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Biomedical subjects

István Préda

Publications and source records attributed to István Préda.

9 recordsLinked to original sources
PubMed2005

Generalized changes in venous distensibility in postthrombotic patients.

INTRODUCTION: In situ biomechanical properties of peripheral large veins were compared between asymptomatic young patients who had previously unilateral femoro-popliteal deep venous thrombosis (DVT) and age-matched, healthy controls; the aim of this study was to assess local or generalized alterations of venous wall biomechanics in postthrombotic patients. PATIENTS AND METHODS: Inner diameters of both common femoral veins, right axillary vein, and right internal jugular veins were measured in two directions by ultrasonography. Venous pressure was altered by posture changes (standing and lying) and by application of graded and controlled Valsalva. Ten postthrombotic young patients without any symptoms and 11 age-matched control subjects were included. RESULTS: In postthrombotic patients, both the affected and unaffected common femoral vein diameters and capacities were larger at low transmural pressures than those for the control group, but they demonstrated significantly less distensibility when higher pressures were applied. Similarly, in the internal jugular vein, capacity without Valsalva was significantly higher in postthrombotic patients and distensibility was reduced (statistically significant in the erect position). Pressure-induced changes in axillary vein diameter were negligible. CONCLUSIONS: In situ diameter and capacity changes, and in situ distensibility of the femoral veins on both sides (i.e., the side of previous thrombosis as well as the disease-free side) and of the jugular veins are reduced in the young DVT patients compared to veins of the age-matched, healthy controls. The pathophysiological mechanism of generalized venous wall changes in these young DVT patients remains unknown.

Adolescent↗
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↗
PubMed2004

Simple, quantitative body surface potential map parameters in the diagnosis of remote Q wave and non-Q wave myocardial infarction.

BACKGROUND: Body surface potential mapping has been shown to be a useful tool in the diagnosis and localization of remote non-Q wave and Q wave myocardial infarction, but human expertise is required to interpret the maps. OBJECTIVE: To identify quantitative body surface potential mapping parameters that could enable a computer-based diagnosis. METHODS: Body surface isopotential maps (63 unipolar leads) were recorded in 86 patients with remote Q wave and 71 patients with remote non-Q wave myocardial infarction. Twenty-four healthy adults served as control subjects. Myocardial infarctions were classified using standard electrocardiogram leads in the acute and chronic phases, and were validated by coronary angiography, ventriculography and thallium scintigraphy. RESULTS: Two simple quantitative parameters with high diagnostic power were identified: the time interval between the peak minimum and the peak maximum potentials (time-shift), and the ratio of these potentials (maximum to minimum ratio [max/min]). Both parameters showed significant differences between infarction patients and normal control subjects, and optimum cut-off values were determined using receiver operating characteristic curves (anterior infarction: time-shift of -4 ms or less, max/min of 0.6 or less; posterior infarction: time-shift of 8 ms or greater, max/min of 1.25 or greater). The sensitivities of the two parameters were 100% and 97%, and the specificities were 99% and 100%, respectively, in the anterior Q wave infarction group, compared with sensitivities of 88% and 100%, and specificities of 94% and 95%, respectively, in the posterior Q wave infarction group. In the anterior non-Q wave infarction group, sensitivity was 35% for both parameters, specificity was 100% for both parameters, and only infarctions associated with a low ejection fraction were detected, indicating that infarction size may influence the power of the tests. CONCLUSIONS: Time-shift and max/min are two new, simple, powerful parameters for infarction diagnosis and may also be suitable for automated, computer-based processing.

Adolescent↗
PubMed2002

[Treatment of unstable coronary disease].

The clinical presentations of ischemic heart disease comprises the term of acute ischaemia syndromes, that include unstable angina pectoris, non-Q-wave myocardial infarction, Q-wave-myocardial infarction and sudden death. Among the different presentations of acute ischemic syndromes, the unstable angina and non-Q-wave myocardial infarction can be regarded together. In both pathologic entity, the plaque rupture, or erosion signifies the primary event, which is the source of the highly thrombogenic substances coming out from the core of the atherosclerotic plaque and entering to the coronary and systemic circulation. They cause a thrombocyte-rich "white" intracoronary thrombus, that is not fully obstructive, or there is adequate collateral circulation, being the pathogenetic substrate that prevents the development of transmural necrosis. The nosologically-bound two clinical entity can be called as "unstable coronary artery disease" (UCAD), since they have uniform etiologic, risk stratification and therapeutic backgrounds and also therapeutic targets that are basically distinct, they are admitted for transmural "ST-elevation" infarction. The review is discussing the therapy and the questions of follow-up of the disease according to the guidelines of the European Society of Cardiology and to the multicenter evidence based studies.

Angina, Unstable↗
PubMed2002

[Etiology, pathogenesis and clinical course of unstable coronary artery disease].

The clinical presentations of ischemic heart disease comprises the term of acute ischaemia syndromes, that include unstable angina pectoris, non-Q-wave myocardial infarction, Q-wave-myocardial infarction and sudden death. Among the different presentations of acute ischemic syndromes, tha unstable angina and non-Q-wave myocardial infarction can be regarded together. In both pathologic entity, the plaque rupture, or erosion signifies the primary event, which is the source of the highly thrombogenic substances coming out from the core of the atherosclerotic plaque and entering to the coronary and systemic circulation. They cause a thrombocyte-rich "white" intracoronary thrombus, that is not fully obstructive, or there is adequate collateral circulation, being the pathogenetic substrate that prevents the development of transmural necrosis. The nosologically-bound two clinical entity can be called as "unstable coronary artery disease" (UCAD), since they have uniform etiologic, risk stratification and therapeutic backgrounds and also therapeutic targets that are basically distinct, they are admitted for transmural "ST-elevation" infarction. The review is discussing the etiology, pathophysiology, the role of inflammation factors, the problems of diagnostics, as well as risk stratification of the disease in the light of the recent guidelines of the European Society of Cardiology and multicenter evidence based studies.

Angina, Unstable↗
PubMed2002

Ventricular tachycardia induced by a pacemaker lead.

The authors present a case of symptomatic non-sustained ventricular tachycardia induced by mechanical irritation of the outflow tract of the right ventricle by a loop in a permanent ventricular pacing lead. Reposition of the lead eliminated the rhythm disturbance.

Electrocardiography↗
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↗