[Clopidogrel resistance: myth or reality].

The efficacy of clopidogrel, as an established anti-platelet agent for the acute coronary syndrome treatment and for the thrombotic complications prevention after percutaneous coronary angioplasty and coronary artery stenting has been supported by the evidence of several major randomized clinical trials. However, some patients treated with clopidogrel have a minor, but still a risk of coronary artery thrombosis and sudden death. Moreover, clopidogrel was not effective in patients after ischemic stroke, as well as it was not effective for the primary prevention of vascular events. Several authors proposed the theory of " clopidogrel-resistance " . However, this theory is based on a limited number of laboratory findings, and was not supported by the evidence of clinical studies. The phenomena of " clopidogrel-resistance " could be masked by the low patient compliance, while the rate of such patients could exceed 30% after one year of treatment. The offered methods for overcoming clopidogrel-resistance include doubling or tripling of the loading dose (600-900 mg vs. 300mg) or administration one or two more potent antiplatelet agents. However, such approach could not only increase the risk of major and fatal bleedings, but could have a potential to reduce patients compliance, and consequently increase the risk of thrombosis. Only multicenter randomized study with hard outcome or ideally survival endpoint, supported by comprehensive serial platelet assessment, strict compliance rules including measurement of clopidogrel metabolite(s) will determine whether " clopidogrel resistance " is a real danger (as suggested by the platelet biomarkers), or an artificial tool (as suggested by the randomized clinical evidence) introduced to help novel antiplatelet agents to gain the vascular market share.

[A morphologic analysis of changes in the lungs and kidneys caused by acetyl glyceryl ether phosphorylcholine and limited by verapamil]. / Morfologicheskii analiz izmenenii v legkikh i pochkakh, vyzvannykh atsetilglitseril'nym éfirom fosforilkholina i ogranichennykh verapamilom.

Histological analysis of lung and kidney after multiple PAF i.v. injection into rabbits was performed. Under these conditions the effect of previously injected of verapamyl, calcium channel blocker, was studied. It was shown that RAF causes inflammatory reaction with cell infiltration, microcirculation disorders and thrombosis in lung and kidney, which may classify as interstitial nephritis, pneumonitis and vasculitis. Verapamyl inhibits vasospasm, abolishes fibrinogen but does not affect cell infiltration and oedema development. Thus, Ca channel-dependent mechanism of vasospasm and thrombogenesis induced by PAF in vivo is confirmed. Perhaps, another possibilities for realising PAF action in vivo may occur.

[Features of thrombophilia in nephrotic syndrome in children]. / Osobennosti trombofilii pri nefroticheskom sindrome v detskom vozraste.

A comprehensive study was made of the hemostatic system in 25 children with the nephrotic syndrome and combined forms of glomerulonephritis. Hypercoagulation and a number of factors preventing thrombosis formation were revealed, namely the presence of so-called thrombin-resistant blocked fibrinogen, a rise of the total antithrombin potential at the expense of proteins differing from antithrombin III, sufficient reserves of plasminogen, and a moderate increase of fibrin degradation products.