Biomedical subjects

Katarina Vargova

Publications and source records attributed to Katarina Vargova.

3 recordsLinked to original sources

PubMed2005

Inverse correlation between coronary blood flow velocity and sICAM-1 level observed in ischemic heart disease patients.

Systemic factors and blood flow velocity related to atherosclerosis have been examined mainly separately or by in vitro studies. The aim of our study was to investigate the association between local coronary blood flow (corrected TIMI frame count, CTFC) and systemic atherosclerosis-related inflammatory parameters such as soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (Il-6), high sensitivity C-reactive protein (hsCRP) and von Willebrand factor (vWF) in humans. We enrolled the following groups of ischemic heart disease (IHD) patients: patients with coronary stenosis and stable (CAD, n = 96) or unstable angina (ACS, n = 27), patients with documented myocardial ischemia and normal coronary angiogram (NEG, n = 68). Patient groups showed only marginal differences in CTFC or sICAM-1 levels. In contrast, when IHD patients were studied individually, general positive correlation was found between CTFC and sICAM-1 level (r = 0.33; in NEG r = 0.25; in CAD r = 0.37; in ACS r = 0.61), being the strongest in ACS. The relation was independent from age, gender, BMI, smoking, hypertension, diabetes, previous myocardial infarction, family history of IHD, medication, hsCRP, IL-6 and vWF levels. (odds ratio, OR = 6.4; CI 95%: 2.43-16.84; p < 0.05). Nevertheless, correlation between CTFC and IL-6, hsCRP, vWF levels was not found. These results indicate inverse correlation between coronary blood flow and adhesion molecule production independently from conventional cardiovascular risk factors and inflammatory markers.

Blood Flow Velocity↗

PubMed2005

[Endothelial function and ischemic heart disease].

The original hypothesis of the development of human atherosclerosis and ischemic heart disease called "response-to-injury" suggested the loss of integrity of the endothelium as the first step of the process. The recent version of this hypothesis emphasizes the term of endothelial dysfunction, that can be triggered by any of the well known cardiovascular risk factors. The atherosclerotic process, starting with endothelial dysfunction is a slow grade inflammatory process, promoting the oxidation of the low density lipoprotein molecules, activation of cell adhesion molecules as well as various ligands and cytokines, and activating immunological processes resulting in the development of unstable atherosclerotic plaque, followed by plaque rupture and formation of atherothrombotic lesions. Among the laboratory methods used for the detection of endothelial dysfunction, the flow mediated vasodilation (FMD) is increasingly known. A novel method is the laser Doppler flowmetry, still adapted to routine clinical tests. Clinical experiments are currently running with the coronarographic evaluation of intravascular flow velocity (slow coronary flow phenomenon), and also with the isolation and clinical evaluation of the circulating endothelial cells in patients with ischemic heart disease.

Arteritis↗

PubMedDate not supplied

Activation of poly(ADP-ribose) polymerase by myocardial ischemia and coronary reperfusion in human circulating leukocytes.

Reactive free radical and oxidant production leads to DNA damage during myocardial ischemia/reperfusion. Consequent overactivation of poly(ADP-ribose) polymerase (PARP) promotes cellular energy deficit and necrosis. We hypothesized that PARP is activated in circulating leukocytes in patients with myocardial infarction and reperfusion during primary percutaneous coronary intervention (PCI). In 15 patients with ST segment elevation acute myocardial infarction, before and after primary PCI and 24 and 96 h later, we determined serum hydrogen peroxide concentrations, plasma levels of the oxidative DNA adduct 8-hydroxy-2'-deoxyguanosine (8OHdG), tyrosine nitration, PARP activation, and translocation of apoptosis-inducing factor (AIF) in circulating leukocytes. Plasma 8OHdG levels and leukocyte tyrosine nitration were rapidly increased by PCI. Similarly, poly(ADP-ribose) content of the leukocytes increased in cells isolated just after PCI, indicating immediate PARP activation triggered by reperfusion of the myocardium. In contrast, serum hydrogen peroxide concentrations and the translocation of AIF gradually increased over time and were most pronounced at 96 h. Reperfusion-related oxidative/nitrosative stress triggers DNA damage, which leads to PARP activation in circulating leukocytes. Translocation of AIF and lipid peroxidation occurs at a later stage. These results represent the first direct demonstration of PARP activation in human myocardial infarction. Future work is required to test whether pharmacological inhibition of PARP may offer myocardial protection during primary PCI.

8-Hydroxy-2'-Deoxyguanosine↗