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3,019 results on '"Hasenfuss, Gerd"'

53. Atrial shunt device for heart failure with preserved and mildly reduced ejection fraction (REDUCE LAP-HF II): a randomised, multicentre, blinded, sham-controlled trial

Author

Akar, Joseph, Ando, Jiro, Anzai, Toshihisa, Asakura, Masanori, Bailey, Steven, Basuray, Anupam, Bauer, Fabrice, Bergmann, Martin, Blair, John, Cavendish, Jeffrey, Chung, Eugene, Cikes, Maja, Dauber, Ira, Donal, Erwan, Eicher, Jean-Christophe, Fail, Peter, Flaherty, James, Freixa, Xavier, Gafoor, Sameer, Gertz, Zachary, Gordon, Robert, Guazzi, Marco, Guerrero-Miranda, Cesar, Gupta, Deepak, Gustafsson, Finn, Hadadi, Cyrus, Hakemi, Emad, Handoko, Louis, Hass, Moritz, Hausleiter, Jorg, Hayward, Christopher, Hickey, Gavin, Hummel, Scott, Hussain, Imad, Isnard, Richard, Izumi, Chisato, Jondeau, Guillaume, Juneman, Elizabeth, Kinugawa, Koichiro, Kipperman, Robert, Krakowiak, Bartek, Krim, Selim, Larned, Joshua, Lewis, Gregory, Lipsic, Erik, Magalski, Anthony, Mazimba, Sula, Mazurek, Jeremy, McGrady, Michele, Mckenzie, Scott, Mehta, Shamir, Mignone, John, Morsli, Hakim, Nair, Ajith, Noel, Thomas, Orford, James, Parikh, Kishan, Patterson, Tiffany, Penicka, Martin, Petrie, Mark, Pieske, Burkert, Post, Martijn, Raake, Philip, Romero, Alicia, Ryan, John, Saito, Yoshihiko, Sakamoto, Takafumi, Sakata, Yasushi, Samara, Michael, Satya, Kumar, Sindone, Andrew, Starling, Randall, Trochu, Jean-Noël, Upadhya, Bharathi, van der Heyden, Jan, van Empel, Vanessa, Varma, Amit, Vest, Amanda, Wengenmayer, Tobias, Westenfeld, Ralf, Westermann, Dirk, Yamamoto, Kazuhiro, Zirlik, Andreas, Shah, Sanjiv J, Borlaug, Barry A, Chung, Eugene S, Cutlip, Donald E, Debonnaire, Philippe, Fail, Peter S, Gao, Qi, Hasenfuß, Gerd, Kahwash, Rami, Kaye, David M, Litwin, Sheldon E, Lurz, Philipp, Massaro, Joseph M, Mohan, Rajeev C, Ricciardi, Mark J, Solomon, Scott D, Sverdlov, Aaron L, Swarup, Vijendra, van Veldhuisen, Dirk J, Winkler, Sebastian, and Leon, Martin B

Published
2022
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55. Dysferlin Enables Tubular Membrane Proliferation in Cardiac Hypertrophy.

Author

Paulke, Nora Josefine, Fleischhacker, Carolin, Wegener, Justus B., Riedemann, Gabriel C., Cretu, Constantin, Mushtaq, Mufassra, Zaremba, Nina, Möbius, Wiebke, Zühlke, Yannik, Wedemeyer, Jasper, Liebmann, Lorenz, Gorshkova, Anastasiia A., Kownatzki-Danger, Daniel, Wagner, Eva, Kohl, Tobias, Wichmann, Carolin, Jahn, Olaf, Urlaub, Henning, Toischer, Karl, and Hasenfuß, Gerd

Published
2024
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56. Transition from asymptomatic to symptomatic systolic chronic heart failure: rationale and design of TransitionCHF.

Author

Sandek, Anja, Edelmann, Frank, Gertler, Christoph, Friede, Tim, Wachter, Rolf, and Hasenfuß, Gerd

Subjects
LEFT ventricular dysfunction, VENTRICULAR ejection fraction, ASYMPTOMATIC patients, CARDIOVASCULAR disease related mortality, HEART failure, AUTOMATIC timers
Abstract

Aims: Chronic systolic heart failure (CHF) is a major health burden. A relevant number of patients shows asymptomatic left ventricular dysfunction (ALVSD) before symptomatic CHF or becomes asymptomatic after initiating heart failure therapy. Clinical course, prognosis, and response to pharmacological and device‐based treatment are largely unknown in these two distinct groups of patients. Current pharmacological and interventional therapies do neither properly address the underlying pathophysiology nor prevent malignant loss of function. New therapeutic paradigms are needed to stop the progression from asymptomatic to symptomatic heart failure. Key questions are what causes progression of clinically asymptomatic New York Heart Association (NYHA) I heart failure to overt heart failure (>NYHA I) in some but not all patients and the underlying reasons for this transition. This requires the identification of disease mechanisms and biomarkers that predict outcome in well‐defined cohorts for innovative preclinical and clinical trials. Methods and results: TransitionCHF is a prospective, multicentre, longitudinal pathophysiological evaluation cohort study in patients with asymptomatic systolic dysfunction NYHA I and left ventricular ejection fraction ≤40%. The cohort comprises both incidental findings and patients who had become asymptomatic after a previous symptomatic event. TransitionCHF has recruited 1000 patients with ALVSD caused by various aetiologies in 20 university heart failure clinics across Germany. Both patients with and without comorbidities at study entry will be recruited. Patients will be systematically investigated and followed up annually over the course of the study. The primary composite endpoint is time to hospitalization for heart failure and cardiovascular death. The secondary endpoints assess time to all‐cause mortality, to cardiovascular mortality, to heart failure mortality, to all‐cause hospitalization, to heart failure hospitalization, and to recurrent heart failure hospitalizations, as well as time to assist device implantation/transplantation. Additional investigations focusing on biomarkers, comorbidities, gender aspects, nutrition, and functional parameters including quality of life will be performed. Conclusions: TransitionCHF will provide a more thorough pathophysiological understanding of the progression of asymptomatic systolic dysfunction into symptomatic heart failure that will help develop therapies tailored to prevent progressive heart failure. [ABSTRACT FROM AUTHOR]

Published
2024
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57. Impact of epicardial adipose tissue on cardiac function and morphology in patients with diastolic dysfunction.

Author

Schulz, Alexander, Backhaus, Sören J., Lange, Torben, Evertz, Ruben, Kutty, Shelby, Kowallick, Johannes T., Hasenfuß, Gerd, and Schuster, Andreas

Subjects
EPICARDIAL adipose tissue, BRAIN natriuretic factor, MAGNETIC resonance, CARDIAC catheterization, HEART failure, DOPPLER echocardiography
Abstract

Aims: This study aimed to identify the impact of increased epicardial adipose tissue (EAT) and its regional distribution on cardiac function in patients with diastolic dysfunction. Methods and results: Sixty‐eight patients with exertional dyspnoea (New York Heart Association ≥II), preserved ejection fraction (≥50%), and diastolic dysfunction (E/e′ ≥ 8) underwent rest and stress right heart catheterization, transthoracic echocardiography, and cardiovascular magnetic resonance (CMR). EAT volumes were depicted from CMR short‐axis stacks. First, the impact of increased EAT above the median was investigated. Second, the association of ventricular and atrial EAT with myocardial deformation at rest and during exercise stress was analysed in a multivariable regression analysis. Patients with high EAT had higher HFA‐PEFF and H2FPEFF scores as well as N‐terminal prohormone of brain natriuretic peptide levels (all P < 0.048). They were diagnosed with manifest heart failure with preserved ejection fraction (HFpEF) more frequently (low EAT: 37% vs. high EAT: 64%; P = 0.029) and had signs of adverse remodelling indicated by higher T1 times (P < 0.001). No differences in biventricular volumetry and left ventricular mass (all P > 0.074) were observed. Patients with high EAT had impaired atrial strain at rest and during exercise stress, and impaired ventricular strain during exercise stress. Regionally increased EAT was independently associated with functional impairment of the adjacent chambers. Conclusions: Patients with diastolic dysfunction and increased EAT show more pronounced signs of diastolic functional failure and adverse structural remodelling. Despite similar morphological characteristics, patients with high EAT show significant cardiac functional impairment, in particular in the atria. Our results indicate that regionally increased EAT directly induces atrial functional failure, which represents a distinct pathophysiological feature in HFpEF. [ABSTRACT FROM AUTHOR]

Published
2024
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59. Atrial Shunt Device Effects on Cardiac Structure and Function in Heart Failure With Preserved Ejection Fraction

Author

Patel, Ravi B., primary, Silvestry, Frank E., additional, Komtebedde, Jan, additional, Solomon, Scott D., additional, Hasenfuß, Gerd, additional, Litwin, Sheldon E., additional, Borlaug, Barry A., additional, Price, Matthew J., additional, Kawash, Rami, additional, Hummel, Scott L., additional, Cutlip, Donald E., additional, Leon, Martin B., additional, van Veldhuisen, Dirk J., additional, Rieth, Andreas J., additional, McKenzie, Scott, additional, Bugger, Heiko, additional, Mazurek, Jeremy A., additional, Kapadia, Samir R., additional, Vanderheyden, Marc, additional, Ky, Bonnie, additional, and Shah, Sanjiv J., additional

Published
2024
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61. Angiotensin Receptor–Neprilysin Inhibition (Sacubitril/Valsartan) Reduces Structural Arterial Stiffness in Middle‐Aged Mice

Author

Schellinger, Isabel N., primary, Dannert, Angelika, additional, Hoffmann, Annet, additional, Chodisetti, Giriprakash, additional, Mattern, Karin, additional, Petzold, Anne, additional, Klöting, Nora, additional, Schuster, Andreas, additional, Wagenhäuser, Markus U., additional, Emrich, Fabian, additional, Stumvoll, Michael, additional, Hasenfuß, Gerd, additional, and Raaz, Uwe, additional

Published
2024
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67. MicroRNA miR-29b regulates diabetic aortic remodeling and stiffening

Author

Schellinger, Isabel N., Wagenhäuser, Markus, Chodisetti, Giriprakash, Mattern, Karin, Dannert, Angelika, Petzold, Anne, Jakubizka-Smorag, Joanna, Emrich, Fabian, Haunschild, Josephina, Schuster, Andreas, Schwob, Elisabeth, Schulz, Kei, Maegdefessel, Lars, Spin, Joshua M., Stumvoll, Michael, Hasenfuß, Gerd, Tsao, Philip S., and Raaz, Uwe

Published
2021
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69. Integration of implantable device therapy in patients with heart failure. A clinical consensus statement from the Heart Failure Association (HFA) and European Heart Rhythm Association (EHRA) of the European Society of Cardiology (ESC)

Author

Mullens, Wilfried, Dauw, Jeroen, Gustafsson, Finn, Mebazaa, Alexandre, Steffel, Jan, Witte, Klaus K., Delgado, Victoria, Linde, Cecilia, Vernooy, Kevin, Anker, Stefan D., Chioncel, Ovidiu, Milicic, Davor, Hasenfuss, Gerd, Ponikowski, Piotr, Stephan von Bardeleben, Ralph, Koehler, Friedrich, Ruschitzka, Frank, Damman, Kevin, Schwammenthal, Ehud, Testani, Jeffrey M., Zannad, Faiez, Boehm, Michael, Cowie, Martin R., Dickstein, Kenneth, Jaarsma, Tiny, Filippatos, Gerasimos, Volterrani, Maurizio, Thum, Thomas, Adamopoulos, Stamatis, Cohen-Solal, Alain, Moura, Brenda, Rakisheva, Amina, Ristic, Arsen, Bayes-Genis, Antoni, Van Linthout, Sophie, Tocchetti, Carlo Gabriele, Savarese, Gianluigi, Skouri, Hadi, Adamo, Marianna, Amir, Offer, Yilmaz, Mehmet Birhan, Simpson, Maggie, Tokmakova, Mariya, Gonzalez, Arantxa, Piepoli, Massimo, Seferovic, Petar, Metra, Marco, Coats, Andrew J. S., Rosano, Giuseppe M. C., Mullens, Wilfried, Dauw, Jeroen, Gustafsson, Finn, Mebazaa, Alexandre, Steffel, Jan, Witte, Klaus K., Delgado, Victoria, Linde, Cecilia, Vernooy, Kevin, Anker, Stefan D., Chioncel, Ovidiu, Milicic, Davor, Hasenfuss, Gerd, Ponikowski, Piotr, Stephan von Bardeleben, Ralph, Koehler, Friedrich, Ruschitzka, Frank, Damman, Kevin, Schwammenthal, Ehud, Testani, Jeffrey M., Zannad, Faiez, Boehm, Michael, Cowie, Martin R., Dickstein, Kenneth, Jaarsma, Tiny, Filippatos, Gerasimos, Volterrani, Maurizio, Thum, Thomas, Adamopoulos, Stamatis, Cohen-Solal, Alain, Moura, Brenda, Rakisheva, Amina, Ristic, Arsen, Bayes-Genis, Antoni, Van Linthout, Sophie, Tocchetti, Carlo Gabriele, Savarese, Gianluigi, Skouri, Hadi, Adamo, Marianna, Amir, Offer, Yilmaz, Mehmet Birhan, Simpson, Maggie, Tokmakova, Mariya, Gonzalez, Arantxa, Piepoli, Massimo, Seferovic, Petar, Metra, Marco, Coats, Andrew J. S., and Rosano, Giuseppe M. C.

Abstract

Implantable devices form an integral part of the management of patients with heart failure (HF) and provide adjunctive therapies in addition to cornerstone drug treatment. Although the number of these devices is growing, only few are supported by robust evidence. Current devices aim to improve haemodynamics, improve reverse remodelling, or provide electrical therapy. A number of these devices have guideline recommendations and some have been shown to improve outcomes such as cardiac resynchronization therapy, implantable cardioverter-defibrillators and long-term mechanical support. For others, more evidence is still needed before large-scale implementation can be strongly advised. Of note, devices and drugs can work synergistically in HF as improved disease control with devices can allow for further optimization of drug therapy. Therefore, some devices might already be considered early in the disease trajectory of HF patients, while others might only be reserved for advanced HF. As such, device therapy should be integrated into HF care programmes. Unfortunately, implementation of devices, including those with the greatest evidence, in clinical care pathways is still suboptimal. This clinical consensus document of the Heart Failure Association (HFA) and European Heart Rhythm Association (EHRA) of the European Society of Cardiology (ESC) describes the physiological rationale behind device-provided therapy and also device-guided management, offers an overview of current implantable device options recommended by the guidelines and proposes a new integrated model of device therapy as a part of HF care.

Published
2024
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71. Functional and prognostic implications of cardiac magnetic resonance feature tracking-derived remote myocardial strain analyses in patients following acute myocardial infarction

Author

Lange, Torben, Stiermaier, Thomas, Backhaus, Sören J., Boom, Patricia C., Kowallick, Johannes T., de Waha-Thiele, Suzanne, Lotz, Joachim, Kutty, Shelby, Bigalke, Boris, Gutberlet, Matthias, Feistritzer, Hans-Josef, Desch, Steffen, Hasenfuß, Gerd, Thiele, Holger, Eitel, Ingo, and Schuster, Andreas

Published
2021
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72. Na V 1.8 as Proarrhythmic Target in a Ventricular Cardiac Stem Cell Model.

Author

Hartmann, Nico, Knierim, Maria, Maurer, Wiebke, Dybkova, Nataliya, Zeman, Florian, Hasenfuß, Gerd, Sossalla, Samuel, and Streckfuss-Bömeke, Katrin

Subjects
HEART cells, BRUGADA syndrome, INDUCED pluripotent stem cells, STEM cells, SODIUM channels, ARRHYTHMIA, SARCOPLASMIC reticulum, PLURIPOTENT stem cells
Abstract

The sodium channel NaV1.8, encoded by the SCN10A gene, has recently emerged as a potential regulator of cardiac electrophysiology. We have previously shown that NaV1.8 contributes to arrhythmogenesis by inducing a persistent Na+ current (late Na+ current, INaL) in human atrial and ventricular cardiomyocytes (CM). We now aim to further investigate the contribution of NaV1.8 to human ventricular arrhythmogenesis at the CM-specific level using pharmacological inhibition as well as a genetic knockout (KO) of SCN10A in induced pluripotent stem cell CM (iPSC-CM). In functional voltage-clamp experiments, we demonstrate that INaL was significantly reduced in ventricular SCN10A-KO iPSC-CM and in control CM after a specific pharmacological inhibition of NaV1.8. In contrast, we did not find any effects on ventricular APD90. The frequency of spontaneous sarcoplasmic reticulum Ca2+ sparks and waves were reduced in SCN10A-KO iPSC-CM and control cells following the pharmacological inhibition of NaV1.8. We further analyzed potential triggers of arrhythmias and found reduced delayed afterdepolarizations (DAD) in SCN10A-KO iPSC-CM and after the specific inhibition of NaV1.8 in control cells. In conclusion, we show that NaV1.8-induced INaL primarily impacts arrhythmogenesis at a subcellular level, with minimal effects on systolic cellular Ca2+ release. The inhibition or knockout of NaV1.8 diminishes proarrhythmic triggers in ventricular CM. In conjunction with our previously published results, this work confirms NaV1.8 as a proarrhythmic target that may be useful in an anti-arrhythmic therapeutic strategy. [ABSTRACT FROM AUTHOR]

Published
2024
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73. Histological assessment of cardiac amyloidosis in patients undergoing transcatheter aortic valve replacement.

Author

Beuthner, Bo Eric, Elkenani, Manar, Evert, Katja, Mustroph, Julian, Jacob, Christoph Friedemann, Paul, Niels Benjamin, Beißbarth, Tim, Zeisberg, Elisabeth Maria, Schnelle, Moritz, Puls, Miriam, Hasenfuß, Gerd, and Toischer, Karl

Subjects
BRAIN natriuretic factor, CARDIAC amyloidosis, CARDIAC patients, HEART valve prosthesis implantation, VENTRICULAR ejection fraction, CARDIAC arrest, PROPENSITY score matching
Abstract

Aims: Studies have reported a strongly varying co‐prevalence of aortic stenosis (AS) and cardiac amyloidosis (CA). We sought to histologically determine the co‐prevalence of AS and CA in patients undergoing transcatheter aortic valve replacement (TAVR). Consequently, we aimed to derive an algorithm to identify cases in which to suspect the co‐prevalence of AS and CA. Methods and results: In this prospective, monocentric study, endomyocardial biopsies of 162 patients undergoing TAVR between January 2017 and March 2021 at the University Medical Centre Göttingen were analysed by one pathologist blinded to clinical data using haematoxylin–eosin staining, Elastica van Gieson staining, and Congo red staining of endomyocardial biopsies. CA was identified in only eight patients (4.9%). CA patients had significantly higher N‐terminal pro‐brain natriuretic peptide (NT‐proBNP) levels (4356.20 vs. 1938.00 ng/L, P = 0.034), a lower voltage‐to‐mass ratio (0.73 vs. 1.46 × 10−2 mVm2/g, P = 0.022), and lower transaortic gradients (Pmean 17.5 vs. 38.0 mmHg, P = 0.004) than AS patients. Concomitant CA was associated with a higher prevalence of post‐procedural acute kidney injury (50.0% vs. 13.1%, P = 0.018) and sudden cardiac death [SCD; P (log‐rank test) = 0.017]. Following propensity score matching, 184 proteins were analysed to identify serum biomarkers of concomitant CA. CA patients expressed lower levels of chymotrypsin (P = 0.018) and carboxypeptidase 1 (P = 0.027). We propose an algorithm using commonly documented parameters—stroke volume index, ejection fraction, NT‐proBNP levels, posterior wall thickness, and QRS voltage‐to‐mass ratio—to screen for CA in AS patients, reaching a sensitivity of 66.6% with a specificity of 98.1%. Conclusions: The co‐prevalence of AS and CA was lower than expected, at 4.9%. Despite excellent 1 year mortality, AS + CA patients died significantly more often from SCD. We propose a multimodal algorithm to facilitate more effective screening for CA containing parameters commonly documented during clinical routine. Proteomic biomarkers may yield additional information in the future. [ABSTRACT FROM AUTHOR]

Published
2024
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77. Challenges in developing and validating machine learning models for TAVI mortality risk prediction: reply

Author

Leha, Andreas, primary, Huber, Cynthia, additional, Friede, Tim, additional, Bauer, Timm, additional, Beckmann, Andreas, additional, Bekeredjian, Raffi, additional, Bleiziffer, Sabine, additional, Herrmann, Eva, additional, Möllmann, Helge, additional, Walther, Thomas, additional, Beyersdorf, Friedhelm, additional, Hamm, Christian, additional, Künzi, Arnaud, additional, Windecker, Stephan, additional, Stortecky, Stefan, additional, Kutschka, Ingo, additional, Hasenfuß, Gerd, additional, Ensminger, Stephan, additional, Frerker, Christian, additional, and Seidler, Tim, additional

Published
2023
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79. Bi-allelic missense disease-causing variants in RPL3L associate neonatal dilated cardiomyopathy with muscle-specific ribosome biogenesis

Author

Ganapathi, Mythily, Argyriou, Loukas, Martínez-Azorín, Francisco, Morlot, Susanne, Yigit, Gökhan, Lee, Teresa M., Auber, Bernd, von Gise, Alexander, Petrey, Donald S., Thiele, Holger, Cyganek, Lukas, Sabater-Molina, María, Ahimaz, Priyanka, Cabezas-Herrera, Juan, Sorlí-García, Moisés, Zibat, Arne, Siegelin, Markus D., Burfeind, Peter, Buchovecky, Christie M., Hasenfuss, Gerd, Honig, Barry, Li, Yun, Iglesias, Alejandro D., and Wollnik, Bernd

Published
2020
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83. Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure

Author

Bengel, Philipp, Dybkova, Nataliya, Tirilomis, Petros, Ahmad, Shakil, Hartmann, Nico, A. Mohamed, Belal, Krekeler, Miriam Celine, Maurer, Wiebke, Pabel, Steffen, Trum, Maximilian, Mustroph, Julian, Gummert, Jan, Milting, Hendrik, Wagner, Stefan, Ljubojevic-Holzer, Senka, Toischer, Karl, Maier, Lars S., Hasenfuss, Gerd, Streckfuss-Bömeke, Katrin, and Sossalla, Samuel

Published
2021
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92. Differential multivariable risk prediction of appropriate shock versus competing mortality - A prospective cohort study to estimate benefits from ICD therapy

Author

Bergau, Leonard, Willems, Rik, Sprenkeler, David J., Fischer, Thomas H., Flevari, Panayota, Hasenfuß, Gerd, Katsaras, Dimitrios, Kirova, Aleksandra, Lehnart, Stephan E., Lüthje, Lars, Röver, Christian, Seegers, Joachim, Sossalla, Samuel, Dunnink, Albert, Sritharan, Rajevaa, Tuinenburg, Anton E., Vandenberk, Bert, Vos, Marc A., Wijers, Sofieke C., Friede, Tim, and Zabel, Markus

Published
2018
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94. Low-flow in aortic valve stenosis patients with reduced ejection fraction does not depend on left ventricular function

Author

Gersch, Svante, primary, Lange, Torben, additional, Beuthner, Bo Eric, additional, Elkenani, Manar, additional, Paul, Niels B, additional, Schnelle, Moritz, additional, Diez, Javier, additional, Zeisberg, Elisabeth M., additional, Puls, Miriam, additional, Hasenfuss, Gerd, additional, Schuster, Andreas, additional, and Toischer, Karl, additional

Published
2023
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95. Machine learning‐based prediction of in‐hospital death for patients with takotsubo syndrome: The InterTAK‐ML model

Author

De Filippo, Ovidio, primary, Cammann, Victoria L., additional, Pancotti, Corrado, additional, Di Vece, Davide, additional, Silverio, Angelo, additional, Schweiger, Victor, additional, Niederseer, David, additional, Szawan, Konrad A., additional, Würdinger, Michael, additional, Koleva, Iva, additional, Dusi, Veronica, additional, Bellino, Michele, additional, Vecchione, Carmine, additional, Parodi, Guido, additional, Bossone, Eduardo, additional, Gili, Sebastiano, additional, Neuhaus, Michael, additional, Franke, Jennifer, additional, Meder, Benjamin, additional, Jaguszewski, Miłosz, additional, Noutsias, Michel, additional, Knorr, Maike, additional, Jansen, Thomas, additional, Dichtl, Wolfgang, additional, von Lewinski, Dirk, additional, Burgdorf, Christof, additional, Kherad, Behrouz, additional, Tschöpe, Carsten, additional, Sarcon, Annahita, additional, Shinbane, Jerold, additional, Rajan, Lawrence, additional, Michels, Guido, additional, Pfister, Roman, additional, Cuneo, Alessandro, additional, Jacobshagen, Claudius, additional, Karakas, Mahir, additional, Koenig, Wolfgang, additional, Pott, Alexander, additional, Meyer, Philippe, additional, Roffi, Marco, additional, Banning, Adrian, additional, Wolfrum, Mathias, additional, Cuculi, Florim, additional, Kobza, Richard, additional, Fischer, Thomas A., additional, Vasankari, Tuija, additional, Airaksinen, K.E. Juhani, additional, Napp, L. Christian, additional, Dworakowski, Rafal, additional, MacCarthy, Philip, additional, Kaiser, Christoph, additional, Osswald, Stefan, additional, Galiuto, Leonarda, additional, Chan, Christina, additional, Bridgman, Paul, additional, Beug, Daniel, additional, Delmas, Clément, additional, Lairez, Olivier, additional, Gilyarova, Ekaterina, additional, Shilova, Alexandra, additional, Gilyarov, Mikhail, additional, El‐Battrawy, Ibrahim, additional, Akin, Ibrahim, additional, Poledniková, Karolina, additional, Toušek, Petr, additional, Winchester, David E., additional, Massoomi, Michael, additional, Galuszka, Jan, additional, Ukena, Christian, additional, Poglajen, Gregor, additional, Carrilho‐Ferreira, Pedro, additional, Hauck, Christian, additional, Paolini, Carla, additional, Bilato, Claudio, additional, Kobayashi, Yoshio, additional, Kato, Ken, additional, Ishibashi, Iwao, additional, Himi, Toshiharu, additional, Din, Jehangir, additional, Al‐Shammari, Ali, additional, Prasad, Abhiram, additional, Rihal, Charanjit S., additional, Liu, Kan, additional, Schulze, P. Christian, additional, Bianco, Matteo, additional, Jörg, Lucas, additional, Rickli, Hans, additional, Pestana, Gonçalo, additional, Nguyen, Thanh H., additional, Böhm, Michael, additional, Maier, Lars S., additional, Pinto, Fausto J., additional, Widimský, Petr, additional, Felix, Stephan B., additional, Braun‐Dullaeus, Ruediger C., additional, Rottbauer, Wolfgang, additional, Hasenfuß, Gerd, additional, Pieske, Burkert M., additional, Schunkert, Heribert, additional, Budnik, Monika, additional, Opolski, Grzegorz, additional, Thiele, Holger, additional, Bauersachs, Johann, additional, Horowitz, John D., additional, Di Mario, Carlo, additional, Bruno, Francesco, additional, Kong, William, additional, Dalakoti, Mayank, additional, Imori, Yoichi, additional, Münzel, Thomas, additional, Crea, Filippo, additional, Lüscher, Thomas F., additional, Bax, Jeroen J., additional, Ruschitzka, Frank, additional, De Ferrari, Gaetano Maria, additional, Fariselli, Piero, additional, Ghadri, Jelena R., additional, Citro, Rodolfo, additional, D'Ascenzo, Fabrizio, additional, and Templin, Christian, additional

Published
2023
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96. Impact of myocardial deformation on risk prediction in patients following acute myocardial infarction

Author

Lange, Torben, primary, Gertz, Roman J., additional, Schulz, Alexander, additional, Backhaus, Sören J., additional, Evertz, Ruben, additional, Kowallick, Johannes T., additional, Hasenfuß, Gerd, additional, Desch, Steffen, additional, Thiele, Holger, additional, Stiermaier, Thomas, additional, Eitel, Ingo, additional, and Schuster, Andreas, additional

Published
2023
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97. Genome-wide analysis of histone marks identifying an epigenetic signature of promoters and enhancers underlying cardiac hypertrophy

Author

Papait, Roberto, Cattaneo, Paola, Kunderfranco, Paolo, Greco, Carolina, Carullo, Pierluigi, Guffanti, Alessandro, Viganò, Valentina, Stirparo, Giuliano Giuseppe, Latronico, Michael VG, Hasenfuss, Gerd, Chen, Ju, and Condorelli, Gianluigi

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Cardiovascular, Human Genome, Heart Disease, Biotechnology, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Aetiology, Underpinning research, Acetylation, Animals, Cardiomegaly, Enhancer Elements, Genetic, Epigenesis, Genetic, Gene Expression Regulation, Developmental, Histones, Methylation, Mice, Promoter Regions, Genetic, Transcription Factors, epigenetic regulation, histone acetylation, histone methylation
Abstract

Cardiac hypertrophy, initially an adaptive response of the myocardium to stress, can progress to heart failure. The epigenetic signature underlying this phenomenon is poorly understood. Here, we report on the genome-wide distribution of seven histone modifications in adult mouse cardiomyocytes subjected to a prohypertrophy stimulus in vivo. We found a set of promoters with an epigenetic pattern that distinguishes specific functional classes of genes regulated in hypertrophy and identified 9,207 candidate active enhancers whose activity was modulated. We also analyzed the transcriptional network within which these genetic elements act to orchestrate hypertrophy gene expression, finding a role for myocyte enhancer factor (MEF)2C and MEF2A in regulating enhancers. We propose that the epigenetic landscape is a key determinant of gene expression reprogramming in cardiac hypertrophy and provide a basis for understanding the role of chromatin in regulating this phenomenon.

Published
2013

98. A Randomized Controlled Trial to Evaluate the Safety and Efficacy of Cardiac Contractility Modulation

Author

Abraham, William T., Kuck, Karl-Heinz, Goldsmith, Rochelle L., Lindenfeld, JoAnn, Reddy, Vivek Y., Carson, Peter E., Mann, Douglas L., Saville, Benjamin, Parise, Helen, Chan, Rodrigo, Wiegn, Phi, Hastings, Jeffrey L., Kaplan, Andrew J., Edelmann, Frank, Luthje, Lars, Kahwash, Rami, Tomassoni, Gery F., Gutterman, David D., Stagg, Angela, Burkhoff, Daniel, and Hasenfuß, Gerd

Published
2018
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99. Long-Term Prognosis of Patients With Takotsubo Syndrome

Author

Ghadri, Jelena R., Kato, Ken, Cammann, Victoria L., Gili, Sebastiano, Jurisic, Stjepan, Di Vece, Davide, Candreva, Alessandro, Ding, Katharina J., Micek, Jozef, Szawan, Konrad A., Bacchi, Beatrice, Bianchi, Rahel, Levinson, Rena A., Wischnewsky, Manfred, Seifert, Burkhardt, Schlossbauer, Susanne A., Citro, Rodolfo, Bossone, Eduardo, Münzel, Thomas, Knorr, Maike, Heiner, Susanne, D’Ascenzo, Fabrizio, Franke, Jennifer, Sarcon, Annahita, Napp, L. Christian, Jaguszewski, Milosz, Noutsias, Michel, Katus, Hugo A., Burgdorf, Christof, Schunkert, Heribert, Thiele, Holger, Bauersachs, Johann, Tschöpe, Carsten, Pieske, Burkert M., Rajan, Lawrence, Michels, Guido, Pfister, Roman, Cuneo, Alessandro, Jacobshagen, Claudius, Hasenfuß, Gerd, Karakas, Mahir, Koenig, Wolfgang, Rottbauer, Wolfgang, Said, Samir M., Braun-Dullaeus, Ruediger C., Banning, Adrian, Cuculi, Florim, Kobza, Richard, Fischer, Thomas A., Vasankari, Tuija, Airaksinen, K.E. Juhani, Opolski, Grzegorz, Dworakowski, Rafal, MacCarthy, Philip, Kaiser, Christoph, Osswald, Stefan, Galiuto, Leonarda, Crea, Filippo, Dichtl, Wolfgang, Empen, Klaus, Felix, Stephan B., Delmas, Clément, Lairez, Olivier, El-Battrawy, Ibrahim, Akin, Ibrahim, Borggrefe, Martin, Horowitz, John, Kozel, Martin, Tousek, Petr, Widimský, Petr, Gilyarova, Ekaterina, Shilova, Alexandra, Gilyarov, Mikhail, Winchester, David E., Ukena, Christian, Bax, Jeroen J., Prasad, Abhiram, Böhm, Michael, Lüscher, Thomas F., Ruschitzka, Frank, and Templin, Christian

Published
2018
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