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István Edes

Publications and source records attributed to István Edes.

28 records · Page 2Linked to original sources
PubMed2004

[Risk and prevention in cardiovascular diseases].

The RCTs are the most important sources of drug therapy related scientific evidence (RCT--Randomised Controlled clinical Trials). In most cases RCTs studying identical or similar clinical issues are slightly or considerably varied. However, for such cases we have the appropriate methodology to compare the more or less different RCT results. This publication was written to provide a general overview of this methodology such as relative and absolute risk reduction (RRR, ARR), odd ratio (OR), number needed to treat and number needed to harm (NNT, NNH).

Cardiovascular Diseases↗
PubMed2004

[Beta-adrenergic receptor blockers in clinical practice].

Discovery of beta receptor system and the class of beta-adrenergic receptor antagonists in the last century has been one of the most important developments in cardiovascular pharmacotherapy. A non-cardioselective beta blocker (propranolol) was introduced in the therapy in the early 1960s. Later, the second generation beta1 selective blockers and finally the third generation blockers (with vasodilator property) appeared on the market. Beta-adrenergic receptor antagonists have become widely used in cardiovascular therapy for the last decades. They were introduced for the treatment of angina pectoris and arrhythmias and later hypertension and there has been a continuing progress in the treatment of several heart diseases (including congestive heart failure which was contraindicated earlier). The recent clinical indications and practical considerations of beta-blockers are summarized in this review.

Adrenergic beta-Antagonists↗
PubMed2004

The effects of levosimendan and OR-1896 on isolated hearts, myocyte-sized preparations and phosphodiesterase enzymes of the guinea pig.

The concentration dependences of the Ca(2+)-sensitizing and the phosphodiesterase-inhibitory effects of levosimendan (the (-) enantiomer of [[4-(1,4,5,6-tetrahydro-4-methyl-6-oxo-3-pyridazinyl)phenyl]hydrazono]propanedinitrile) and its active metabolite, OR-1896 (the (-) enantiomer of N-[4-(1,4,5,6-tetrahydro-4-methyl-6-oxo-3-pyridazinyl)phenyl] acetamide), were compared with their positive inotropic effects to reveal their mechanisms of action in guinea pig hearts. In Langendorff-perfused hearts, left ventricular +dP/dt(max) increased by 26+/-4% and 25+/-3% (mean+/-S.E.M.), with EC(50) values of 15+/-2 and 25+/-1 nM for levosimendan and OR-1896, respectively. In permeabilized myocyte-sized preparations, levosimendan and OR-1896 both increased isometric force production via Ca(2+) sensitization (at pCa 6.2), by 51+/-7% and 52+/-6%, with EC(50) values of 8+/-1 and 36+/-7 nM (P<0.05), respectively. Thus, the two molecules could be defined as Ca(2+) sensitizers and positive inotropes with very similar concentration dependences. However, major differences appeared when the phosphodiesterase-inhibitory effects of levosimendan and OR-1896 were probed on the two phosphodiesterase isoforms (phosphodiesterases III and IV) dominant in the left ventricular cardiac tissue. Levosimendan was a 40-fold more potent and a 3-fold more selective phosphodiesterase III inhibitor (IC(50) for phosphodiesterase III=2.5 nM, and IC(50) for phosphodiesterase IV=25 microM, selectivity factor approximately 10000) than OR-1896 (IC(50) for phosphodiesterase III=94 nM, and IC(50) for phosphodiesterase IV=286 microM, selectivity factor approximately 3000). Hence, our data support the hypothesis that levosimendan and OR-1896 both exert positive inotropy via a Ca(2+)-sensitizing mechanism and not via simultaneous inhibition of the phosphodiesterases III and IV isozymes in the myocardium at their maximal free plasma concentrations.

Acetamides↗
PubMed2004

99mTc-MIBI SPECT assessment of the effects of aneurysm resection on the left ventricular morphology.

OBJECTIVE: 99mTc-MIBI SPECT is a widely used myocardial perfusion investigation technique, but few data are available concerning its use to assess the morphological characteristics of a left ventricular aneurysm (LVA) before and after LVA resection. METHODS AND RESULTS: Pre- and postoperative rest 99mTc-MIBI SPECT images were analysed in order to characterize the features of LVAs and the changes in the 3D scintigraphic parameters after apical LVA resection in 6 patients. In the middle horizontal slice an angle was defined to quantify the apical divergence associated with the LVA. After resection, the changes in the divergence angles (DA) were measured as were the changes in the left ventricular volumes (LVV) by volumetric calculations. The mean DA decreased from an average of 38.50 degrees +/- 11.32 degrees preoperatively to 24 degrees +/- 11.84 degrees postoperatively (p = 0.03). The mean LVV also decreased significantly: from 443 +/- 87 ml to 317 +/- 74 ml (p = 0.003). The resectable LVAs were associated with a very low isotope uptake in the apical segments (< 20% relative activity). A DA < 20 degrees was also characteristic of anatomical LVA in all patients. A regression curve plotting divergence angle and the number of left ventricular segments below 20% relative activity showed a significant correlation between them (r = 0.86, p = 0.003). CONCLUSIONS: The significant decreases of DA and LVV after resection reflect favourable morphological changes in the left ventricle (reverse remodelling). We consider 99mTc-MIBI SPECT a useful method for apical LVA detection, it allows an analysis of the morphological (and indirectly the functional) results of the surgery.

Cardiac Surgical Procedures↗
PubMed2003

Calpain-1-dependent degradation of troponin I mutants found in familial hypertrophic cardiomyopathy.

The mechanism by which mutations of the cardiac troponin I (cTnI) gene evoke familial hypertrophic cardiomyopathy (fHCM) is unknown. In this investigation the potential effects of three fHCM-related cTnI mutations on Calpain-1-induced cTnI degradation were tested, and a study was made of whether additional conformational changes due to troponin complex formation and protein kinase A-induced phosphorylation affect the intensity of cTnI proteolysis. Purified recombinant wild-type cTnI and three of its fHCM-related missense mutants (R145G, G203S and K206Q), alone or in the troponin complex (i.e. together with troponin C and troponin T), in the non-phosphorylated or protein kinase A-bisphosphorylated forms were proteolyzed in vitro in the presence of Calpain-1 (0.05-2.5 U) at 30 degrees C. Following incubation with Calpain-1 for 0.5, 30, 60 or 120 min, the extent of protein degradation was evaluated through the use of Western immunoblotting and densitometry. The results indicated that both the wild-type and the mutant cTnI molecules were susceptible to Calpain-1. However, the degradation of the cTnI molecules in the troponin complex was less intense than that of the non-complexed forms. Moreover, phosphorylation by protein kinase A conferred effective protection against cTnI proteolysis. The data suggested that mutations in the central inhibitory domain (R145G) and in the C-terminal region (G203S and K206Q) of cTnI do not affect its Calpain-1-mediated degradation, or the phosphorylation-induced protection against proteolysis.

Blotting, Western↗
PubMed2002

[The role of PET scan among cardiologic imaging methods].

The PET technique has been available for myocardial viability studies in Hungary since 1994. The early comparative results showed that FDG-PET identified more potentially reversible myocardial damages than [201Tl]-scintigraphy, defining the viability either by preserved metabolic activity of 50% or by metabolism-perfusion mismatch. According to the follow up of revascularized patients in our cases, FDG-PET had a positive predictive value for functional recovery at 80%. In our opinion, it is the detection of glucose metabolism that predicts with the greatest accuracy segments of hibernating myocardial tissue that will recover after revascularization. Unlike dobutamine echocardiography, PET can detect viable ventricular segments in the myocardium of lost contractile material often seen in the histological studies of chronically ischemic myocardium. The FDG-PET method can be regarded as the gold standard of myocardial viability.

Adult↗
PubMedDate not supplied

Radiation-induced coronary artery disease in Hodgkin's disease.

PURPOSE: Secondary malignant tumours and cardiovascular complications are of great importance among the late complications after treatment for Hodgkin's disease (HD) because they may significantly reduce the patients' life expectancy. We report on coronary artery disease (CAD) after treatment for HD. METHODS AND MATERIALS: We present the case of two female patients with HD who received mediastinal irradiation after which complete remission was achieved. In 12 and 19 years after the onset of the disease, control examinations revealed ischaemic heart disease, which was confirmed by coronary arteriography and solved by stent implantation in one of the patients and bypass surgery in the other one. CONCLUSIONS: Ischaemic heart disease was due to early CAD, which was associated with mediastinal irradiation accompanied by hypothyroidism, hyperlipidaemia and, possibly, early menopause, all posing an increased risk for the cardiologic disease. Our cases may serve as a warning example to carefully plan the management (low dose, involved field irradiation) of newly diagnosed patients as well as the cardiologic follow-up of patients with HD.

Adult↗
PubMedDate not supplied

Activation of the poly(ADP-ribose) polymerase pathway in human heart failure.

Poly(ADP-ribose) polymerase (PARP) activation has been implicated in the pathogenesis of acute and chronic myocardial dysfunction and heart failure. The goal of the present study was to investigate PARP activation in human heart failure, and to correlate PARP activation with various indices of apoptosis and oxidative and nitrosative stress in healthy (donor) and failing (NYHA class III-IV) human heart tissue samples. Higher levels of oxidized protein end-products were found in failing hearts compared with donor heart samples. On the other hand, no differences in tyrosine nitration (a marker of peroxynitrite generation) were detected. Activation of PARP was demonstrated in the failing hearts by an increased abundance of poly-ADP ribosylated proteins. Immunohistochemical analysis revealed that PARP activation was localized to the nucleus of the cardiomyocytes from the failing hearts. The expression of full-length PARP-1 was not significantly different in donor and failing hearts. The expression of caspase-9, in contrast, was significantly higher in the failing than in the donor hearts. Immunohistochemical analysis was used to detect the activation of mitochondrial apoptotic pathways. We found no significant translocation of apoptosis-inducing factor (AIF) into the nucleus. Overall, the current data provide evidence of oxidative stress and PARP activation in human heart failure. Interventional studies with antioxidants or PARP inhibitors are required to define the specific roles of these factors in the pathogenesis of human heart failure.

Adenosine Diphosphate Ribose↗