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1.

001-es BibID:BIBFORM020592
Első szerző:Böhm, Michael
Cím:Erectile dysfunction predicts cardiovascular events in high-risk patients receiving telmisartan, ramipril, or both : the ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial/Telmisartan Randomized AssessmeNt Study in ACE iNtolerant subjects with cardiovascular Disease (ONTARGET/TRANSCEND) Trials / Bohm, M., Baumhakel, M., Teo, K., Sleight, P., Probstfield, J., Gao, P., Mann, J. F., Diaz, R., Dagenais, G. R., Jennings, G. L. R., Liu, L., Jansky, P., Yusuf, S., the ONTARGET/TRANSCEND Erectile Dysfunction Substudy Investigators
Dátum:2010
ISSN:0009-7322
Megjegyzések:Although erectile dysfunction (ED) is associated with cardiovascular risk factors and atherosclerosis, it is not known whether the presence of ED is predictive of future events in individuals with cardiovascular disease. We evaluated whether ED is predictive of mortality and cardiovascular outcomes, and because inhibition of the renin-angiotensin system in high-risk patients reduces cardiovascular events, we also tested the effects on ED of randomized treatments with telmisartan, ramipril, and the combination of the 2 drugs (ONTARGET), as well as with telmisartan or placebo in patients who were intolerant of angiotensin-converting enzyme inhibitors (TRANSCEND). METHODS AND RESULTS: In a prespecified substudy, 1549 patients underwent double-blind randomization, with 400 participants assigned to receive ramipril, 395 telmisartan, and 381 the combination thereof (ONTARGET), as well as 171 participants assigned to receive telmisartan and 202 placebo (TRANSCEND). ED was evaluated at baseline, at 2-year follow-up, and at the penultimate visit before closeout. ED was predictive of all-cause death (hazard ratio [HR] 1.84, 95% confidence interval [CI] 1.21 to 2.81, P=0.005) and the composite primary outcome (HR 1.42, 95% CI 1.04 to 1.94, P=0.029), which consisted of cardiovascular death (HR 1.93, 95% CI 1.13 to 3.29, P=0.016), myocardial infarction (HR 2.02, 95% CI 1.13 to 3.58, P=0.017), hospitalization for heart failure (HR 1.2, 95% CI 0.64 to 2.26, P=0.563), and stroke (HR 1.1, 95% CI 0.64 to 1.9, P=0.742). The study medications did not influence the course or development of ED. CONCLUSIONS: ED is a potent predictor of all-cause death and the composite of cardiovascular death, myocardial infarction, stroke, and heart failure in men with cardiovascular disease. Trial treatment did not significantly improve or worsen ED. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT 00153101.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation. - 121 : 12 (2010), p. 1439-1446. -
További szerzők:Baumhäkel, Magnus Teo, Koon Sleight, Peter Probstfield, Jeffrey Gao, Peggy Mann, Johannes F. Diaz, Rafael Dagenais, Gilles R. Jennings, Garry L. R. Liu, Lisheng Jansky, Petr Yusuf, Salim (1929-2008) (belgyógyász) Czuriga István (1948-2018) (kardiológus) the ONTARGET/TRANSCEND Erectile Dysfunction Substudy Investigators
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2.

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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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.
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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.
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5.

001-es BibID:BIBFORM023026
Első szerző:Cheng, Caroline
Cím:Heme Oxygenase 1 Determines Atherosclerotic Lesion Progression Into a Vulnerable Plaque / Cheng, C., Noordeloos, A. M., Jeney, V., Soares, M. P., Moll, F., Pasterkamp, G., Serruys, P. W., Duckers, H. J.
Dátum:2009
ISSN:0009-7322
Megjegyzések:Background-The molecular regulation for the transition from stable to vulnerable plaque remains to be elucidated. Heme oxygenase 1 (HO-1) and its metabolites have been implicated in the cytoprotective defense against oxidative injury in atherogenesis. In this study, we sought to assess the role of HO-1 in the progression toward plaque instability in carotid artery disease in patients and in a murine model of vulnerable plaque development. Methods and Results-Atherectomy biopsy from 112 patients with clinical carotid artery disease was collected and stratified according to characteristics of plaque vulnerability. HO-1 expression correlated closely with features of vulnerable human atheromatous plaque (P<0.005), including macrophage and lipid accumulation, and was inversely correlated with intraplaque vascular smooth muscle cells and collagen deposition. HO-1 expression levels correlated with the plaque destabilizing factors matrix metalloproteinase-9, interleukin-8, and interleukin-6. Likewise, in a vulnerable plaque model using apolipoprotein E(-/-) mice, HO-1 expression was upregulated in vulnerable versus stable lesions. HO-1 induction by cobalt protoporphyrin impeded lesion progression into vulnerable plaques, indicated by a reduction in necrotic core size and intraplaque lipid accumulation, whereas cap thickness and vascular smooth muscle cells were increased. In contrast, inhibition of HO-1 by zinc protoporphyrin augmented plaque vulnerability. Plaque stabilizing was prominent after adenoviral transduction of HO-1 compared with sham virus-treated animals, providing proof that the observed effects on plaque vulnerability were HO-1 specific. Conclusions-Here we demonstrate in a well-defined patient group and a murine vulnerable plaque model that HO-1 induction reverses plaque progression from a vulnerable plaque to a more stable phenotype as part of a compensatory atheroprotective response.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation. - 119 : 23 (2009), p. 3017-3027. -
További szerzők:Noordeloos, Annemarie M. Jeney Viktória (1971-) (vegyész, kémia tanár) Soares, Miguel P. Moll, Frans Pasterkamp, Gerard Serruys, Patrick W. Duckers, Henricus J.
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6.

001-es BibID:BIBFORM117739
035-os BibID:(cikkazonosító)e011105 (Scopus)85182262507
Első szerző:Dauw, Jeroen
Cím:Protocolized Natriuresis-Guided Decongestion Improves Diuretic Response : the Multicenter ENACT-HF Study / Jeroen Dauw, Kristina Charaya, Małgorzata Lelonek, Isabel Zegri-Reiriz, Samer Nasr, Cynthia P. Paredes-Paucar, Attila Borbély, Fatih Erdal, Riad Benkouar, Marta Cobo-Marcos, Gonzalo Barge-Caballero, Varghese George, Cornelia Zara, Noel T. Ross, Diane Barker, Annop Lekhakul, Simone Frea, Azmee M. Ghazi, Dorit Knappe, Nawal Doghmi, Milka Klincheva, Inês Fialho, Virginia Bovolo, Hajo Findeisen, Imad A. Alhaddad, Alessandro Galluzzo, Rafael de la Espriella, Ramzi Tabbalat, Òscar Miró, Jagdeep S. Singh, Petra Nijst, Matthias Dupont, Pieter Martens, Wilfried Mullens
Dátum:2024
ISSN:1941-3289 1941-3297
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Circulation: Heart Failure. - 17 (2024), p. 1-10. -
További szerzők:Charaya, Kristina Lelonek, Malgorzata Zegri-Reiriz, Isabel Nasr, Samer Paredes-Paucar, Cynthia P. Borbély Attila (1978-) (kardiológus) Erdal, Fatih Benkouar, Riad Cobo-Marcos, Marta Barge-Caballero, Gonzalo George, Varghese Zara, Cornelia Ross, Noel T. Barker, Diane Lekhakul, Annop Frea, Simone Ghazi, Azmee M. Knappe, Dorit Doghmi, Nawal Klincheva, Milka Fialho, Inês Bovolo, Virginia Findeisen, Hajo Alhaddad, Imad A. Galluzzo, Alessandro Espriella, Rafael de la Tabbalat, Ramzi Miró, Òscar Singh, Jagdeep S. Nijst, Petra Dupont, Matthias Martens, Pieter Mullens, Wilfried
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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.
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8.

001-es BibID:BIBFORM004326
Első szerző:Gyöngyösi Mariann
Cím:Serial Noninvasive In Vivo Positron Emission Tomographic Tracking of Percutaneously Intramyocardially Injected Autologous Porcine Mesenchymal Stem Cells Modified for Transgene Reporter Gene Expression / Gyöngyösi M., Blanco J., Márián T., Trón L., Hemetsberger R., Rodriguez J., Font G., Pavo I.J., Kertész I., Balkay L., Pavo N., Posa A., Emri M., Galuska L., Kraitchman D. L., Wojta J., Huber K., Glogar D.
Dátum:2008
Megjegyzések:Background: Porcine bone marrow-derived mesenchymal stem cells (MSCs) were stably transfected with a lentiviral vector for transgene expression of the trifusion protein renilla luciferase, red fluorescent protein and herpes simplex truncated thymidine kinase (LV-RL-RFP-tTK; positron emission tomography [PET] reporter gene) for in vivo noninvasive tracking of the intramyocardially delivered MSC fate. Methods and Results: A closed-chest, reperfused myocardial infarction was created in farm pigs. Sixteen days after myocardial infarction, LV-RL-RFP-tTK-MSCs were injected intramyocardially using electromechanical mapping guidance in the infarct border zone (n=7). PET-computed tomographic metabolic and perfusion imaging was performed after an intravenous injection of 10 mCi [18F]-FHBG and 13N-ammonia PET at 30?2 hours and 7 days after LV-RL-RFP-tTK-MSC treatment. Fusion imaging of the [18F]-FHBG PET-computed tomography with MRI was used to determine the myocardial location of the injected LV-RL-RFP-tTK-MSCs. Seven days after injections, [18F]-FHBG PET showed a decreased cardiac uptake with a mild increased pericardial and pleura uptake in the treated animals, which was confirmed by the measurement of luciferase activity. At 10 days, infarct size by MRI in the LV-RL-RFP-tTK-MSC-treated animals was smaller than controls (n=7) (23.3?1.5% versus 30.2?3.5%, P<0.005). The presence of the LV-RL-RFP-tTK-MSCs (5.8?1.1% of the injected cells) in the myocardium 10 days after intramyocardial delivery was confirmed histologically.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
cells
imaging
infarction
mapping
revascularization
Megjelenés:Circulation: Cardiovascular Imaging. - 1 : 2 (2008), p. 94-103. -
További szerzők:Blanco, Jeronimo Márián Teréz (1950-) (radiobiológus) Trón Lajos (1941-) (biofizikus) Hemetsberger, Rayyan Rodriguez, Julio Font Gusztáv Pávó Imre J. Kertész István (1966-) (vegyész) Balkay László (1963-) (biofizikus) Pavo, Noemi Pósa Anikó Emri Miklós (1962-) (fizikus) Galuska László (1946-) (belgyógyász, izotópdiagnoszta) Kraitchman, Dara L. Wojta, Johann Huber, Kurt Glogar, Dietmar
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9.

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.
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10.

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.
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11.

001-es BibID:BIBFORM005642
Első szerző:Heerebeek, Loek, van
Cím: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. J., Schalkwijk, C. G., Bronzwaer, J. G. F., Diamant, M., Borbely, A., van der Velden, J., Stienen, G. J. M., Laarman, G. J., Niessen, H. W. M., Paulus, W. J.
Dátum:2008
ISSN:1524-4539 (Electronic)
Megjegyzések:Excessive diastolic left ventricular stiffness is an important contributor to heart failure in patients with diabetes mellitus. Diabetes is presumed to increase stiffness through myocardial deposition of collagen and advanced glycation end products (AGEs). Cardiomyocyte resting tension also elevates stiffness, especially in heart failure with normal left ventricular ejection fraction (LVEF). The contribution to diastolic stiffness of fibrosis, AGEs, and cardiomyocyte resting tension was assessed in diabetic heart failure patients with normal or reduced LVEF. METHODS AND RESULTS: Left ventricular endomyocardial biopsy samples were procured in 28 patients with normal LVEF and 36 patients with reduced LVEF, all without coronary artery disease. Sixteen patients with normal LVEF and 10 with reduced LVEF had diabetes mellitus. Biopsy samples were used for quantification of collagen and AGEs and for isolation of cardiomyocytes to measure resting tension. Diabetic heart failure patients had higher diastolic left ventricular stiffness irrespective of LVEF. Diabetes mellitus increased the myocardial collagen volume fraction only in patients with reduced LVEF (from 14.6+/-1.0% to 22.4+/-2.2%, P<0.001) and increased cardiomyocyte resting tension only in patients with normal LVEF (from 5.1+/-0.7 to 8.5+/-0.9 kN/m2, P=0.006). Diabetes increased myocardial AGE deposition in patients with reduced LVEF (from 8.8+/-2.5 to 24.1+/-3.8 score/mm2; P=0.005) and less so in patients with normal LVEF (from 8.2+/-2.5 to 15.7+/-2.7 score/mm2, P=NS). CONCLUSIONS: Mechanisms responsible for the increased diastolic stiffness of the diabetic heart differ in heart failure with reduced and normal LVEF: Fibrosis and AGEs are more important when LVEF is reduced, whereas cardiomyocyte resting tension is more important when LVEF is normal.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Case-Control Studies
Diabetes Complications/ physiopathology
Diabetes Mellitus/physiopathology
Diastole
Female
Fibrosis
Glycosylation End Products, Advanced
Heart Failure/etiology/ pathology
Heart Ventricles/pathology
Humans
Male
Middle Aged
Muscle Tonus
Myocytes, Cardiac/ physiology
Stroke Volume
Megjelenés:Circulation. - 117 : 1 (2008), p. 43-51. -
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:elektronikus változat
DOI
Borító:

12.

001-es BibID:BIBFORM092742
035-os BibID:(WOS)000530378100008 (Scopus)85083912431 (cikkazonosító)e008130
Első szerző:Hegyi Bence (élettanász)
Cím:Balance Between Rapid Delayed Rectifier K+ Current and Late Na+ Current on Ventricular Repolarization : an Effective Antiarrhythmic Target? / Bence Hegyi, Ye Chen-Izu, Leighton T. Izu, Sridharan Rajamani, Luiz Belardinelli, Donald M. Bers, Tamas Bányász
Dátum:2020
ISSN:1941-3149 1941-3084
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Circulation-Arrhythmia and Electrophysiology. - 13 : 4 (2020), p. 336-349. -
További szerzők:Chen-Izu, Ye Izu, Leighton T. Rajamani, Sridharan Belardinelli, Luiz Bers, Donald M. Bányász Tamás (1960-) (élettanász)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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