after coronary angioplasty. The indication of angioplasty was either acute or chronic. All patients received combined aspirin + clopidogrel but only for four weeks in the control group or for one year in the treatment group. The combined primary endpoint was decreased by 26.9%. In all the 3 trials the risk of bleeding was slightly but significantly increased by the combined aspirin + clopidogrel treatment. Clinical application: based on the results of the 3 trials it is concluded that combined aspirin + clopidogrel treatment is indicated in all patients with acute coronary syndrome, independently from the treatment strategy. The treatment should be continued for one year. This is also applicable for all patients treated with coronary angioplasty.]

Lege Artis Medicinae

JULY 10, 2001

[Platelet aggregation inhibitors in the prevention of coronary coronary artery disease. „Handle with care!"]

NAGY Viktor

[Platelets play pivotal role in the pathophysiology of unstable angina, acute myocardial infarction and in complications following percutaneous coronary intervention. Three classes of platelet-inhibiting drugs, aspirin, thienopyridines and platelet glycoprotein IIb/IIIa inhibitors are now commonly used for the prevention and treatment of the disorders of coronary artery thrombosis. For the last several decades, aspirin has been the sole option for antiplatelet therapy in the treatment and prevention of the manifestations of cardiovascular disease. However, a wider selection of antiplatelet agents, including the thienopyridines (ticlopidine and clopidogrel) and the platelet glycoprotein IIb/IIIa receptor antagonists are available today. This review summarizes these drugs and scientific data that have led to their use in primary and secundary prevention, unstable angina, myocardial infarction and percutaneous coronary intervention.]