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• W2165883922 abstract "In the current issue of Cardiology Journal,Qi-ming Liu et al. [1] present the study in which theyprove that in the group of patients with microva-scular angina (myocardial ischemia without steno-sis in coronary arteries confirmed by means of se-veral methods) more intense lipid disorders occurthan in the control group (precisely selected interms of gender and age) and additionally that it isassociated with endothelial function impairment.This function was evaluated by measuring theextent of flow mediated dilatation of brachial artery(FMD, flow mediated dilatation). The negativecorrelation between concentration of lipoprote-in (a) and LDL cholesterol and FMD [1] was alsodemonstrated.This work touches upon the present questions— the problem of microvascular angina pathogene-sis, that is of syndrome X as well as the problem ofendothelial dysfunction and methods of its investi-gation.In patients with syndrome X among others thefollowing disorder s were diagnosed: decreased den-sity of capillary vessels in the myocardium [2], in-creased blood viscosity [3], platelet aggregation di-sorders [4], hormone disorders [5], abnormal reac-tions of autonomous nervous system [6] andvariously expressed endothelial dysfunction [7].Endothelial dysfunction is regarded as the firststage in the development of atherosclerosis [8]. Itis not a local process, but it refers to all arterialvessels. It was proved that all classical risk factorscan impair the function of endothelial [9–12]. In oneof our papers we demonstrated that endothelial dys-function assessed with FMD intensifies with theincreasing number of co-existing atherosclerosisrisk factors [13].Endothelial dysfunction is primarily associa-ted with decrease of nitric oxide (NO) secretionby endothelial cells, but also with the increase ofconcentration of von Willebrand factor (vWF), en-dothelin (ET), plasminogen activator inhibitor-1(PAI-1) and with tPA (tissue plasminogen activa-tor) concentration decrease [14]. This results inreduced dilatation ability, predisposition to intrava-scular thrombosis, leucocyte adhesion to vascularwall, intense proliferation of smooth muscle cellsin tunica intima [9]. Since the credible measure-ment of NO secretion is impossible because of itsinstability, the research in order to find other me-thods of endothelial function assessment was con-ducted. For this evaluation could assess the con-centration of other substances secreted by endothe-lial cells. Endothelial-dependent dilatation of one ofeasily accesible arteries, such as brachial artery, canalso be evaluated. Artery dilatation is caused by therelease of nitric oxide provoked by ‘shear stress’generated by hyperemia which follows the manome-ter cuff release. The latter method (FMD), as sim-ple and easily repeatable, is accepted and recommen-ded as the way of endothelial function assessment.The Working Group was created for this method [15].But so far standarization of the FMD research out-comes and norms has not been achieved [16]. TheFMD values considered as reference oscillate in widerange from 4 to 10% [16].Until recently there was no research whichwould demonstrate the correlation between concen-tration of substances secreted by endothelium andFMD. In one of the recently published papers Maaset al. proved a direct relation between the decre-ase of systemic NO production by endothelial NOsynthase (eNOS) and reduction of FMD [9]. In oneof our studies we documented that patients withsyndrome X have significantly higher PAI-1 con-centrations than healthy people and patients with" @default.
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• W2165883922 date "2008-01-01" @default.
• W2165883922 modified "2023-09-23" @default.
• W2165883922 title "In search of understanding the endothelium." @default.
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