CCL

Összesen 17 találat.
#/oldal:
Részletezés:
Rendezés:

1.

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.
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

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.
Internet cím:elektronikus változat
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

001-es BibID:BIBFORM010417
Első szerző:Borbély Attila (kardiológus)
Cím:Transcriptional and posttranslational modifications of titin : implications for diastole / Borbely, A., van Heerebeek, L., Paulus, W. J.
Dátum:2009
ISSN:1524-4571 (Electronic)
Tárgyszavak:Orvostudományok Klinikai orvostudományok szerkesztőségi anyag
Alternative Splicing
Animals
Cyclic AMP-Dependent Protein Kinases
Cyclic GMP-Dependent Protein Kinases
Diabetes Complications
Diacetyl
derivatives
Diastole
Elasticity
Extracellular Matrix
Gelsolin
Heart Failure, Diastolic
Humans
Mice
Muscle Proteins
Myocytes, Cardiac
Phosphorylation
Protein Isoforms
Protein Kinases
Protein Processing, Post-Translational
Rats
Sarcomeres
Triiodothyronine
Ventricular Remodeling
Megjelenés:Circulation Research. - 104 : 1 (2009), p. 12-14. -
További szerzők:Heerebeek, Loek, van Paulus, Walter J.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

4.

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.
Internet cím:DOI
elektronikus változat
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

5.

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)
Internet cím:elektronikus változat
DOI
Borító:

6.

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
Internet cím:Szerző által megadott URL
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

7.

001-es BibID:BIBFORM023507
Első szerző:Falcao-Pires, Ines
Cím:Diabetes Mellitus Worsens Diastolic Left Ventricular Dysfunction in Aortic Stenosis Through Altered Myocardial Structure and Cardiomyocyte Stiffness / Falcao-Pires, I., Hamdani, N., Borbely, A., Gavina, C., Schalkwijk, C. G., van der Velden, J., van Heerebeek, L., Stienen, G. J. M., Niessen, H. W. M., Leite-Moreira, A. F., Paulus, W. J.
Dátum:2011
ISSN:0009-7322
Megjegyzések:Aortic stenosis (AS) and diabetes mellitus (DM) are frequent comorbidities in aging populations. In heart failure, DM worsens diastolic left ventricular (LV) dysfunction, thereby adversely affecting symptoms and prognosis. Effects of DM on diastolic LV function were therefore assessed in aortic stenosis, and underlying myocardial mechanisms were identified. Methods and Results-Patients referred for aortic valve replacement were subdivided into patients with AS and no DM (AS; n=46) and patients with AS and DM (AS-DM; n=16). Preoperative Doppler echocardiography and hemodynamics were implemented with perioperative LV biopsies. Histomorphometry and immunohistochemistry quantified myocardial collagen volume fraction and myocardial advanced glycation end product deposition. Isolated cardiomyocytes were stretched to 2.2-gamma m sarcomere length to measure resting tension (Fpassive). Expression and phosphorylation of titin isoforms were analyzed with gel electrophoresis with ProQ Diamond and SYPRO Ruby stains. Reduced LV end-diastolic distensibility in AS-DM was evident from higher LV end-diastolic pressure (21±1 mm Hg for AS versus 28±4 mm Hg for AS-DM; P=0.04) at comparable LV end-diastolic volume index and attributed to higher myocardial collagen volume fraction (AS, 12.9±1.1% versus AS-DM, 18.2±2.6%; P<0.001), more advanced glycation end product deposition in arterioles, venules, and capillaries (AS, 14.4±2.1 score per 1 mm2 versus AS-DM, 31.4±6.1 score per 1 mm2; P=0.03), and higher Fpassive (AS, 3.5±1.7 kN/m2 versus AS-DM, 5.1±0.7 kN/m2; P=0.04). Significant hypophosphorylation of the stiff N2B titin isoform in AS-DM explained the higher Fpassive and normalization of Fpassive after in vitro treatment with protein kinase A. Conclusions-Worse diastolic LV dysfunction in AS-DM predisposes to heart failure and results from more myocardial fibrosis, more intramyocardial vascular advanced glycation end product deposition, and higher cardiomyocyte Fpassive, which was related to hypophosphorylation of the N2B titin isoform.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
aortic valve stenosis
myocytes
cardiac
diabetes mellitus
diastole
fibrosis
titin
myofilamentary proteins
Megjelenés:Circulation. - 124 : 10 (2011), p. 1151-1159. -
További szerzők:Hamdani, Nazha Borbély Attila (1978-) (kardiológus) Gavina, Cristina Schalkwijk, Casper G. Velden, Jolanda, van der Heerebeek, Loek, van Stienen, Ger J. M. Niessen, Hans W. M. Leite-Moreira, Adelino F. Paulus, Walter J.
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

8.

001-es BibID:BIBFORM014718
Első szerző:Hamdani, Nazha
Cím:More severe cellular phenotype in human idiopathic dilated cardiomyopathy compared to ischemic heart disease / Hamdani Nazha, Borbély Attila, Veenstra Sophie P. G. R., Kooij Viola, Vrydag Wim, Zaremba Ruud, Remedios Cris, Niessen Hans W. M., Michel Martin C., Paulus Walter J., Stienen Ger J. M., van der Velden Jolanda
Dátum:2010
ISSN:0142-4319
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Muscle Research And Cell Motility. - 31 : 4 (2010), p. 289-301. -
További szerzők:Borbély Attila (1978-) (kardiológus) Veenstra, Sophie P. G. R. Kooij, Viola Vrydag, Wim Zaremba, Ruud Remedios, Cris Niessen, Hans W. M. Michel, Martin C. Paulus, Walter J. Stienen, Ger J. M. Velden, Jolanda, van der
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

9.

001-es BibID:BIBFORM010421
Első szerző:Hamdani, Nazha
Cím:Distinct myocardial effects of beta-blocker therapy in heart failure with normal and reduced left ventricular ejection fraction / Hamdani, N., Paulus, W. J., van Heerebeek, L., Borbely, A., Boontje, N. M., Zuidwijk, M. J., Bronzwaer, J. G., Simonides, W. S., Niessen, H. W., Stienen, G. J. M., van der Velden, J.
Dátum:2009
ISSN:0195-668X (Print)
Megjegyzések:Left ventricular (LV) myocardial structure and function differ in heart failure (HF) with normal (N) and reduced (R) LV ejection fraction (EF). This difference could underlie an unequal outcome of trials with beta-blockers in heart failure with normal LVEF (HFNEF) and heart failure with reduced LVEF (HFREF) with mixed results observed in HFNEF and positive results in HFREF. To investigate whether beta-blockers have distinct myocardial effects in HFNEF and HFREF, myocardial structure, cardiomyocyte function, and myocardial protein composition were compared in HFNEF and HFREF patients without or with beta-blockers. METHODS AND RESULTS: Patients, free of coronary artery disease, were divided into beta-(HFNEF) (n = 16), beta+(HFNEF) (n = 16), beta-(HFREF) (n = 17), and beta+(HFREF) (n = 22) groups. Using LV endomyocardial biopsies, we assessed collagen volume fraction (CVF) and cardiomyocyte diameter (MyD) by histomorphometry, phosphorylation of myofilamentary proteins by ProQ-Diamond phosphostained 1D-gels, and expression of beta-adrenergic signalling and calcium handling proteins by western immunoblotting. Cardiomyocytes were also isolated from the biopsies to measure active force (F(active)), resting force (F(passive)), and calcium sensitivity (pCa(50)). Myocardial effects of beta-blocker therapy were either shared by HFNEF and HFREF, unique to HFNEF or unique to HFREF. Higher F(active), higher pCa(50), lower phosphorylation of troponin I and myosin-binding protein C, and lower beta(2) adrenergic receptor expression were shared. Higher F(passive), lower CVF, lower MyD, and lower expression of stimulatory G protein were unique to HFNEF and lower expression of inhibitory G protein was unique to HFREF. CONCLUSION: Myocardial effects unique to either HFNEF or HFREF could contribute to the dissimilar outcome of beta-blocker therapy in both HF phenotypes.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Adrenergic beta-Antagonists
Aged
Cross-Sectional Studies
Female
Heart Failure
Humans
Male
Microfilament Proteins
Middle Aged
Myocardium
Myocytes, Cardiac
Phosphorylation
Stroke Volume
Ventricular Dysfunction, Left
Megjelenés:European Heart Journal. - 30 : 15 (2009), p. 1863-1872. -
További szerzők:Paulus, Walter J. Heerebeek, Loek, van Borbély Attila (1978-) (kardiológus) Boontje, Nicky M. Zuidwijk, Marian J. Bronzwaer, Jean G. F. Simonides, Warner S. Niessen, Hans W. M. Stienen, Ger J. M. Velden, Jolanda, van der
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

10.

001-es BibID:BIBFORM005631
Első szerző:Hamdani, Nazha
Cím:Myofilament dysfunction in cardiac disease from mice to men / Hamdani, N., de Waard, M., Messer, A. E., Boontje, N. M., Kooij, V., van Dijk, S., Versteilen, A., Lamberts, R., Merkus, D., Dos Remedios, C., Duncker, D. J., Borbely, A., Papp, Z., Paulus, W., Stienen, G. J. M., Marston, S. B., van der Velden, J.
Dátum:2008
ISSN:0142-4319 (Print)
Megjegyzések:In healthy human myocardium a tight balance exists between receptor-mediated kinases and phosphatases coordinating phosphorylation of regulatory proteins involved in cardiomyocyte contractility. During heart failure, when neurohumoral stimulation increases to compensate for reduced cardiac pump function, this balance is perturbed. The imbalance between kinases and phosphatases upon chronic neurohumoral stimulation is detrimental and initiates cardiac remodelling, and phosphorylation changes of regulatory proteins, which impair cardiomyocyte function. The main signalling pathway involved in enhanced cardiomyocyte contractility during increased cardiac load is the beta-adrenergic signalling route, which becomes desensitized upon chronic stimulation. At the myofilament level, activation of protein kinase A (PKA), the down-stream kinase of the beta-adrenergic receptors (beta-AR), phosphorylates troponin I, myosin binding protein C and titin, which all exert differential effects on myofilament function. As a consequence of beta-AR down-regulation and desensitization, phosphorylation of the PKA-target proteins within the cardiomyocyte may be decreased and alter myofilament function. Here we discuss involvement of altered PKA-mediated myofilament protein phosphorylation in different animal and human studies, and discuss the roles of troponin I, myosin binding protein C and titin in regulating myofilament dysfunction in cardiac disease. Data from the different animal and human studies emphasize the importance of careful biopsy procurement, and the need to investigate localization of kinases and phosphatases within the cardiomyocyte, in particular their co-localization with cardiac myofilaments upon receptor stimulation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Muscle Research and Cell Motility. - 29 : 6-8 (2008), p. 189-201. -
További szerzők:de Waard, Monique Messer, Andrew E. Boontje, Nicky M. Kooij, Viola Dijk, Sabine, van Versteilen, Amanda Lamberts, Regis Merkus, Daphne Dos Remedios, Cris Duncker, Dirk J. Borbély Attila (1978-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász) Paulus, Walter J. Stienen, Ger J. M. Marston, Steven B. Velden, Jolanda, van der
Internet cím:elektronikus változat
DOI
Borító:

11.

001-es BibID:BIBFORM030333
Első szerző:Heerebeek, Loek, van
Cím:Response to Letter Regarding Article, "Diastolic Stiffness of the Failing Diabetic Heart : Importance of Fibrosis, Advanced Glycation End Products, and Myocyte Resting Tension" / van Heerebeek L., Hamdani N., Handoko M. L., Falcao-Pires I., Musters R. J., Kupreishvili K., Ijsselmuiden A. J., Schalkwijk C. G., Bronzwaer J. G., Diamant M., Borbely A., van der Velden J., Stienen G. J. M., Laarman G. J., Niessen H. W., Paulus W. J.
Dátum:2008
ISSN:0009-7322
Tárgyszavak:Orvostudományok Elméleti orvostudományok levél
Megjelenés:Circulation. - 117 (2008), p. e484. -
További szerzők:Hamdani, Nazha Handoko, Martin Louis Falcao-Pires, Ines Musters, René J. Kupreishvili, Koba Ijsselmuiden, Alexander J. J. Schalkwijk, Casper G. Bronzwaer, Jean G. F. Diamant, Michaela Borbély Attila (1978-) (kardiológus) Velden, Jolanda, van der Stienen, Ger J. M. Laarman, Gerrit J. Niessen, Hans W. M. Paulus, Walter J.
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM014721
Első szerző:Heerebeek, Loek, van
Cím:Myocardial Structure and Function Differ in Systolic and Diastolic Heart Failure / van Heerebeek L., Borbély A., Niessen H. W. M., Bronzwaer J. G. F., van der Velden J., Stienen G. J., Linke W. A., Laarman G. J., Paulus W. J.
Dátum:2006
ISSN:0009-7322
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation. - 113 : 16 (2006), p. 1966-1973. -
További szerzők:Borbély Attila (1978-) (kardiológus) Niessen, Hans W. M. Bronzwaer, Jean G. F. Velden, Jolanda, van der Stienen, Ger J. M. Linke, Wolfgang A. Laarman, Gerrit J. Paulus, Walter J.
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1 2