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001-es BibID:BIBFORM015074
Első szerző:Borbély Attila (kardiológus)
Cím:Cardiomyocyte Stiffness in Diastolic Heart Failure / Borbély A., van der Velden J., Papp Z., Bronzwaer J. G. F., Edes I., Stienen G. J. M., Paulus W. J.
Dátum:2005
ISSN:0009-7322
Megjegyzések:Heart failure with preserved left ventricular (LV) ejection fraction (EF) is increasingly recognized and usually referred to as diastolic heart failure (DHF). Its pathogenetic mechanism remains unclear, partly because of a lack of myocardial biopsy material. Endomyocardial biopsy samples obtained from DHF patients were therefore analyzed for collagen volume fraction (CVF) and sarcomeric protein composition and compared with control samples. Single cardiomyocytes were isolated from these biopsy samples to assess cellular contractile performance.METHODS AND RESULTS: DHF patients (n=12) had an LVEF of 71+/-11%, an LV end-diastolic pressure (LVEDP) of 28+/-4 mm Hg, and no significant coronary artery stenoses. DHF patients had higher CVFs (7.5+/-4.0%, P<0.05) than did controls (n=8, 3.8+/-2.0%), and no conspicuous changes in sarcomeric protein composition were detected. Cardiomyocytes, mechanically isolated and treated with Triton X-100 to remove all membranes, were stretched to a sarcomere length of 2.2 microm and activated with solutions containing varying [Ca2+]. Compared with cardiomyocytes of controls, cardiomyocytes of DHF patients developed a similar total isometric force at maximal [Ca2+], but their resting tension (F(passive)) in the absence of Ca2+ was almost twice as high (6.6+/-3.0 versus 3.5+/-1.7 kN/m2, P<0.001). F(passive) and CVF combined yielded stronger correlations with LVEDP than did either alone. Administration of protein kinase A (PKA) to DHF cardiomyocytes lowered F(passive) to control values.CONCLUSIONS: DHF patients had stiffer cardiomyocytes, as evident from a higher F(passive) at the same sarcomere length. Together with CVF, F(passive) determined in vivo diastolic LV dysfunction. Correction of this high F(passive) by PKA suggests that reduced phosphorylation of sarcomeric proteins is involved in DHF.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation. - 111 : 6 (2005), p. 774-781. -
További szerzők:Velden, Jolanda, van der Papp Zoltán (1965-) (kardiológus, élettanász) Bronzwaer, Jean G. F. Édes István (1952-) (kardiológus) Stienen, Ger J. M. Paulus, Walter J.
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DOI
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2.

001-es BibID:BIBFORM010416
Első szerző:Borbély Attila (kardiológus)
Cím:Molecular determinants of heart failure with normal left ventricular ejection fraction / Borbely, A., Papp, Z., Edes, I., Paulus, W. J.
Dátum:2009
ISSN:1734-1140 (Print)
Megjegyzések:In population-based studies, heart failure with normal left ventricular (LV) ejection fraction (HFNEF) is now increasingly recognized and referred to as diastolic heart failure. However, the pathogenic mechanisms underlying HFNEF are incompletely understood, mainly because of limited availability of human myocardial biopsy material. Nevertheless, recent studies have examined in vivo hemodynamics, in vitro cardiomyocyte function, myofilamentary protein composition, collagen content and deposition of advanced glycation end products from LV endomyocardial biopsies. These measures were compared between HFNEF patients, subjects without symptoms of heart failure (controls), patients with heart failure and reduced ejection function (HFREF), and patients with HFNEF and HFREF with diabetes mellitus. This article summarizes the various findings of these studies and focuses on the possible correlations among altered LV myocardial structure, cardiomyocyte function, myofilamentary proteins, and extracellular matrices. These findings revealed novel mechanisms responsible for diastolic LV dysfunction, and they have important therapeutic implications, particularly HFNEF, for which a specific heart failure treatment strategy is largely lacking.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Diabetes Complications
Fibrosis
Glycosylation End Products, Advanced
Heart Failure, Diastolic
Hemodynamics
Humans
Microfilaments
Myocardium
Myocytes, Cardiac
Ventricular Dysfunction, Left
Ventricular Function, Left
Megjelenés:Pharmacological Reports. - 61 : 1 (2009), p. 139-145. -
További szerzők:Papp Zoltán (1965-) (kardiológus, élettanász) Édes István (1952-) (kardiológus) Paulus, Walter J.
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3.

001-es BibID:BIBFORM010415
Első szerző:Borbély Attila (kardiológus)
Cím:Hypophosphorylation of the Stiff N2B titin isoform raises cardiomyocyte resting tension in failing human myocardium / Borbely, A., Falcao-Pires, I., van Heerebeek, L., Hamdani, N., Edes, I., Gavina, C., Leite-Moreira, A. F., Bronzwaer, J. G. F., Papp, Z., van der Velden, J., Stienen, G. J. M., Paulus, W. J.
Dátum:2009
ISSN:1524-4571 (Electronic)
Megjegyzések:High diastolic stiffness of failing myocardium results from interstitial fibrosis and elevated resting tension (F(passive)) of cardiomyocytes. A shift in titin isoform expression from N2BA to N2B isoform, lower overall phosphorylation of titin, and a shift in titin phosphorylation from N2B to N2BA isoform can raise F(passive) of cardiomyocytes. In left ventricular biopsies of heart failure (HF) patients, aortic stenosis (AS) patients, and controls (CON), we therefore related F(passive) of isolated cardiomyocytes to expression of titin isoforms and to phosphorylation of titin and titin isoforms. Biopsies were procured by transvascular technique (44 HF, 3 CON), perioperatively (25 AS, 4 CON), or from explanted hearts (4 HF, 8 CON). None had coronary artery disease. Isolated, permeabilized cardiomyocytes were stretched to 2.2-microm sarcomere length to measure F(passive). Expression and phosphorylation of titin isoforms were analyzed using gel electrophoresis with ProQ Diamond and SYPRO Ruby stains and reported as ratio of titin (N2BA/N2B) or of phosphorylated titin (P-N2BA/P-N2B) isoforms. F(passive) was higher in HF (6.1+/-0.4 kN/m(2)) than in CON (2.3+/-0.3 kN/m(2); P<0.01) or in AS (2.2+/-0.2 kN/m(2); P<0.001). Titin isoform expression differed between HF (N2BA/N2B=0.73+/-0.06) and CON (N2BA/N2B=0.39+/-0.05; P<0.001) and was comparable in HF and AS (N2BA/N2B=0.59+/-0.06). Overall titin phosphorylation was also comparable in HF and AS, but relative phosphorylation of the stiff N2B titin isoform was significantly lower in HF (P-N2BA/P-N2B=0.77+/-0.05) than in AS (P-N2BA/P-N2B=0.54+/-0.05; P<0.01). Relative hypophosphorylation of the stiff N2B titin isoform is a novel mechanism responsible for raised F(passive) of human HF cardiomyocytes.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Aged
Biopsy
Elasticity
Female
Heart Failure
Humans
Male
Middle Aged
Muscle Proteins
Myocardium
Myocytes, Cardiac
Phosphorylation
Protein Isoforms
Protein Kinases
Sarcomeres
Megjelenés:Circulation Research. - 104 : 6 (2009), p. 780-786. -
További szerzők:Falcao-Pires, Ines Heerebeek, Loek, van Hamdani, Nazha Édes István (1952-) (kardiológus) Gavina, Cristina Leite-Moreira, Adelino F. Bronzwaer, Jean G. F. Papp Zoltán (1965-) (kardiológus, élettanász) Velden, Jolanda, van der Stienen, Ger J. M. Paulus, Walter J.
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elektronikus változat
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4.

001-es BibID:BIBFORM003575
Első szerző:Borbély Attila (kardiológus)
Cím:Peroxynitrite-induced alpha-actinin nitration and contractile alterations in isolated human myocardial cells / Borbély A., Tóth A., Édes I., Virág L., Papp J. G., Varró A., Paulus W. J., van der Velden J., Stienen G. J. M., Papp Z.
Dátum:2005
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
myocytes
contractile function
peroxynitrite
alpha-actinin
human myocardium
Megjelenés:Cardiovascular Research. - 67 : 2 (2005), p. 225-233. -
További szerzők:Tóth Attila (1971-) (biológus) Édes István (1952-) (kardiológus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Paulus, Walter J. Velden, Jolanda, van der Stienen, Ger J. M. Papp Zoltán (1965-) (kardiológus, élettanász)
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DOI
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5.

001-es BibID:BIBFORM030682
Első szerző:Czuriga Dániel (kardiológus)
Cím:Cellular mechanisms for diastolic dysfunction in the human heart / Czuriga D., Paulus W. J., Czuriga I., Edes I., Papp Z., Borbély A.
Dátum:2012
Megjegyzések:Left ventricular (LV) diastolic dysfunction is an important contributor to many different cardiovascular diseases. LV diastolic dysfunction can manifest itself as slow LV relaxation, slow LV filling or high diastolic LV stiffness. Diastolic abnormalities have been described in the senescent heart, in heart failure with normal ejection fraction (HFNEF), in diabetic cardiomyopathy, in aortic valve stenosis (AVS), in hypertrophic cardiomyopathy (HCM), as well as in Fabry disease (FD), however, exact cellular and molecular alterations behind the diastolic deterioration in these diseases are not yet completely characterized. Several studies thoroughly investigated altered cardiomyocyte function, changes of contractile myofilaments, extracellular collagen deposition and advanced glycation end products (AGEs) cross-linking in the background of diastolic dysfunction. These clinical and experimental data suggest that underlying mechanisms of LV diastolic dysfunction are divergent in different cardiac pathologies, therefore the present review aims to summarize mechanisms at the cellular level of diastolic abnormalities in various cardiovascular diseases.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Cardiomyocytes
Contractile dysfunction
Diabetes mellitus
Diastole
Fibrosis
Human heart
Megjelenés:Current Pharmaceutical Biotechnology. - 13 : 13 (2012), p. 2532-2538. -
További szerzők:Paulus, Walter J. Czuriga István (1948-2018) (kardiológus) Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Borbély Attila (1978-) (kardiológus)
Pályázati támogatás:MEDIA-261409
FP7
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6.

001-es BibID:BIBFORM003763
Első szerző:Paulus, Walter J.
Cím:How to diagnose diastolic heart failure : a consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of the European Society of Cardiology / Paulus, W. J., Tschope, C., Sanderson, J. E., Rusconi, C., Flachskampf, F. A., Rademakers, F. E., Marino, P., Smiseth, O. A., De Keulenaer, G., Leite-Moreira, A. F., Borbely, A., Edes, I., Handoko, M. L., Heymans, S., Pezzali, N., Pieske, B., Dickstein, K., Fraser, A. G., Brutsaert, D. L.
Dátum:2007
Megjegyzések:Diastolic heart failure (DHF) currently accounts for more than 50% of all heart failure patients. DHF is also referred to as heart failure with normal left ventricular (LV) ejection fraction (HFNEF) to indicate that HFNEF could be a precursor of heart failure with reduced LVEF. Because of improved cardiac imaging and because of widespread clinical use of plasma levels of natriuretic peptides, diagnostic criteria for HFNEF needed to be updated. The diagnosis of HFNEF requires the following conditions to be satisfied: (i) signs or symptoms of heart failure; (ii) normal or mildly abnormal systolic LV function; (iii) evidence of diastolic LV dysfunction. Normal or mildly abnormal systolic LV function implies both an LVEF &gt; 50% and an LV end-diastolic volume index (LVEDVI) &lt;97 mL/m(2). Diagnostic evidence of diastolic LV dysfunction can be obtained invasively (LV end-diastolic pressure &gt;16 mmHg or mean pulmonary capillary wedge pressure &gt;12 mmHg) or non-invasively by tissue Doppler (TD) (E/E' &gt; 15). If TD yields an E/E' ratio suggestive of diastolic LV dysfunction (15 &gt; E/E' &gt; 8), additional non-invasive investigations are required for diagnostic evidence of diastolic LV dysfunction. These can consist of blood flow Doppler of mitral valve or pulmonary veins, echo measures of LV mass index or left atrial volume index, electrocardiographic evidence of atrial fibrillation, or plasma levels of natriuretic peptides. If plasma levels of natriuretic peptides are elevated, diagnostic evidence of diastolic LV dysfunction also requires additional non-invasive investigations such as TD, blood flow Doppler of mitral valve or pulmonary veins, echo measures of LV mass index or left atrial volume index, or electrocardiographic evidence of atrial fibrillation. A similar strategy with focus on a high negative predictive value of successive investigations is proposed for the exclusion of HFNEF in patients with breathlessness and no signs of congestion. The updated strategies for the diagnosis and exclusion of HFNEF are useful not only for individual patient management but also for patient recruitment in future clinical trials exploring therapies for HFNEF
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Biological Markers
blood
Consensus
diagnosis
Diagnosis,Differential
Diastole
Echocardiography
Echocardiography,Doppler
Heart Failure
Humans
methods
Natriuretic Peptides
physiology
Stroke Volume
therapy
ultrasonography
Megjelenés:European Heart Journal. - 28 : 20 (2007), p. 2539-2550. -
További szerzők:Tschöpe, Carsten Sanderson, John E. Rusconi, Cesare Flachskampf, Frank A. Rademakers, Frank E. Marino, Paolo Smiseth, Otto A. De Keulenaer, Gilles Leite-Moreira, Adelino F. Borbély Attila (1978-) (kardiológus) Édes István (1952-) (kardiológus) Handoko, Martin Louis Heymans, Stephane Pezzali, Natalia Pieske, Burkert Dickstein, Kenneth Fraser, Alan G. Brutsaert, Dirk L.
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DOI
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7.

001-es BibID:BIBFORM065084
Első szerző:Úri Katalin
Cím:Circulating ACE2 activity correlates with cardiovascular disease development / Katalin Úri, Miklós Fagyas, Attila Kertész, Attila Borbély, Csaba Jenei, Orsolya Bene, Zoltán Csanádi, Walter J. Paulus, István Édes, Zoltán Papp, Attila Tóth, Erzsébet Lizanecz
Dátum:2016
Megjegyzések:Abstract It was shown recently that Angiotensin Converting Enzyme activity is limited by endogenous inhibition in vivo, highlighting the importance of Angiotensin II elimination (ACE2). Potential contribution of the ACE2 to cardiovascular disease progression was addressed. Serum ACE2 activities were measured in different clinical states (healthy, n=45; hypertensive, n=239; heart failure (HF) with reduced ejection fraction (HFrEF), n=141 and HF with preserved ejection fraction (HFpEF), n=47). ACE2 activity was significantly higher in hypertensive patients (24.8?0.8U/ml) than that in healthy volunteers (16.2?0.8U/ml, P=0.01). ACE2 activity further increased in HFrEF patients (43.9?2.1U/ml, P=0.001) but not in HFpEF patients (24.6?1.9U/ml) when compared to hypertensive patients. Serum ACE2 activity negatively correlated with left ventricular systolic function in HFrEF, but not in hypertensive, HFpEF or healthy populations. Serum ACE2 activity had a fair diagnostic value to differentiate HFpEF from HFrEF patients in this study.Serum ACE2 activity correlates with cardiovascular disease development: it increases when hypertension developes and further increases when the cardiovascular disease further progresses to systolic dysfunction, suggesting that ACE2 metabolism plays a role in these processes. In contrast, serum ACE2 activity does not change when hypertension progresses to HFpEF, suggesting a different pathomechanism for HFpEF and proposing a biomarker based identification of these HF forms.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Angiotensin converting enzyme 2
diastolic heart failure
systolic heart failure
hypertension
renin-angiotensin-aldosterone system
biomarker
Megjelenés:Journal of the Renin-Angiotensin-Aldosterone System 17 : 4 (2016), p. 1-11. -
További szerzők:Fagyas Miklós (1984-) (orvos) Kertész Attila Béla (1973-) (kardiológus) Borbély Attila (1978-) (kardiológus) Jenei Csaba (1976-) (kardiológus) Bene Orsolya (1980-) (kardiológus) Csanádi Zoltán (1960-) (kardiológus) Paulus, Walter J. Édes István (1952-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus) Lizanecz Erzsébet (1978-) (orvos)
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