Faculty of Medicine

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    Effect of angiotensin II type 1 (AT1) receptor antagonist on the endothelial dysfunction in spontaneously hypertensive rats in correlation with the nitric oxide system
    (Comenius University, School of Medicine - AEPRESS SRO, 2003)
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    Korneti, Petar
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    Jovanoska, E
    Hypertension is associated with impaired endothelial function, which can be explained by a decrease in nitric oxide (NO) generation or by an enhanced inactivation of NO after its release from endothelial cells. The aim of this study was to investigate the effect of long-term treatment with losartan, an angiotensin II (AT1) receptor antagonist, on endothelial dysfunction in an animal model of hypertension in relation to the nitric oxide system. Losartan was administered to 48 sixteen-week-old spontaneously hypertensive rats, in a dose of 10 mg/kg bw/daily in drinking water, for 12 weeks. Systolic blood pressure (SBP) was measured at the beginning, after 4, 8 and 12 weeks of treatment, by the tail-cuff plethysmographic method. At each mentioned time point, a group of 12 animals was sacrificed and blood was withdrawn from the abdominal aorta. Plasma samples were used for determination of total nitrate/nitirite levels, cyclic guanosine monophosphate (cGMP) and endothelin (ET) 1 levels. Statistical evaluation of the results was performed by the use of a computer statistical programme Statistica for Windows 5.0. Losartan produced a significant decrease of SBP at all time points. On the other hand, long-term treatment with this AT1 receptor antagonist produced a significant increase of nitrate/nitrite and cGMP plasma levels. When we compared the values of SBP with plasma nitrate/nitrite as well as with cGMP values, a statistically significant correlation was established. A statistically significant decrease in plasma endothelin 1 values was found during the whole study period. Also, a positive correlation between SBP and plasma endothelin 1 concentrations was observed. Long-term losartan (AT1 receptor antagonist) treatment, apart from its blood pressure lowering effect in hypertension, has beneficial effects on the endothelial dysfunction which is at least partially due to the activation of the nitric oxide system. (Tab. 1, Fig. 2, Ref. 33.)
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    The Role of Endothelial Dysfunction in the Pathogenesis of Pregnancy-Related Pathological Conditions: A Review
    (Walter de Gruyter GmbH, 2023-07)
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    Milivojevic, Vladimir
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    Rankovic, Ivan
    In the recent decades, endothelial dysfunction (ED) has been recognized as a significant contributing factor in the pathogenesis of many pathological conditions. In interaction with atherosclerosis, hypercholesterolemia, and hypertension, ED plays a crucial role in the pathogenesis of coronary artery disease, chronic renal disease, and microvascular complications in diabetes mellitus. Although ED plays a significant role in the pathogenesis of several pregnancy-related disorders such as preeclampsia, HELLP syndrome, fetal growth restriction, and gestational diabetes mellitus, the exact pathogenetic mechanisms are still a matter of debate. The increased prevalence of these entities in patients with preexisting vascular diseases highlights the essential pathological role of the preexisting ED in these patients. The abnormal uteroplacental circulation and the release of soluble factors from the ischemic placenta into the maternal bloodstream are the main causes of the maternal ED underlying the characteristic preeclamptic phenotype. Besides the increased risk for maternal and fetal poor outcomes, the preexisting ED also increases the risk of development of future cardiovascular diseases in these patients. This study aimed to look deeper into the role of ED in the pathogenesis of several pregnancy-related hypertensive and liver diseases. Hopefully, it could contribute to improvement of the awareness, knowledge, and management of these conditions and also to the reduction of the adverse outcomes and additional long-term cardiovascular complications.
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    Cardiovascular disease and COVID-19: a consensus paper from the ESC Working Group on Coronary Pathophysiology & Microcirculation, ESC Working Group on Thrombosis and the Association for Acute CardioVascular Care (ACVC), in collaboration with the European Heart Rhythm Association (EHRA)
    (Oxford University Press (OUP), 2021-09-16)
    Cenko, Edina
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    Badimon, Lina
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    Bugiardini, Raffaele
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    Claeys, Marc J
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    De Luca, Giuseppe
    The cardiovascular system is significantly affected in coronavirus disease-19 (COVID-19). Microvascular injury, endothelial dysfunction and thrombosis resulting from viral infection or indirectly related to the intense systemic inflammatory and immune responses are characteristic features of severe COVID-19. Pre-existing cardiovascular disease and viral load are linked to myocardial injury and worse outcomes. The vascular response to cytokine production and the interaction between SARS-CoV-2 and ACE2 receptor may lead to a significant reduction in cardiac contractility and subsequent myocardial dysfunction. In addition, a considerable proportion of patients who have been infected with SARS-CoV-2 do not fully recover and continue to experience a large number of symptoms and post-acute complications in the absence of a detectable viral infection. This conditions often referred to as "post-acute COVID-19" may have multiple causes. Viral reservoirs or lingering fragments of viral RNA or proteins contribute to the condition. Systemic inflammatory response to COVID-19 has the potential to increase myocardial fibrosis which in turn may impair cardiac remodelling. Here we summarize the current knowledge of cardiovascular injury and post-acute sequelae of COVID-19. As the pandemic continues and new variants emerge, we can advance our knowledge of the underlying mechanisms only by integrating our understanding of the pathophysiology with the corresponding clinical findings. Identification of new biomarkers of cardiovascular complications, and development of effective treatments for COVID-19 infection are of crucial importance.
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    Von-Willebrand factor as a predictor of three-month mortality in patients with liver cirrhosis compared to MELD score
    (Universa Press, 2019)
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    Misevski Jane
    Introduction and aim : Endothelial dysfunction is involved in the pathogenesis of portal hypertension and in the progression of liver disease. As an indicator of endothelial dysfunction, von Willebrand factor (vWF-Ag) can be a useful mortality predictor in patients with liver cirrhosis. The aim of the study is to compare the predictive value of vWF-Ag with the predictive value of MELD score regarding the three-month mortality in patients with liver cirrhosis. Materials and methods : In 70 patients with cirrhosis and portal hypertension we measured the vWF-Ag concentration and we followed the patients for 90 days. We registered all manifestations and complications of liver cirrhosis and the three-month mortality was the main end-point. Results : We registered mean vWF-Ag of 341.9±155.8%, median 312%, IQR (214-410), vWF-Ag significantly correlated with MELD score (R=0.3713 ; p<0.05) and vWF-Ag median was higher in the uncensored compared to the median in the censored patients (p<0.0067). vWF-Ag and MELD score were significantly associated with three-month mortality, with no significant difference in the diagnostic performance between the two parameters [AUC=0.735, p=0.007 for vWF-Ag ; AUC=0.885, p=0.000 for MELD score], (Z=-1.473, p=0.1407). Conclusion : In patients with liver cirrhosis vWF-Ag is a relevant predictor of three-month mortality that equals the MELD score.