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3. Advancing the care of individuals with cancer through innovation & technology: Proceedings from the cardiology oncology innovation summit 2020 and 2021

Author

Brown, Sherry-Ann, Beavers, Craig, Bauer, Brenton, Cheng, Richard K, Berman, Generika, Marshall, Catherine H, Guha, Avirup, Jain, Prantesh, Steward, Austin, DeCara, Jeanne M, Olaye, Iredia M, Hansen, Kathryn, Logan, Jim, Bergom, Carmen, Glide-Hurst, Carri, Loh, Irving, Gambril, John Alan, MacLeod, James, Maddula, Ragasnehith, McGranaghan, Peter J, Batra, Akshee, Campbell, Courtney, Hamid, Abdulaziz, Gunturkun, Fatma, Davis, Robert, Jefferies, John, Fradley, Michael, Albert, Katherine, Blaes, Anne, Choudhuri, Indrajit, Ghosh, Arjun K, Ryan, Thomas D, Ezeoke, Ogochukwu, Leedy, Douglas J, Williams, Wadsworth, Roman, Sebastian, Lehmann, Lorenz, Sarkar, Abdullah, Sadler, Diego, Polter, Elizabeth, Ruddy, Kathryn J, Bansal, Neha, Yang, Eric, Patel, Brijesh, Cho, David, Bailey, Alison, Addison, Daniel, Rao, Vijay, Levenson, Joshua E, Itchhaporia, Dipti, Watson, Karol, Gulati, Martha, Williams, Kim, Lloyd-Jones, Donald, Michos, Erin, Gralow, Julie, and Martinez, Hugo

Published
2024

7. Cardiomuscular Biomarkers in the Diagnosis and Prognostication of Immune Checkpoint Inhibitor Myocarditis.

Author

Lehmann, Lorenz, Heckmann, Markus, Bailly, Guillaume, Finke, Daniel, Procureur, Adrien, Power, John, Stein, Frederic, Bretagne, Marie, Ederhy, Stephane, Fenioux, Charlotte, Hamwy, Omar, Funck-Brentano, Elisa, Romano, Emanuela, Pieroni, Laurence, Münster, Jan, Allenbach, Yves, Anquetil, Céline, Leonard-Louis, Sarah, Palaskas, Nicolas, Hayek, Salim, Katus, Hugo, Giannitsis, Evangelos, Frey, Norbert, Kaya, Ziya, Moslehi, Javid, Prifti, Edi, and Salem, Joe-Elie

Subjects
biomarkers, drug-related side effects and adverse reactions, immune checkpoint inhibitors, myocarditis, pharmacology, troponins, Humans, Myocarditis, Immune Checkpoint Inhibitors, Biomarkers, Creatine Kinase, Prognosis, Troponin T
Abstract

BACKGROUND: Immune checkpoint inhibitors (ICIs) are approved for multiple cancers but can result in ICI-associated myocarditis, an infrequent but life-threatening condition. Elevations in cardiac biomarkers, specifically troponin-I (cTnI), troponin-T (cTnT), and creatine kinase (CK), are used for diagnosis. However, the association between temporal elevations of these biomarkers with disease trajectory and outcomes has not been established. METHODS: We analyzed the diagnostic accuracy and prognostic performances of cTnI, cTnT, and CK in patients with ICI myocarditis (n=60) through 1-year follow-up in 2 cardio-oncology units (APHP Sorbonne, Paris, France and Heidelberg, Germany). A total of 1751 (1 cTnT assay type), 920 (4 cTnI assay types), and 1191 CK sampling time points were available. Major adverse cardiomyotoxic events (MACE) were defined as heart failure, ventricular arrhythmia, atrioventricular or sinus block requiring pacemaker, respiratory muscle failure requiring mechanical ventilation, and sudden cardiac death. Diagnostic performance of cTnI and cTnT was also assessed in an international ICI myocarditis registry. RESULTS: Within 72 hours of admission, cTnT, cTnI, and CK were increased compared with upper reference limits (URLs) in 56 of 57 (98%), 37 of 42 ([88%] P=0.03 versus cTnT), and 43 of 57 ([75%] P

Published
2023

8. Abatacept/Ruxolitinib and Screening for Concomitant Respiratory Muscle Failure to Mitigate Fatality of Immune-Checkpoint Inhibitor Myocarditis.

Author

Salem, Joe-Elie, Bretagne, Marie, Abbar, Baptiste, Leonard-Louis, Sarah, Ederhy, Stéphane, Redheuil, Alban, Boussouar, Samia, Nguyen, Lee S, Procureur, Adrien, Stein, Frederic, Fenioux, Charlotte, Devos, Perrine, Gougis, Paul, Dres, Martin, Demoule, Alexandre, Psimaras, Dimitri, Lenglet, Timothee, Maisonobe, Thierry, De Chambrun, Marc Pineton, Hekimian, Guillaume, Straus, Christian, Gonzalez-Bermejo, Jesus, Klatzmann, David, Rigolet, Aude, Guillaume-Jugnot, Perrine, Champtiaux, Nicolas, Benveniste, Olivier, Weiss, Nicolas, Saheb, Samir, Rouvier, Philippe, Plu, Isabelle, Gandjbakhch, Estelle, Kerneis, Mathieu, Hammoudi, Nadjib, Zahr, Noel, Llontop, Claudia, Morelot-Panzini, Capucine, Lehmann, Lorenz, Qin, Juan, Moslehi, Javid J, Rosenzwajg, Michelle, Similowski, Thomas, and Allenbach, Yves

Subjects
Lung, Clinical Research, Rare Diseases, Humans, Myocarditis, Immune Checkpoint Inhibitors, Abatacept, Antineoplastic Agents, Immunological, Myotoxicity, Myositis, Respiratory Muscles, Oncology and Carcinogenesis
Abstract

Immune-checkpoint-inhibitor (ICI)-associated myotoxicity involves the heart (myocarditis) and skeletal muscles (myositis), which frequently occur concurrently and are highly fatal. We report the results of a strategy that included identification of individuals with severe ICI myocarditis by also screening for and managing concomitant respiratory muscle involvement with mechanical ventilation, as well as treatment with the CTLA4 fusion protein abatacept and the JAK inhibitor ruxolitinib. Forty cases with definite ICI myocarditis were included with pathologic confirmation of concomitant myositis in the majority of patients. In the first 10 patients, using recommended guidelines, myotoxicity-related fatality occurred in 60%, consistent with historical controls. In the subsequent 30 cases, we instituted systematic screening for respiratory muscle involvement coupled with active ventilation and treatment using ruxolitinib and abatacept. The abatacept dose was adjusted using CD86 receptor occupancy on circulating monocytes. The myotoxicity-related fatality rate was 3.4% (1/30) in these 30 patients versus 60% in the first quartile (P < 0.0001). These clinical results are hypothesis-generating and need further evaluation.SignificanceEarly management of respiratory muscle failure using mechanical ventilation and high-dose abatacept with CD86 receptor occupancy monitoring combined with ruxolitinib may be promising to mitigate high fatality rates in severe ICI myocarditis. See related commentary by Dougan, p. 1040. This article is highlighted in the In This Issue feature, p. 1027.

Published
2023

9. Versorgung von Patienten mit kardialer Amyloidose: Konsensuspapier der Deutschen Gesellschaft für Kardiologie – Herz- und Kreislaufforschung e. V. (DGK), AG 40 Onkologische Kardiologie, und der Deutschen Gesellschaft für Hämatologie und medizinische Onkologie e. V. (DGHO), der Deutschen Gesellschaft für Neurologie e. V. (DGN) und der Deutschen Gesellschaft für Nephrologie e. V. (DGfN)

Author

Pfister, Roman, Hagenacker, Tim, Heemann, Uwe, Hegenbart, Ute, Heidecker, Bettina, Kruck, Sebastian, Knebel, Fabian, Lehmann, Lorenz, Morbach, Caroline, Rischpler, Christoph, Schulze, P. Christian, Yilmaz, Ali, and Perings, Christian

Published
2024
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11. Thymus alterations and susceptibility to immune checkpoint inhibitor myocarditis

Author

Fenioux, Charlotte, Abbar, Baptiste, Boussouar, Samia, Bretagne, Marie, Power, John R., Moslehi, Javid J., Gougis, Paul, Amelin, Damien, Dechartres, Agnès, Lehmann, Lorenz H., Courand, Pierre-Yves, Cautela, Jennifer, Alexandre, Joachim, Procureur, Adrien, Rozes, Antoine, Leonard-Louis, Sarah, Qin, Juan, Cheynier, Rémi, Charmeteau-De Muylder, Benedicte, Redheuil, Alban, Tubach, Florence, Cadranel, Jacques, Milon, Audrey, Ederhy, Stéphane, Similowski, Thomas, Johnson, Douglas B., Pizzo, Ian, Catalan, Toniemarie, Benveniste, Olivier, Hayek, Salim S., Allenbach, Yves, Rosenzwajg, Michelle, Dolladille, Charles, and Salem, Joe-Elie

Published
2023
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12. Coronary artery disease and revascularization associated with immune checkpoint blocker myocarditis: Report from an international registry.

Author

Nowatzke, Joseph, Guedeney, Paul, Palaskas, Nicholas, Lehmann, Lorenz, Ederhy, Stephane, Zhu, Han, Cautela, Jennifer, Francis, Sanjeev, Courand, Pierre-Yves, Deswal, Anita, Ewer, Steven, Aras, Mandar, Arangalage, Dimitri, Ghafourian, Kambiz, Fenioux, Charlotte, Finke, Daniel, Peretto, Giovanni, Zaha, Vlad, Itzhaki Ben Zadok, Osnat, Tajiri, Kazuko, Akhter, Nausheen, Levenson, Joshua, Baldassarre, Lauren, Salem, Joe-Elie, Huang, Shi, Collet, Jean-Philippe, Power, John, and Moslehi, Javid

Subjects
Acute coronary syndrome, Coronary revascularization, Immune checkpoint blockers, Immune-related adverse events, Myocarditis, Humans, Coronary Artery Disease, Immune Checkpoint Inhibitors, Retrospective Studies, Myocarditis, Prognosis, Registries, Risk Factors
Abstract

PURPOSE: Immune checkpoint blocker (ICB) associated myocarditis (ICB-myocarditis) may present similarly and/or overlap with other cardiac pathology including acute coronary syndrome presenting a challenge for prompt clinical diagnosis. METHODS: An international registry was used to retrospectively identify cases of ICB-myocarditis. Presence of coronary artery disease (CAD) was defined as coronary artery stenosis >70% in patients undergoing coronary angiogram. RESULTS: Among 261 patients with clinically suspected ICB-myocarditis who underwent a coronary angiography, CAD was present in 59/261 patients (22.6%). Coronary revascularization was performed during the index hospitalisation in 19/59 (32.2%) patients. Patients undergoing coronary revascularization less frequently received steroids administration within 24 h of admission compared to the other groups (p = 0.029). Myocarditis-related 90-day mortality was 9/17 (52.7%) in the revascularised cohort, compared to 5/31 (16.1%) in those not revascularized and 25/156 (16.0%) in those without CAD (p = 0.001). Immune-related adverse event-related 90-day mortality was 9/17 (52.7%) in the revascularized cohort, compared to 6/31 (19.4%) in those not revascularized and 31/156 (19.9%) in no CAD groups (p = 0.007). All-cause 90-day mortality was 11/17 (64.7%) in the revascularized cohort, compared to 13/31 (41.9%) in no revascularization and 60/158 (38.0%) in no CAD groups (p = 0.10). After adjustment of age and sex, coronary revascularization remained associated with ICB-myocarditis-related death at 90 days (hazard ratio [HR] = 4.03, 95% confidence interval [CI] 1.84-8.84, p

Published
2022

13. Hormonal therapies up-regulate MANF and overcome female susceptibility to immune checkpoint inhibitor myocarditis

Author

Zhang, Yaohua, Sun, Chengcao, Li, Yajuan, Qin, Juan, Amancherla, Kaushik, Jing, Ying, Hu, Qingsong, Liang, Ke, Zhang, Zhao, Ye, Youqiong, Huang, Lisa A, Nguyen, Tina K, Egranov, Sergey D, Zhao, Zilong, Wu, Andrew, Xi, Yutao, Yao, Jun, Hung, Mien-Chie, Calin, George A, Cheng, Jie, Lim, Bora, Lehmann, Lorenz H, Salem, Joe-Elie, Johnson, Douglas B, Curran, Michael A, Yu, Dihua, Han, Leng, Darabi, Radbod, Yang, Liuqing, Moslehi, Javid J, and Lin, Chunru

Subjects
Cardiovascular, Estrogen, Heart Disease, 5.1 Pharmaceuticals, Aetiology, 2.1 Biological and endogenous factors, Development of treatments and therapeutic interventions, Humans, Female, Male, Mice, Animals, Myocarditis, Immune Checkpoint Inhibitors, Estrogen Receptor beta, Myocytes, Cardiac, Estradiol, Nerve Growth Factors, Biological Sciences, Medical and Health Sciences
Abstract

Immune checkpoint inhibitors (ICIs) have been increasingly used in combination for cancer treatment but are associated with myocarditis. Here, we report that tumor-bearing mice exhibited response to treatment with combinatorial anti-programmed cell death 1 and anti-cytotoxic T lymphocyte antigen-4 antibodies but also presented with cardiovascular toxicities observed clinically with ICI therapy, including myocarditis and arrhythmia. Female mice were preferentially affected with myocarditis compared to male mice, consistent with a previously described genetic model of ICI myocarditis and emerging clinical data. Mechanistically, myocardial tissue from ICI-treated mice, the genetic mouse model, and human heart tissue from affected patients with ICI myocarditis all exhibited down-regulation of MANF (mesencephalic astrocyte-derived neurotrophic factor) and HSPA5 (heat shock 70-kDa protein 5) in the heart; this down-regulation was particularly notable in female mice. ICI myocarditis was amplified by heart-specific genetic deletion of mouse Manf and was attenuated by administration of recombinant MANF protein, suggesting a causal role. Ironically, both MANF and HSPA5 were transcriptionally induced by liganded estrogen receptor β and inhibited by androgen receptor. However, ICI treatment reduced serum estradiol concentration to a greater extent in female compared to male mice. Treatment with an estrogen receptor β-specific agonist and androgen depletion therapy attenuated ICI-associated cardiac effects. Together, our data suggest that ICI treatment inhibits estradiol-dependent expression of MANF/HSPA5 in the heart, curtailing the cardiomyocyte response to immune injury. This endocrine-cardiac-immune pathway offers new insights into the mechanisms of sex differences in cardiac disease and may offer treatment strategies for ICI myocarditis.

Published
2022

15. Publisher Correction: Thymus alterations and susceptibility to immune checkpoint inhibitor myocarditis

Author

Fenioux, Charlotte, Abbar, Baptiste, Boussouar, Samia, Bretagne, Marie, Power, John R., Moslehi, Javid J., Gougis, Paul, Amelin, Damien, Dechartres, Agnès, Lehmann, Lorenz H., Courand, Pierre-Yves, Cautela, Jennifer, Alexandre, Joachim, Procureur, Adrien, Rozes, Antoine, Leonard-Louis, Sarah, Qin, Juan, Cheynier, Rémi, Charmeteau-De Muylder, Benedicte, Redheuil, Alban, Tubach, Florence, Cadranel, Jacques, Milon, Audrey, Ederhy, Stéphane, Similowski, Thomas, Johnson, Douglas B., Pizzo, Ian, Catalan, Toniemarie, Benveniste, Olivier, Hayek, Salim S., Allenbach, Yves, Rosenzwajg, Michelle, Dolladille, Charles, and Salem, Joe-Elie

Published
2024
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16. A Genetic Mouse Model Recapitulates Immune Checkpoint Inhibitor-Associated Myocarditis and Supports a Mechanism-Based Therapeutic Intervention.

Author

Wei, Spencer, Meijers, Wouter, Axelrod, Margaret, Anang, Nana-Ama, Screever, Elles, Wescott, Elizabeth, Johnson, Douglas, Whitley, Elizabeth, Lehmann, Lorenz, Courand, Pierre-Yves, Mancuso, James, Himmel, Lauren, Lebrun-Vignes, Benedicte, Wleklinski, Matthew, Knollmann, Bjorn, Srinivasan, Jayashree, Li, Yu, Atolagbe, Oluwatomisin, Rao, Xiayu, Zhao, Yang, Wang, Jing, Ehrlich, Lauren, Sharma, Padmanee, Salem, Joe-Elie, Balko, Justin, Moslehi, Javid, and Allison, James

Subjects
Animals, Biomarkers, Tumor, Cardiotoxicity, Disease Management, Disease Models, Animal, Disease Susceptibility, Electrocardiography, Humans, Immune Checkpoint Inhibitors, Mice, Molecular Targeted Therapy, Myocarditis, Neoplasms
Abstract

Immune checkpoint inhibitors (ICI) targeting CTLA4 or PD-1/PD-L1 have transformed cancer therapy but are associated with immune-related adverse events, including myocarditis. Here, we report a robust preclinical mouse model of ICI-associated myocarditis in which monoallelic loss of Ctla4 in the context of complete genetic absence of Pdcd1 leads to premature death in approximately half of mice. Premature death results from myocardial infiltration by T cells and macrophages and severe ECG abnormalities, closely recapitulating the clinical and pathologic hallmarks of ICI-associated myocarditis observed in patients. Using this model, we show that Ctla4 and Pdcd1 functionally interact in a gene dosage-dependent manner, providing a mechanism by which myocarditis arises with increased frequency in the setting of combination ICI therapy. We demonstrate that intervention with CTLA4-Ig (abatacept) is sufficient to ameliorate disease progression and additionally provide a case series of patients in which abatacept mitigates the fulminant course of ICI myocarditis. SIGNIFICANCE: We provide a preclinical model of ICI-associated myocarditis which recapitulates this clinical syndrome. Using this model, we demonstrate that CTLA4 and PD-1 (ICI targets) functionally interact for myocarditis development and that intervention with CTLA4-Ig (abatacept) attenuates myocarditis, providing mechanistic rationale and preclinical support for therapeutic clinical studies.See related commentary by Young and Bluestone, p. 537.This article is highlighted in the In This Issue feature, p. 521.

Published
2021

18. Author Correction: Thymus alterations and susceptibility to immune checkpoint inhibitor myocarditis

Author

Fenioux, Charlotte, Abbar, Baptiste, Boussouar, Samia, Bretagne, Marie, Power, John R., Moslehi, Javid J., Gougis, Paul, Amelin, Damien, Dechartres, Agnès, Lehmann, Lorenz H., Courand, Pierre-Yves, Cautela, Jennifer, Alexandre, Joachim, Procureur, Adrien, Rozes, Antoine, Leonard-Louis, Sarah, Qin, Juan, Cheynier, Rémi, Charmeteau-De Muylder, Benedicte, Redheuil, Alban, Tubach, Florence, Cadranel, Jacques, Milon, Audrey, Ederhy, Stéphane, Similowski, Thomas, Johnson, Douglas B., Pizzo, Ian, Catalan, Toniemarie, Benveniste, Olivier, Hayek, Salim S., Allenbach, Yves, Rosenzwajg, Michelle, Dolladille, Charles, and Salem, Joe-Elie

Published
2023
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19. Common mechanistic pathways in cancer and heart failure. A scientific roadmap on behalf of the Translational Research Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC).

Author

de Boer, Rudolf, Hulot, Jean-Sébastien, Tocchetti, Carlo, Aboumsallem, Joseph, Ameri, Pietro, Anker, Stefan, Bauersachs, Johann, Bertero, Edoardo, Coats, Andrew, Čelutkienė, Jelena, Chioncel, Ovidiu, Dodion, Pierre, Eschenhagen, Thomas, Farmakis, Dimitrios, Bayes-Genis, Antoni, Jäger, Dirk, Jankowska, Ewa, Kitsis, Richard, Konety, Suma, Larkin, James, Lehmann, Lorenz, Lenihan, Daniel, Maack, Christoph, Moslehi, Javid, Müller, Oliver, Nowak-Sliwinska, Patrycja, Piepoli, Massimo, Ponikowski, Piotr, Pudil, Radek, Rainer, Peter, Ruschitzka, Frank, Sawyer, Douglas, Seferovic, Petar, Suter, Thomas, Thum, Thomas, van der Meer, Peter, Van Laake, Linda, von Haehling, Stephan, Heymans, Stephane, Lyon, Alexander, and Backs, Johannes

Subjects
Angiogenesis, Cancer, Cardio-oncology, Cardiotoxicity, Clonal haematopoiesis, Extracellular matrix, Heart failure, Inflammation, Metabolism, Comorbidity, Heart Failure, Humans, Inflammation, Neoplasms, Risk Factors
Abstract

The co-occurrence of cancer and heart failure (HF) represents a significant clinical drawback as each disease interferes with the treatment of the other. In addition to shared risk factors, a growing body of experimental and clinical evidence reveals numerous commonalities in the biology underlying both pathologies. Inflammation emerges as a common hallmark for both diseases as it contributes to the initiation and progression of both HF and cancer. Under stress, malignant and cardiac cells change their metabolic preferences to survive, which makes these metabolic derangements a great basis to develop intersection strategies and therapies to combat both diseases. Furthermore, genetic predisposition and clonal haematopoiesis are common drivers for both conditions and they hold great clinical relevance in the context of personalized medicine. Additionally, altered angiogenesis is a common hallmark for failing hearts and tumours and represents a promising substrate to target in both diseases. Cardiac cells and malignant cells interact with their surrounding environment called stroma. This interaction mediates the progression of the two pathologies and understanding the structure and function of each stromal component may pave the way for innovative therapeutic strategies and improved outcomes in patients. The interdisciplinary collaboration between cardiologists and oncologists is essential to establish unified guidelines. To this aim, pre-clinical models that mimic the human situation, where both pathologies coexist, are needed to understand all the aspects of the bidirectional relationship between cancer and HF. Finally, adequately powered clinical studies, including patients from all ages, and men and women, with proper adjudication of both cancer and cardiovascular endpoints, are essential to accurately study these two pathologies at the same time.

Published
2020

20. Coronary artery disease and revascularization associated with immune checkpoint blocker myocarditis: Report from an international registry

Author

Aghel, Nazanin, Alexandre, Joachim, Aonuma, Kazutaka, Asnani, Aarti H., Behling, Juliane, Bilen, Mehmet, Bottinor, Wendy, Cariou, Eve, Chahine, Johnny, Chan, Weiting, Chauhan, Aman, Cohen, Max, Crusz, Shanthini, Fernando, Suran, Florido, Roberta, Frigeri, Mauro, Fukushima, Satoshi, Gaughan, Elizabeth, Geisler, Benjamin P., Gilstrap, Lauren, Grohe, Christian, Guha, Avirup, Habib, Manhal, Haegler-Laube, Eva, Haydon, Andrew, Hayek, Salim, Hughes, Andrew, Imai, Rysk, Katsume, Yumi, Kimura, Hideki, Koo Lin, Lily, Lenneman, Carrie, Leong, Daryl, Makker, Vicky, Martinez-Calle, Nicolas, Moey, Melissa, Mohri, Masahiro, Morimoto, Ryota, Moritoki, Yoshinobu, Narezkina, Anna, Nicol, Martin, Nooka, Ajay, Orimoloye, Olusola, Patel, Milan, Perl, Michal, Piriou, Nicolas, Raikhelkar, Jayant K., Raza, Yasmin, Rao, Anjali, Reddy, Sunil, Seki, Nobuhiko, Stangl, Karl, Stewart, Andrew, Stringer, Bryan, Tamarappoo, Balaji K., Tamura, Yuichi, Thuny, Frank, Tierney, Sean, Tresorier, Romain, Ullah, Waqas, Von Hunolstein, Jean-Jacques, Warner, Ellen, Weppler, Allison, Nowatzke, Joseph, Guedeney, Paul, Palaskas, Nicholas, Lehmann, Lorenz, Ederhy, Stephane, Zhu, Han, Cautela, Jennifer, Francis, Sanjeev, Courand, Pierre-Yves, Deswal, Anita, Ewer, Steven M., Aras, Mandar, Arangalage, Dimitri, Ghafourian, Kambiz, Fenioux, Charlotte, Finke, Daniel, Peretto, Giovanni, Zaha, Vlad, Itzhaki Ben Zadok, Osnat, Tajiri, Kazuko, Akhter, Nausheen, Levenson, Joshua, Baldassarre, Lauren, Power, John, Huang, Shi, Collet, Jean-Philippe, Moslehi, Javid, and Salem, Joe-Elie

Published
2022
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27. Versorgung von Patienten mit kardialer Amyloidose

Author

Pfister, Roman, primary, Hagenacker, Tim, additional, Heemann, Uwe, additional, Hegenbart, Ute, additional, Heidecker, Bettina, additional, Kruck, Sebastian, additional, Knebel, Fabian, additional, Lehmann, Lorenz, additional, Morbach, Caroline, additional, Rischpler, Christoph, additional, Schulze, P. Christian, additional, Yilmaz, Ali, additional, and Perings, Christian, additional

Published
2023
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28. Advancing the care of individuals with cancer through innovation & technology: Proceedings from the cardiology oncology innovation summit 2020 and 2021

Author

Brown, Sherry-Ann, primary, Beavers, Craig, additional, Bauer, Brenton, additional, Cheng, Richard K., additional, Berman, Generika, additional, Marshall, Catherine H., additional, Guha, Avirup, additional, Jain, Prantesh, additional, Steward, Austin, additional, DeCara, Jeanne M., additional, Olaye, Iredia M., additional, Hansen, Kathryn, additional, Logan, Jim, additional, Bergom, Carmen, additional, Glide-Hurst, Carri, additional, Loh, Irving, additional, Gambril, John Alan, additional, MacLeod, James, additional, Maddula, Ragasnehith, additional, McGranaghan, Peter J., additional, Batra, Akshee, additional, Campbell, Courtney, additional, Hamid, Abdulaziz, additional, Gunturkun, Fatma, additional, Davis, Robert, additional, Jefferies, John, additional, Fradley, Michael, additional, Albert, Katherine, additional, Blaes, Anne, additional, Choudhuri, Indrajit, additional, Ghosh, Arjun K., additional, Ryan, Thomas D., additional, Ezeoke, Ogochukwu, additional, Leedy, Douglas J., additional, Williams, Wadsworth, additional, Roman, Sebastian, additional, Lehmann, Lorenz, additional, Sarkar, Abdullah, additional, Sadler, Diego, additional, Polter, Elizabeth, additional, Ruddy, Kathryn J., additional, Bansal, Neha, additional, Yang, Eric, additional, Patel, Brijesh, additional, Cho, David, additional, Bailey, Alison, additional, Addison, Daniel, additional, Rao, Vijay, additional, Levenson, Joshua E., additional, Itchhaporia, Dipti, additional, Watson, Karol, additional, Gulati, Martha, additional, Williams, Kim, additional, Lloyd-Jones, Donald, additional, Michos, Erin, additional, Gralow, Julie, additional, and Martinez, Hugo, additional

Published
2023
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30. Epigenetic regulation of cardiac electrophysiology in atrial fibrillation: HDAC2 determines action potential duration and suppresses NRSF in cardiomyocytes

Author

Lugenbiel, Patrick, Govorov, Katharina, Syren, Pascal, Rahm, Ann-Kathrin, Wieder, Teresa, Wunsch, Maximilian, Weiberg, Nadine, Manolova, Emili, Gramlich, Dominik, Rivinius, Rasmus, Finke, Daniel, Lehmann, Lorenz H., Schweizer, Patrick A., Frank, Derk, El Tahry, Fadwa A., Bruehl, Claus, Heimberger, Tanja, Sandke, Steffi, Weis, Tanja, Most, Patrick, Schmack, Bastian, Ruhparwar, Arjang, Karck, Matthias, Frey, Norbert, Katus, Hugo A., and Thomas, Dierk

Published
2021
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36. The lipid-droplet-associated protein ABHD5 protects the heart through proteolysis of HDAC4

Author

Jebessa, Zegeye H., Shanmukha, Kumar D., Dewenter, Matthias, Lehmann, Lorenz H., Xu, Chang, Schreiter, Friederike, Siede, Dominik, Gong, Xue-Min, Worst, Barbara C., Federico, Giuseppina, Sauer, Sven W., Fischer, Tamas, Wechselberger, Lisa, Müller, Oliver J., Sossalla, Samuel, Dieterich, Christoph, Most, Patrick, Gröne, Herrmann-Josef, Moro, Cedric, Oberer, Monika, Haemmerle, Guenter, Katus, Hugo A., Tyedmers, Jens, and Backs, Johannes

Published
2019
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40. Cardiological parameters predict mortality and cardiotoxicity in oncological patients.

Author

Romann, Sebastian W., Finke, Daniel, Heckmann, Markus B., Hund, Hauke, Giannitsis, Evangelos, Katus, Hugo A., Frey, Norbert, and Lehmann, Lorenz H.

Subjects
BRAIN natriuretic factor, CANCER patients, CARDIOTOXICITY, CARDIOVASCULAR diseases risk factors, VENTRICULAR ejection fraction
Abstract

Aims: Oncological patients suspected at risk for cardiotoxicity are recommended to undergo intensified cardiological surveillance. We investigated the value of cardiac biomarkers and patient‐related risk factors [age, cardiovascular risk factors (CVRFs), and cardiac function] for the prediction of all‐cause mortality (ACM) and the development of cardiotoxicity. Methods and results: Between January 2016 and December 2020, patients with oncological diseases admitted to the Cardio‐Oncology Unit at the Heidelberg University Hospital were included. They were evaluated by medical history, physical examination, 12‐lead electrocardiogram, 2D echocardiography, and cardiac biomarkers [high‐sensitivity cardiac troponin T (hs‐cTnT) and N‐terminal pro‐brain natriuretic peptide (NT‐proBNP)]. The primary endpoint was defined as ACM and the secondary endpoint was defined as cardiotoxicity, as defined by the European Society of Cardiology. Of the 1971 patients enrolled, the primary endpoint was reached by 490 patients (25.7%) with a median of 363.5 [interquartile range (IQR) 121.8, 522.5] days after presentation. Hs‐cTnT of ≥ 7 ng/L [odds ratio (OR) 1.82, P < 0.001] and NT‐proBNP (OR 1.98, P < 0.001) were independent predictors of ACM, while reduced left ventricular ejection fraction was not associated with increased ACM (P = 0.85). The secondary endpoint was reached by 182 patients (9.2%) with a median of 793.5 [IQR 411.2, 1165.0] days. Patients with multiple CVRFs (defined as high risk, n = 886) had an increased risk of cardiotoxicity (n = 100/886, 11.3%; hazard ratio 1.57, P = 0.004). They showed elevated baseline values of hs‐cTnT (OR 1.60, P = 0.006) and NT‐proBNP (OR 4.00, P < 0.001) and had an increased risk of ACM (OR 1.43, P = 0.031). Conclusions: In cancer patients, CVRF accumulation predicts cardiotoxicity whereas elevated hs‐cTnT or NT‐proBNP levels are associated with ACM. Accordingly, less intensive surveillance protocols may be warranted in patients with low cardiac biomarker levels and absence of CVRFs. [ABSTRACT FROM AUTHOR]

Published
2024
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43. Abstract 15365: Natural History of Immune Checkpoint Inhibitor Associated Myocarditis With Preserved Ejection Fraction

Author

Nowatzke, Joseph, Power, John R, Meijers, Wouter C, Orimoloye, Olusola, Fenioux, Charlotte, Tamura, Yuichi, Cautela, Jennifer, Lehmann, Lorenz H, Finke, Daniel, Hayek, Salim, Azam, Tariq U, Asnani, Aarti, Mehegan, Tyler, Weppler, Alison, Baik, Alan H, Aras, Mandar A, Narezkina, Anna, Arangalage, Dimitri, rocher, fanny, Alexandre, Gerard, Palaskas, Nicolas L, Salem, Joe-elie, and Moslehi, Javid

Published
2020
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44. Abstract 14843: Electrocardiographic Manifestations of Immune Checkpoint Inhibitor Associated Myocarditis

Author

Power, John R, Alexandre, Joachim, Choudhary, Arrush, ozbay, benay, Palaskas, Nicolas L, Lehmann, Lorenz H, Finke, Daniel, Cautela, Jennifer, Thuny, Franck, Tamura, Yuichi, Hayek, Salim S, Azam, Tariq U, Asnani, Aarti, Mehegan, Tyler, Aras, Mandar A, Baik, Alan H, Gilstrap, Lauren, Laufer-Perl, Michal, Arangalage, Dimitri, Ewer, Steven, Martini, Matthew, Nowatzke, Joseph, Orimoloye, Olusola A, Brinkley, Douglas M, Meijers, Wouter C, Fenioux, Charlotte, EDERHY, Stephane, Moslehi, Javid J, and Salem, Joe-elie

Published
2020
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47. Heart-Specific Immune Responses in an Animal Model of Autoimmune-Related Myocarditis Mitigated by an Immunoproteasome Inhibitor and Genetic Ablation

Author

Bockstahler, Mariella, Fischer, Andrea, Goetzke, Carl Christoph, Neumaier, Hannah Louise, Sauter, Martina, Kespohl, Meike, Müller, Anna-Maria, Meckes, Christin, Salbach, Christian, Schenk, Mirjam, Heuser, Arnd, Landmesser, Ulf, Weiner, January, Meder, Benjamin, Lehmann, Lorenz, Kratzer, Adelheid, Klingel, Karin, Katus, Hugo A., Kaya, Ziya, and Beling, Antje

Published
2020
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48. A proteolytic fragment of histone deacetylase 4 protects the heart from failure by regulating the hexosamine biosynthetic pathway

Author

Lehmann, Lorenz H, Jebessa, Zegeye H, Kreusser, Michael M, Horsch, Axel, He, Tao, Kronlage, Mariya, Dewenter, Matthias, Sramek, Viviana, Oehl, Ulrike, Krebs-Haupenthal, Jutta, von der Lieth, Albert H, Schmidt, Andrea, Sun, Qiang, Ritterhoff, Julia, Finke, Daniel, Völkers, Mirko, Jungmann, Andreas, Sauer, Sven W, Thiel, Christian, Nickel, Alexander, Kohlhaas, Michael, Schäfer, Michaela, Sticht, Carsten, Maack, Christoph, Gretz, Norbert, Wagner, Michael, El-Armouche, Ali, Maier, Lars S, Londoño, Juan E Camacho, Meder, Benjamin, Freichel, Marc, Gröne, Hermann-Josef, Most, Patrick, Müller, Oliver J, Herzig, Stephan, Furlong, Eileen E M, Katus, Hugo A, and Backs, Johannes

Subjects
Heart failure -- Prevention -- Research, Quantitative trait loci -- Research, Gene expression -- Research, Histones -- Physiological aspects -- Research, Biological sciences, Health
Abstract

The stress-responsive epigenetic repressor histone deacetylase 4 (HDAC4) regulates cardiac gene expression. Here we show that the levels of an N-terminal proteolytically derived fragment of HDAC4, termed HDAC4-NT, are lower in failing mouse hearts than in healthy control hearts. Virus-mediated transfer of the portion of the Hdac4 gene encoding HDAC4-NT into the mouse myocardium protected the heart from remodeling and failure; this was associated with decreased expression of Nr4a1, which encodes a nuclear orphan receptor, and decreased NR4A1-dependent activation of the hexosamine biosynthetic pathway (HBP). Conversely, exercise enhanced HDAC4-NT levels, and mice with a cardiomyocyte-specific deletion of Hdac4 show reduced exercise capacity, which was characterized by cardiac fatigue and increased expression of Nr4a1. Mechanistically, we found that NR4A1 negatively regulated contractile function in a manner that depended on the HBP and the calcium sensor STIM1. Our work describes a new regulatory axis in which epigenetic regulation of a metabolic pathway affects calcium handling. Activation of this axis during intermittent physiological stress promotes cardiac function, whereas its impairment in sustained pathological cardiac stress leads to heart failure., Author(s): Lorenz H Lehmann [1, 2, 3]; Zegeye H Jebessa [1, 2]; Michael M Kreusser [1, 2, 3]; Axel Horsch [1, 2]; Tao He [1, 2]; Mariya Kronlage [1, 2, [...]

Published
2018
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50. Patient‐reported ability to walk 4 m and to wash: New clinical endpoints and predictors of survival in patients with pre‐terminal cancer

Author

Anker, Markus S., primary, Lena, Alessia, additional, Roeland, Eric J., additional, Porthun, Jan, additional, Schmitz, Sebastian, additional, Hadzibegovic, Sara, additional, Sikorski, Philipp, additional, Wilkenshoff, Ursula, additional, Fröhlich, Ann‐Kathrin, additional, Ramer, Luisa Valentina, additional, Rose, Matthias, additional, Eucker, Jan, additional, Rassaf, Tienush, additional, Totzeck, Matthias, additional, Lehmann, Lorenz H., additional, von Haehling, Stephan, additional, Coats, Andrew J.S., additional, Friede, Tim, additional, Butler, Javed, additional, Anker, Stefan D., additional, Riess, Hanno, additional, Landmesser, Ulf, additional, Bullinger, Lars, additional, Keller, Ulrich, additional, and Ahn, Johann, additional

Published
2023
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