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1. Penetrating extracranial vertebral artery injuries

Author

Rowe, Vincent L., primary, Asensio, Juan A., additional, Dabestani, Parinaz J., additional, Kessler, John J., additional, Wenzl, Florian A., additional, Miljkovic, Stephanie S., additional, Kotaru, Tharun R., additional, Kalamchi, Louay D., additional, Becker, Tyson, additional, Fernandez, Carlos, additional, and Cornell, David, additional

Published
2024
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4. Popliteal vessel injuries: Complex anatomy and high amputation rates

Author

Asensio, Juan A., primary, Dabestani, Parinaz J., additional, Kessler, John J., additional, Miljkovic, Stephanie S., additional, Kotaru, Tharun R., additional, Kalamchi, Louay D., additional, Jessie, Elliot J., additional, Cannon, Jeremy W., additional, Wenzl, Florian A., additional, Bradley, Matthew, additional, Humphries, Ashley, additional, and García-Núñez, Luis Manuel, additional

Published
2024
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5. Brachial vessel injuries: High morbidity and low mortality injuries

Author

Perez-Alonso, Alejandro, primary, Asensio, Juan A., additional, Dabestani, Parinaz J., additional, Kessler, John J., additional, Miljkovic, Stephanie S., additional, Kotaru, Tharun R., additional, Kalamchi, Louay D., additional, Fernandez-Moure, Joseph S., additional, Kasotakis, George, additional, Agarwal, Suresh, additional, Wenzl, Florian A., additional, Polk, Travis, additional, and Grabo, Dan, additional

Published
2024
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6. Contributors

Author

Abelson, Jennifer, primary, Aboutanos, Michel B., additional, Abraham, Peter J., additional, Abualruz, Abdul Rahman, additional, Agarwal, Suresh, additional, Agrawal, Devendra K., additional, Alverdy, John C., additional, Aly, Ahmed, additional, Amato, Stas, additional, Anstadt, Michael J., additional, Asensio, Juan A., additional, Avery, Martin, additional, Bailey, Jeffrey A., additional, Barie, Philip S., additional, Becker, Tyson, additional, Beckerman, Daniel, additional, Bedrick, Edward J., additional, Benson, Jamie, additional, Berne, John D., additional, Berry, Cherisse, additional, Berry, Stepheny, additional, Bhat, Sneha G., additional, Bowie, Jason M., additional, Bowyer, Mark W., additional, Bozeman, Matthew C., additional, Bradley, Matthew, additional, Brakenridge, Scott, additional, Brandes, Steven B., additional, Brenner, Megan, additional, Britt, L.D., additional, Brown, Carlos V., additional, Brown, Ian E., additional, Brown, J. Christian, additional, Brown, Tommy, additional, Buckman, Robert F., additional, Burlew, Clay Cothren, additional, Byers, Patricia M., additional, Caban, Kim M., additional, Cancio, Leopoldo C., additional, Cannon, Jeremy W., additional, Cantlie, Shawn M., additional, Carroll, Eben A., additional, Champion, Howard R., additional, Childs, Ed W., additional, Chiu, William C., additional, Christmas, A. Britton, additional, Cioffi, William G., additional, Cocanour, Christine S., additional, Cohen, Mitchell J., additional, Coimbra, Raul, additional, Cook, Alan, additional, Cornell, David L., additional, Cotton, Bryan A., additional, Couture, Daniel E., additional, Cox, Thomas B., additional, Cristancho, Luis Alfonso Bustamante, additional, Croce, Martin A., additional, Croft, Chasen A., additional, Cubano, Miguel A., additional, Dabestani, Parinaz J., additional, Danton, Gary H., additional, Davis, Christopher S., additional, Davis, Kimberly, additional, de Moya, Marc A., additional, Desai, Urmen, additional, Destiné, Henson, additional, Diebel, Lawrence N., additional, Doucet, Jay J., additional, DuBose, Joseph J., additional, Dubov, Wayne E., additional, Duchesne, Juan C., additional, Durham, Rodney M., additional, Durso, Anthony M., additional, Eastridge, Brian, additional, Efron, David T., additional, Efron, Philip A., additional, Elster, Eric, additional, Esposito, Thomas J., additional, Fakhry, Samir M., additional, Feliciano, David V., additional, Fernandez, Carlos, additional, Fernandez-Moure, Joseph S., additional, Fernández, Luis G., additional, Fiorentino, Michele, additional, Firstenberg, Michael S., additional, Flint, Lewis M., additional, Fredericks, Charles J., additional, Fry, Donald E., additional, Galán, Ricardo, additional, Galante, Joseph M., additional, Galvagno, Samuel M., additional, Garcia, Ana Maria, additional, García, Erwin Rodriguez, additional, García-Núñez, Col Luis Manuel, additional, Gentilello, Larry M., additional, Ghanta, Ravi K., additional, Gigena, Alejandro, additional, Gilani, Ramyar, additional, Glance, Laurent G., additional, Goldman, Matthew, additional, Gonzalez, Ernest A., additional, Gonzalez, Richard P., additional, Grabo, Daniel, additional, Gross, Ronald I., additional, Gummadi, Sriharsha, additional, Guerrero, Whitney M., additional, Gunter, Oliver L., additional, Gurney, Jennifer M., additional, Gutiérrez, Jorge A., additional, Hall, Chad, additional, Hauser, Carl J., additional, Henry, Sharon, additional, Hirshberg, Ashen, additional, Holcomb, John B., additional, Hosmer, David, additional, Hoth, J. Jason, additional, Gomez, Tatiana Hoyos, additional, Hoyt, David B., additional, Humphries, Ashley, additional, Iyengar, Rahul, additional, Jawa, Randeep S., additional, Jessie, Elliot, additional, Johannigman, Jay, additional, Aquino Jose, Victor M., additional, Jurkovich, Gregory J., additional, Kalamchi, Louay, additional, Kapil, Aditi M., additional, Karmy-Jones, Riyad, additional, Kasotakis, George, additional, Kelley, Kathryn C., additional, Keskey, Robert, additional, Kessler, John J., additional, Kim, Dennis Y., additional, Kiraly, Laszlo, additional, Kirton, Orlando C., additional, Kotaru, Tharun R., additional, Kunac, Anastasia, additional, Kwolek, Kinga, additional, Lallemand, Michael S., additional, Ledgerwood, Anna M., additional, Lee, Amanda, additional, Leeper, Christine M., additional, Li, Zhongyu, additional, Libby, Matthew, additional, Lim, Robert B., additional, Liveris, Anna, additional, Livingston, David H., additional, Lobb, Jennifer, additional, Loftus, Tyler J., additional, Lucas, Charles E., additional, Luchette, Fred A., additional, Lundeberg, Megan R., additional, Mackersie, Robert C., additional, Mackey, Kevin E., additional, Magnotti, Louis J., additional, Mah, John W., additional, Maldonado, William Sánchez, additional, Malhotra, Ajai K., additional, Malone, Debra L., additional, Marini, Corrado P., additional, Martin, Matthew J., additional, Marttos, Antonio C., additional, Martyak, Michael T., additional, Mathew, Prakash J., additional, Mattox, Kenneth L., additional, Mayberry, John C., additional, Mazzini, Federico N., additional, McNelis, John, additional, Meallet, Mario A., additional, Meerkov, Meir B.L., additional, Meizoso, Jonathan P., additional, Meredith, J. Wayne, additional, Michetti, Christopher P., additional, Miljkovic, Stephanie S., additional, Miller, Keith R., additional, Miller, Preston R., additional, Minei, Joseph P., additional, Mitchell, Frank L., additional, Moas, Victor M., additional, Mohr, Alicia M., additional, Molnar, Joseph A., additional, Moore, Ernest E., additional, Moore, Frederick A., additional, Moutinho, Manuel, additional, Moysidis, Stavros, additional, Munera, Felipe, additional, Naiditch, Jessica A., additional, Napolitano, Lena M., additional, Narayan, Mayur, additional, Nash, Nicholas A., additional, Nicholson, Kristina J., additional, Nicholson, Susannah, additional, Norwood, Scott H., additional, Nunn, Andrew M., additional, O’Shea, Anne, additional, Osler, Turner M., additional, Pachter, H. Leon, additional, Paladino, Lorenzo, additional, Panthaki, Zubin Jal, additional, Parikh, Manish, additional, Pasquale, Michael D., additional, Patel, Purvi P., additional, Peitzman, Andrew B., additional, Peralta, Ruben, additional, Perez-Alonso, Alejandro J., additional, Pestana, Ivo A., additional, Petrone, Patrizio, additional, Pierre, Edgar J., additional, Pilson, Holly, additional, Polk, Travis, additional, Puyana, Juan Carlos, additional, Quintana, David, additional, Rai, Vikrant, additional, Rajasingh, Charlotte, additional, Ranney, Stephen, additional, Reisbig, Mark D., additional, Reiser, Bibiana Jin, additional, Remick, Kyle N., additional, Rhee, Peter, additional, Rich, Norman M., additional, Richardson, J. David, additional, Richart, Charles M., additional, Rivas, Luis A., additional, Robles, Anamaria J., additional, Rodriguez, Aurelio, additional, Rosengart, Matthew, additional, Rosenthal, Martin D., additional, Rotondo, Michael F., additional, Rowe, Vincent L., additional, Rubano, Jerry A., additional, Rubiano, Andrés M., additional, Ruggero, John M., additional, Rushing, Amy, additional, Salim, Ali, additional, Saillant, Noelle Nugent, additional, Sally, Mitchell B., additional, Salsamendi, Jason, additional, Sanford, Arthur P., additional, Savetamal, Alisa, additional, Scalea, Thomas M., additional, Schecter, William, additional, Schipper, Paul H., additional, Schreiber, Martin A., additional, Schroll, Rebecca W., additional, Schulingkamp, Danielle, additional, Schulman, Carl I., additional, Schulz, John T., additional, Shackelford, Stacy A., additional, Shadis, Ryan, additional, Shapiro, Marc J., additional, Shatz, David V., additional, Shiroff, Adam M., additional, Sicard, Gregorio, additional, Sifri, Ziad C., additional, Sing, Ronald F., additional, Sisley, Amy, additional, Smith, Brian P., additional, Smith, R. Stephen, additional, Singares, Eduardo Smith, additional, Sola, Richard, additional, Spain, David A., additional, Spencer, Audrey L., additional, Stavas, Joseph, additional, Stawicki, Stanislaw P., additional, Stein, Deborah M., additional, Stewart, Nakosi, additional, Stirparo, Joseph J., additional, Strong, Bethany L., additional, Sukumar, Mithran S., additional, Tadlock, Matthew D., additional, Taylor, John R., additional, Thaller, Seth R., additional, Thomas, Bradley W., additional, Thompson, Ashley M., additional, Tieu, Brandon H., additional, Tillou, Areti, additional, Tinkoff, Glen H., additional, Tisherman, Samuel A., additional, Todd, S. Rob, additional, Tominaga, Gail T., additional, Trammell, Amy Phillips, additional, Trunkey, Donald D., additional, Tuggle, David, additional, Upchurch, Gilbert R., additional, Van, Philbert, additional, VanDerHeyden, Nicole, additional, Vanzant, Erin L., additional, Wall, Matthew J., additional, Wenzl, Florian A., additional, Whitlow, Christopher T., additional, Wiegand, Lucas R., additional, Williams, Timothy K., additional, Wilson, Jonathan L., additional, Yeh, D. Dante, additional, Youngblood, Charles F., additional, and Zhang, Wei, additional

Published
2024
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7. Biomarker-enhanced cardiovascular risk prediction in patients with cancer: a prospective cohort study

Author

Kraler, Simon, Liberale, Luca, Nopp, Stephan, Englisch, Cornelia, Grilz, Ella, Lapikova-Bryhinska, Tetiana, Akhmedov, Alexander, Carbone, Federico, Ramoni, Davide, Tirandi, Amedeo, Scuricini, Alessandro, Isoppo, Simone, Tortorella, Curzia, La Rosa, Federica, Michelauz, Cristina, Frè, Federica, Gavoci, Aurora, Lisa, Anna, Suter, Thomas M., von Eckardstein, Arnold, Wenzl, Florian A., Pabinger, Ingrid, Lüscher, Thomas F., Montecucco, Fabrizio, Ay, Cihan, and Moik, Florian

Published
2024
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8. Temporal Trends in Takotsubo Syndrome: Results From the International Takotsubo Registry

Author

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

Published
2024
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11. Sex-specific evaluation and redevelopment of the GRACE score in non-ST-segment elevation acute coronary syndromes in populations from the UK and Switzerland: a multinational analysis with external cohort validation

Author

Wenzl, Florian A, Kraler, Simon, Ambler, Gareth, Weston, Clive, Herzog, Sereina A, Räber, Lorenz, Muller, Olivier, Camici, Giovanni G, Roffi, Marco, Rickli, Hans, Fox, Keith A A, de Belder, Mark, Radovanovic, Dragana, Deanfield, John, and Lüscher, Thomas F

Published
2022
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13. Artificial intelligence in cardiovascular medicine: clinical applications.

Author

Lüscher, Thomas F, Wenzl, Florian A, D'Ascenzo, Fabrizio, Friedman, Paul A, and Antoniades, Charalambos

Subjects
MACHINE learning, HUMAN facial recognition software, ARTIFICIAL intelligence, DEEP learning, PHENOTYPIC plasticity
Abstract

Clinical medicine requires the integration of various forms of patient data including demographics, symptom characteristics, electrocardiogram findings, laboratory values, biomarker levels, and imaging studies. Decision-making on the optimal management should be based on a high probability that the envisaged treatment is appropriate, provides benefit, and bears no or little potential harm. To that end, personalized risk–benefit considerations should guide the management of individual patients to achieve optimal results. These basic clinical tasks have become more and more challenging with the massively growing data now available; artificial intelligence and machine learning (AI/ML) can provide assistance for clinicians by obtaining and comprehensively preparing the history of patients, analysing face and voice and other clinical features, by integrating laboratory results, biomarkers, and imaging. Furthermore, AI/ML can provide a comprehensive risk assessment as a basis of optimal acute and chronic care. The clinical usefulness of AI/ML algorithms should be carefully assessed, validated with confirmation datasets before clinical use, and repeatedly re-evaluated as patient phenotypes change. This review provides an overview of the current data revolution that has changed and will continue to change the face of clinical medicine radically, if properly used, to the benefit of physicians and patients alike. [ABSTRACT FROM AUTHOR]

Published
2024
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14. Safety and effectiveness of glycoprotein IIb/IIIa inhibitors in acute coronary syndromes: insights from the SPUM-ACS study

Author

Bruno, Francesco, primary, Wenzl, Florian A, additional, De Filippo, Ovidio, additional, Kraler, Simon, additional, Giacobbe, Federico, additional, Roffi, Marco, additional, Muller, Olivier, additional, Räber, Lorenz, additional, Templin, Christian, additional, Maria De Ferrari, Gaetano, additional, D'Ascenzo, Fabrizio, additional, and Lüscher, Thomas F, additional

Published
2024
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16. Body temperature, systemic inflammation and risk of adverse events in patients with acute coronary syndromes.

Author

van der Stouwe, Jan Gerrit, Godly, Konstantin, Kraler, Simon, Godly, Julia, Matter, Christian M., Wenzl, Florian A., von Eckardstein, Arnold, Räber, Lorenz, Mach, François, Obeid, Slayman, Templin, Christian, Lüscher, Thomas F., and Niederseer, David

Abstract

Background: Inflammatory processes can trigger acute coronary syndromes (ACS) which may increase core body temperature (BT), a widely available low‐cost marker of systemic inflammation. Herein, we aimed to delineate baseline characteristics of ST‐segment elevation myocardial infarction (STEMI) and non‐ST‐segment elevation ACS (NSTE‐ACS) patients stratified by initial BT and to assess its predictive utility towards major adverse cardiovascular events (MACE) after the index ACS. Methods: From 2012 until 2017, a total of 1044 ACS patients, 517 with STEMI and 527 with NSTE‐ACS, were prospectively recruited at the University Hospital Zurich. BT was measured by digital tympanic thermometer along with high‐sensitivity C‐reactive protein (hs‐CRP) and cardiac troponin‐T (hs‐cTnT) levels prior to coronary angiography. Patients were stratified according to initial BT and uni‐ and multivariable regression models were fit to assess associations of BT with future MACE risk. Results: Among patients with STEMI, BT was not predictive of 1‐year MACE, but a U‐shaped relationship between BT and MACE risk was noted in those with NSTE‐ACS (p =.029), translating into a 2.4‐fold (HR, 2.44, 95% CI, 1.16–5.16) increased 1‐year MACE risk in those with BT >36.8°C (reference: 36.6–36.8°C). Results remained robust in multivariable‐adjusted analyses accounting for sex, age, diabetes, renal function and hs‐cTnT. However, when introducing hs‐CRP, the BT‐MACE association did not prevail. Conclusions: In prospectively recruited patients with ACS, initial BT shows a U‐shaped relationship with 1‐year MACE risk among those with NSTE‐ACS, but not in those with STEMI. BT is a broadly available low‐cost marker to identify ACS patients with high inflammatory burden, at high risk for recurrent ischaemic events, and thus potentially suitable for an anti‐inflammatory intervention. Registration: ClinicalTrials.gov Identifier: NCT01000701. [ABSTRACT FROM AUTHOR]

Published
2024
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21. Circulating GDF11 exacerbates myocardial injury in mice and associates with increased infarct size in humans

Author

Kraler, Simon, primary, Balbi, Carolina, additional, Vdovenko, Daria, additional, Lapikova-Bryhinska, Tetiana, additional, Camici, Giovanni G, additional, Liberale, Luca, additional, Bonetti, Nicole, additional, Canestro, Candela Diaz, additional, Burger, Fabienne, additional, Roth, Aline, additional, Carbone, Federico, additional, Vassalli, Giuseppe, additional, Mach, François, additional, Bhasin, Shalender, additional, Wenzl, Florian A, additional, Muller, Olivier, additional, Räber, Lorenz, additional, Matter, Christian M, additional, Montecucco, Fabrizio, additional, Lüscher, Thomas F, additional, and Akhmedov, Alexander, additional

Published
2023
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23. Circulating Long Noncoding RNA Signatures Associate With Incident Diabetes in Older Adults: A Prospective Analysis From the VITA Cohort Study

Author

Wenzl, Florian A, Mengozzi, Alessandro, Mohammed, Shafeeq A, Pugliese, Nicola Riccardo, Mongelli, Alessia, Gorica, Era, Ambrosini, Samuele, Riederer, Peter, Fischer, Peter, Hinterberger, Margareta, Puspitasari, Yustina, Lüscher, Thomas F, Camici, Giovanni G, Matter, Christian M, Fadini, Gian Paolo, Virdis, Agostino, Masi, Stefano, Ruschitzka, Frank, Grünblatt, Edna, Paneni, Francesco, Costantino, Sarah, University of Zurich, Paneni, Francesco, and Costantino, Sarah

Subjects
Advanced and Specialized Nursing, 2902 Advanced and Specialized Nursing, Endocrinology, Diabetes and Metabolism, 610 Medicine & health, 10058 Department of Child and Adolescent Psychiatry, Internal Medicine, 11459 Center for Molecular Cardiology, Diabetes and Metabolism, 2712 Endocrinology, Diabetes and Metabolism, Endocrinology, 2724 Internal Medicine, 10076 Center for Integrative Human Physiology, 10209 Clinic for Cardiology, 10064 Neuroscience Center Zurich
Abstract

OBJECTIVE Long noncoding RNAs (lncRNAs) are involved in diabetogenesis in experimental models, yet their role in humans is unclear. We investigated whether circulating lncRNAs associate with incident type 2 diabetes in older adults. RESEARCH DESIGN AND METHODS A preselected panel of lncRNAs was measured in serum of individuals without diabetes (n = 296) from the Vienna Transdanube Aging study, a prospective community-based cohort study. Participants were followed up over 7.5 years. A second cohort of individuals with and without type 2 diabetes (n = 90) was used to validate our findings. RESULTS Four lncRNAs (ANRIL, MIAT, RNCR3, and PLUTO) were associated with incident type 2 diabetes and linked to hemoglobin A1c trajectories throughout the 7.5-year follow-up. Similar results (for MIAT and PLUTO also in combined analysis) were obtained in the validation cohort. CONCLUSIONS We found a set of circulating lncRNAs that independently portends incident type 2 diabetes in older adults years before disease onset.

Published
2023

24. Modification of the GRACE Risk Score for Risk Prediction in Patients With Acute Coronary Syndromes

Author

Georgiopoulos, Georgios, primary, Kraler, Simon, additional, Mueller-Hennessen, Matthias, additional, Delialis, Dimitrios, additional, Mavraganis, Georgios, additional, Sopova, Kateryna, additional, Wenzl, Florian A., additional, Räber, Lorenz, additional, Biener, Moritz, additional, Stähli, Barbara E., additional, Maneta, Eleni, additional, Spray, Luke, additional, Iglesias, Juan F., additional, Coelho-Lima, Jose, additional, Tual-Chalot, Simon, additional, Muller, Olivier, additional, Mach, François, additional, Frey, Norbert, additional, Duerschmied, Daniel, additional, Langer, Harald F., additional, Katus, Hugo, additional, Roffi, Marco, additional, Camici, Giovanni G., additional, Mueller, Christian, additional, Giannitsis, Evangelos, additional, Spyridopoulos, Ioakim, additional, Lüscher, Thomas F., additional, Stellos, Konstantinos, additional, and Stamatelopoulos, Kimon, additional

Published
2023
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25. Dipeptidyl peptidase 3 plasma levels predict cardiogenic shock and mortality in acute coronary syndromes

Author

Wenzl, Florian A, primary, Bruno, Francesco, additional, Kraler, Simon, additional, Klingenberg, Roland, additional, Akhmedov, Alexander, additional, Ministrini, Stefano, additional, Santos, Karine, additional, Godly, Konstantin, additional, Godly, Julia, additional, Niederseer, David, additional, Manka, Robert, additional, Bergmann, Andreas, additional, Camici, Giovanni G, additional, von Eckardstein, Arnold, additional, Stähli, Barbara, additional, Muller, Olivier, additional, Roffi, Marco, additional, Räber, Lorenz, additional, and Lüscher, Thomas F, additional

Published
2023
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26. Low-density lipoprotein electronegativity and risk of death after acute coronary syndromes: A case-cohort analysis

Author

Kraler, Simon, primary, Wenzl, Florian A., additional, Vykoukal, Jody, additional, Fahrmann, Johannes F., additional, Shen, Ming-Yi, additional, Chen, Der-Yuan, additional, Chang, Kuan-Cheng, additional, Chang, Ching-Kun, additional, von Eckardstein, Arnold, additional, Räber, Lorenz, additional, Mach, François, additional, Nanchen, David, additional, Matter, Christian M., additional, Liberale, Luca, additional, Camici, Giovanni G., additional, Akhmedov, Alexander, additional, Chen, Chu-Huang, additional, and Lüscher, Thomas F., additional

Published
2023
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28. Initial systolic blood pressure associates with systemic inflammation, myocardial injury and outcomes in patients with acute coronary syndromes

Author

Winzap, Patric A, primary, Kraler, Simon, additional, Obeid, Slayman, additional, Wenzl, Florian A, additional, Templin, Christian, additional, Klingenberg, Roland, additional, von Eckardstein, Arnold, additional, Roffi, Marco, additional, Muller, Olivier, additional, Räber, Lorenz, additional, and Lüscher, Thomas F, additional

Published
2023
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29. Circulating long noncoding RNA signatures associate with incident diabetes in older adults: a prospective analysis from the VITA cohort study

Author

Wenzl, Florian A., primary, Mengozzi, Alessandro, primary, Mohammed, Shafeeq A., primary, Pugliese, Nicola Riccardo, primary, Mongelli, Alessia, primary, Gorica, Era, primary, Ambrosini, Samuele, primary, Riederer, Peter, primary, Fischer, Peter, primary, Hinterberger, Margareta, primary, Puspitasari, Yustina, primary, Lüscher, Thomas F., primary, Camici, Giovanni G., primary, Matter, Christian M., primary, Fadini, Gian Paolo, primary, Virdis, Agostino, primary, Masi, Stefano, primary, Ruschitzka, Frank, primary, Grünblatt, Edna, primary, Paneni, Francesco, primary, and Costantino, Sarah, primary

Published
2023
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30. Modification of the GRACE Risk Score for Risk Prediction in Patients With Acute Coronary Syndromes

Author

Georgiopoulos, Georgios, Kraler, Simon, Mueller-Hennessen, Matthias, Delialis, Dimitrios, Mavraganis, Georgios, Sopova, Kateryna, Wenzl, Florian A, Räber, Lorenz, Biener, Moritz, Stähli, Barbara E, Maneta, Eleni, Spray, Luke, Iglesias, Juan F, Coelho-Lima, Jose, Tual-Chalot, Simon, Muller, Olivier, Mach, François, Frey, Norbert, Duerschmied, Daniel, Langer, Harald F, Katus, Hugo, Roffi, Marco, Camici, Giovanni G, Mueller, Christian, Giannitsis, Evangelos, Spyridopoulos, Ioakim, Lüscher, Thomas F, Stellos, Konstantinos, Stamatelopoulos, Kimon, Georgiopoulos, Georgios, Kraler, Simon, Mueller-Hennessen, Matthias, Delialis, Dimitrios, Mavraganis, Georgios, Sopova, Kateryna, Wenzl, Florian A, Räber, Lorenz, Biener, Moritz, Stähli, Barbara E, Maneta, Eleni, Spray, Luke, Iglesias, Juan F, Coelho-Lima, Jose, Tual-Chalot, Simon, Muller, Olivier, Mach, François, Frey, Norbert, Duerschmied, Daniel, Langer, Harald F, Katus, Hugo, Roffi, Marco, Camici, Giovanni G, Mueller, Christian, Giannitsis, Evangelos, Spyridopoulos, Ioakim, Lüscher, Thomas F, Stellos, Konstantinos, and Stamatelopoulos, Kimon

Abstract

IMPORTANCE The Global Registry of Acute Coronary Events (GRACE) risk score, a guideline-recommended risk stratification tool for patients presenting with acute coronary syndromes (ACS), does not consider the extent of myocardial injury. OBJECTIVE To assess the incremental predictive value of a modified GRACE score incorporating high-sensitivity cardiac troponin (hs-cTn) T at presentation, a surrogate of the extent of myocardial injury. DESIGN, SETTING, AND PARTICIPANTS This retrospectively designed longitudinal cohort study examined 3 independent cohorts of 9803 patients with ACS enrolled from September 2009 to December 2017; 2 ACS derivation cohorts (Heidelberg ACS cohort and Newcastle STEMI cohort) and an ACS validation cohort (SPUM-ACS study). The Heidelberg ACS cohort included 2535 and the SPUM-ACS study 4288 consecutive patients presenting with a working diagnosis of ACS. The Newcastle STEMI cohort included 2980 consecutive patients with ST-elevation myocardial infarction treated with primary percutaneous coronary intervention. Data were analyzed from March to June 2023. EXPOSURES In-hospital, 30-day, and 1-year mortality risk estimates derived from an updated risk score that incorporates continuous hs-cTn T at presentation (modified GRACE). MAIN OUTCOMES AND MEASURES The predictive value of continuous hs-cTn T and modified GRACE risk score compared with the original GRACE risk score. Study end points were all-cause mortality during hospitalization and at 30 days and 1 year after the index event. RESULTS Of 9450 included patients, 7313 (77.4%) were male, and the mean (SD) age at presentation was 64.2 (12.6) years. Using continuous rather than binary hs-cTn T conferred improved discrimination and reclassification compared with the original GRACE score (in-hospital mortality: area under the receiver operating characteristic curve [AUC], 0.835 vs 0.741; continuous net reclassification improvement [NRI], 0.208; 30-day mortality: AUC, 0.828 vs 0.740; NRI, 0.312; 1-y

Published
2023

31. Occlusion of the infarct-related coronary artery presenting as acute coronary syndrome with and without ST-elevation: impact of inflammation and outcomes in a real-world prospective cohort

Author

Bruno, Francesco; https://orcid.org/0000-0003-0019-0273, Adjibodou, Boris, Obeid, Slayman, Kraler, Simon C; https://orcid.org/0000-0002-8245-7287, Wenzl, Florian A; https://orcid.org/0000-0001-6654-9918, Akhtar, M Majid, Denegri, Andrea, Roffi, Marco; https://orcid.org/0000-0002-3051-0170, Muller, Olivier; https://orcid.org/0000-0003-2441-5799, von Eckardstein, Arnold; https://orcid.org/0000-0002-1666-2266, Räber, Lorenz; https://orcid.org/0000-0003-0824-3026, Templin, Christian, Lüscher, Thomas F, Bruno, Francesco; https://orcid.org/0000-0003-0019-0273, Adjibodou, Boris, Obeid, Slayman, Kraler, Simon C; https://orcid.org/0000-0002-8245-7287, Wenzl, Florian A; https://orcid.org/0000-0001-6654-9918, Akhtar, M Majid, Denegri, Andrea, Roffi, Marco; https://orcid.org/0000-0002-3051-0170, Muller, Olivier; https://orcid.org/0000-0003-2441-5799, von Eckardstein, Arnold; https://orcid.org/0000-0002-1666-2266, Räber, Lorenz; https://orcid.org/0000-0003-0824-3026, Templin, Christian, and Lüscher, Thomas F

Abstract

Background Patients with ST-segment elevation typically feature total coronary occlusion (TCO) of the infarct-related artery (IRA) on angiography, which may result in worse outcomes. Yet, relying solely on electrocardiogram (ECG) findings may be misleading and those presenting with non-ST-segment elevation acute coronary syndromes (NSTE-ACSs) may have TCO as well. Herein, we aimed to delineate clinical characteristics and outcomes of patients with ACS stratified by IRA location. Methods A total of 4787 ACS patients were prospectively recruited between 2009 and 2017 in SPUM-ACS (ClinicalTrials.gov Identifier: NCT01000701). The primary endpoint was major adverse cardiovascular events (MACEs), a composite of all-cause death, non-fatal myocardial infarction and non-fatal stroke at 1 year. Multivariable-adjusted survival models were fitted using backward selection. Results A total of 4412 ACS patients were included in this analysis, 56.0% (n = 2469) ST-elevation myocardial infarction (STEMI) and 44.0% (n = 1943) NSTE-ACS. The IRA was the right coronary artery (RCA) in 33.9% (n = 1494), the left-anterior descending coronary artery (LAD) in 45.6% (n = 2013), and the left circumflex (LCx) in 20.5% (n = 905) patients. In STEMI patients, TCO (defined as TIMI 0 flow at angiography) was observed in 55% of cases with LAD, in 63% with RCA, and in 55% with LCx. In those presenting with NSTE-ACS, TCO was more frequent in those with LCx and RCA as compared to the LAD (27 and 24%, respectively, vs. 9%, P < 0.001). Among patients with NSTE-ACS, occlusion of the LCx was associated with an increased risk of MACE during 1 year after the index ACS (fully adjusted hazard ratio 1.68, 95% confidence interval 1.10–2.59, P = 0.02; reference: RCA and LAD). Features of patients with NSTE-ACS associated with TCO of the IRA included elevated lymphocyte and neutrophil counts, higher levels of high-sensitivity C reactive protein (hs-CRP) and high-sensitivity cardiac troponin T, lower eGFR, and no

Published
2023

32. Low-density lipoprotein electronegativity and risk of death after acute coronary syndromes: A case-cohort analysis

Author

Kraler, Simon, Wenzl, Florian A, Vykoukal, Jody, Fahrmann, Johannes F, Shen, Ming-Yi, Chen, Der-Yuan, Chang, Kuan-Cheng, Chang, Ching-Kun, von Eckardstein, Arnold, Räber, Lorenz, Mach, François, Nanchen, David, Matter, Christian M, Liberale, Luca, Camici, Giovanni G, Akhmedov, Alexander, Chen, Chu-Huang, Lüscher, Thomas F, Kraler, Simon, Wenzl, Florian A, Vykoukal, Jody, Fahrmann, Johannes F, Shen, Ming-Yi, Chen, Der-Yuan, Chang, Kuan-Cheng, Chang, Ching-Kun, von Eckardstein, Arnold, Räber, Lorenz, Mach, François, Nanchen, David, Matter, Christian M, Liberale, Luca, Camici, Giovanni G, Akhmedov, Alexander, Chen, Chu-Huang, and Lüscher, Thomas F

Abstract

Background and aims Low-density lipoprotein (LDL)-cholesterol (LDL-C) promotes atherosclerotic cardiovascular disease (ASCVD), with changes in LDL electronegativity modulating its pro-atherogenic/pro-thrombotic effects. Whether such alterations associate with adverse outcomes in patients with acute coronary syndromes (ACS), a patient population at particularly high cardiovascular risk, remains unknown. Methods This is a case-cohort study using data from a subset of 2619 ACS patients prospectively recruited at four university hospitals in Switzerland. Isolated LDL was chromatographically separated into LDL particles with increasing electronegativity (L1-L5), with the L1-L5 ratio serving as a proxy of overall LDL electronegativity. Untargeted lipidomics revealed lipid species enriched in L1 (least) vs. L5 (most electronegative subfraction). Patients were followed at 30 days and 1 year. The mortality endpoint was reviewed by an independent clinical endpoint adjudication committee. Multivariable-adjusted hazard ratios (aHR) were calculated using weighted Cox regression models. Results Changes in LDL electronegativity were associated with all-cause mortality at 30 days (aHR, 2.13, 95% CI, 1.07–4.23 per 1 SD increment in L1/L5; p=.03) and 1 year (1.84, 1.03–3.29; p=.04), with a notable association with cardiovascular mortality (2.29; 1.21–4.35; p=.01; and 1.88; 1.08–3.28; p=.03). LDL electronegativity superseded several risk factors for the prediction of 1-year death, including LDL-C, and conferred improved discrimination when added to the updated GRACE score (area under the receiver operating characteristic curve 0.74 vs. 0.79, p=.03). Top 10 lipid species enriched in L1 vs. L5 were: cholesterol ester (CE) (18:2), CE (20:4), free fatty acid (FA) (20:4), phosphatidyl-choline (PC) (36:3), PC (34:2), PC (38:5), PC (36:4), PC (34:1), triacylglycerol (TG) (54:3), and PC (38:6) (all p < .001), with CE (18:2), CE (20:4), PC (36:3), PC (34:2), PC (38:5), PC (36:4), TG (54:3), an

Published
2023

34. Cardiovascular Biomarkers for the Prediction of Adverse Cardiovascular Events and Mortality in Patients with Cancer

Author

Moik, Florian, primary, Kraler, Simon, additional, Montecucco, Fabrizio, additional, Liberale, Luca, additional, Nopp, Stephan, additional, Englisch, Cornelia, additional, Lapikova-Bryhinska, Tetiana, additional, Akhmedov, Alexander, additional, von Eckardstein, Arnold, additional, Wenzl, Florian A., additional, Pabinger, Ingrid, additional, Lüscher, Thomas F., additional, and Ay, Cihan, additional

Published
2022
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35. SGLT-2 inhibition by empagliflozin has no effect on experimental arterial thrombosis in a murine model of low-grade inflammation

Author

Liberale, Luca, primary, Kraler, Simon, additional, Puspitasari, Yustina M, additional, Bonetti, Nicole R, additional, Akhmedov, Alexander, additional, Ministrini, Stefano, additional, Montecucco, Fabrizio, additional, Marx, Nikolaus, additional, Lehrke, Michael, additional, Hartmann, Niels Ulrik K, additional, Beer, Jürg H, additional, Wenzl, Florian A, additional, Paneni, Francesco, additional, Lüscher, Thomas F, additional, and Camici, Giovanni G, additional

Published
2022
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36. Soluble lectin-like oxidized low-density lipoprotein receptor-1 predicts premature death in acute coronary syndromes

Author

Kraler, Simon, Wenzl, Florian A, Georgiopoulos, Georgios, Obeid, Slayman, Liberale, Luca, von Eckardstein, Arnold, Muller, Olivier, Mach, François, Räber, Lorenz, Losdat, Sylvain, Schmiady, Martin O, Stellos, Konstantinos, Stamatelopoulos, Kimon, Camici, Giovanni G, Srdic, Annie, Paneni, Francesco, Akhmedov, Alexander, Lüscher, Thomas F, University of Zurich, Akhmedov, Alexander, and Lüscher, Thomas F

Subjects
Inflammation, Mortality, Premature, 610 Medicine & health, Acute coronary syndromes, Atherosclerosis, Scavenger Receptors, Class E, Lipids, Plaque, Atherosclerotic, 2705 Cardiology and Cardiovascular Medicine, 10020 Clinic for Cardiac Surgery, LOX-1, 540 Chemistry, 10209 Clinic for Cardiology, Humans, Acute Coronary Syndrome, Cardiology and Cardiovascular Medicine, Biomarkers, 10038 Institute of Clinical Chemistry
Abstract

The lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) and its shedding product [soluble LOX-1 (sLOX-1)] are implicated in atherosclerotic cardiovascular disease (ASCVD) pathogenesis. Herein, we examined the relationship of sLOX-1 with both fatal events and plaque progression in patients with acute coronary syndromes (ACS).Plasma sLOX-1 was assessed at baseline in ACS and chronic coronary syndrome (CCS) patients prospectively recruited in the multicentre SPUM-ACS study, with sex- and age-matched healthy subjects serving as additional controls (n = 2924). Compared with both CCS and controls, ACS patients showed markedly elevated sLOX-1 levels (median, 2.00 and 2.00 vs. 35.08 pg/mL; P 0.0001) which were independently associated with increased mortality risk over 30-day [tertile (T)3: adjusted hazard ratio (HR), 3.11; 95% confidence interval (CI), 1.44-10.61; P = 0.0055] and 1-year intervals (T3: adjusted HR, 2.04; 95% CI, 1.19-3.92; P = 0.0098). Results remained consistent after adjustment for GRACE 2.0 (T3: adjusted HR, 1.86; 95% CI, 1.04-3.74; P = 0.0391) and were primarily driven by the pronounced relationship of sLOX-1 with cardiovascular mortality at 30 days (T3: adjusted HR, 3.81; 95% CI, 1.62-19.62; P = 0.0036) and at 1 year (T3: adjusted HR, 2.29; 95% CI, 1.19-5.34; P = 0.0148). In ACS patients undergoing serial intracoronary imaging and statin therapy, sLOX-1 dropped significantly in those with coronary plaque regression at 1 year (ΔsLOX-1: -4.64 ± 1.80; P = 0.0057), and showed a good discrimination for predicting plaque progression (area under the curve = 0.74; 95% CI, 0.59-0.86; P = 0.0031).Plasma sLOX-1 levels are increased during ACS and predict fatal events beyond traditional and emerging risk factors. Persistently high sLOX-1 associates with coronary plaque progression in patients with established ASCVD.NCT01000701.Experimental evidence has implicated the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) and its shedding product [soluble LOX-1 (sLOX-1)] in atherosclerosis. The aim was to study the relationship of sLOX-1 with mortality and plaque progression in patients with acute coronary syndromes (ACS).Acute coronary syndrome patients displayed elevated sLOX-1 levels, with those in the highest tertile being at increased multivariable-adjusted risk of death from any [hazard ratio (HR) 2.04; P = 0.0098] and cardiovascular causes (HR, 2.29; P = 0.0148). Dynamics of sLOX-1 showed good discrimination for predicting plaque progression.Plasma levels of sLOX-1 are increased during ACS and predict fatal events beyond established risk factors. Trajectories of sLOX-1 mirror coronary plaque progression after the index ACS. Soluble LOX-1 is a novel biomarker of coronary plaque vulnerability and progression.

Published
2022

37. SGLT-2 inhibition by empagliflozin has no effect on experimental arterial thrombosis in a murine model of low-grade inflammation.

Author

Liberale, Luca, Kraler, Simon, Puspitasari, Yustina M, Bonetti, Nicole R, Akhmedov, Alexander, Ministrini, Stefano, Montecucco, Fabrizio, Marx, Nikolaus, Lehrke, Michael, Hartmann, Niels-Ulrik K, Beer, Jürg H, Wenzl, Florian A, Paneni, Francesco, Lüscher, Thomas F, and Camici, Giovanni G

Subjects
EMPAGLIFLOZIN, THROMBOSIS, BLOOD sugar, LABORATORY mice, INSULIN resistance, ENDOTHELIAL cells
Abstract

Aims Low-grade inflammation couples dysmetabolic states to insulin resistance and atherosclerotic cardiovascular (CV) disease (ASCVD). Selective sodium–glucose co-transporter 2 (SGLT-2) inhibition by empagliflozin improves clinical outcomes in patients with ASCVD independently of its glucose lowering effects. Yet, its mechanism of action remains largely undetermined. Here, we aimed to test whether empagliflozin affects arterial thrombus formation in baseline (BSL) conditions or low-grade inflammatory states, a systemic milieu shared among patients with ASCVD. Methods and results Sixteen-week-old C57BL/6 mice were randomly assigned to acute administration of empagliflozin (25 mg/kg body weight) or vehicle, of which a subgroup was pre-treated biweekly over 4 weeks with super-low-dose lipopolysaccharide (LPS; 5 ng/kg body weight), before carotid thrombosis was induced by photochemical injury. The between-group difference in Doppler-flow probe detected time-to-occlusion remained within the predefined equivalence margin (Δ = |10.50|), irrespective of low-grade inflammation (95% confidence interval, –9.82 to 8.85 and –9.20 to 9.69), while glucose dropped by 1.64 and 4.84 mmoL/L, respectively. Ex vivo platelet aggregometry suggested similar activation status, corroborated by unchanged circulating platelet-factor 4 plasma levels. In concert, carotid PAI-1 expression and tissue factor (TF) activity remained unaltered upon SGLT-2 inhibition, and no difference in plasma D-dimer levels was detected, suggesting comparable coagulation cascade activation and fibrinolytic activity. In human aortic endothelial cells pre-treated with LPS, empagliflozin neither changed TF activity nor PAI-1 expression. Accordingly, among patients with established ASCVD or at high CV risk randomized to a daily dose of 10 mg empagliflozin signatures of thrombotic (i.e. TF) and fibrinolytic activity (i.e. PAI-1) remained unchanged, while plasma glucose declined significantly during 3 months of follow-up. Conclusion SGLT-2 inhibition by empagliflozin does not impact experimental arterial thrombus formation, neither under BSL conditions nor during sustained low-grade inflammation, and has no impact on proxies of thrombotic/fibrinolytic activity in patients with ASCVD. The beneficial pleiotropic effects of empagliflozin are likely independent of pathways mediating arterial thrombosis. [ABSTRACT FROM AUTHOR]

Published
2023
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38. The BET Protein Inhibitor Apabetalone Rescues Diabetes-Induced Impairment of Angiogenic Response by Epigenetic Regulation of Thrombospondin-1

Author

Mohammed, Shafeeq A., primary, Albiero, Mattia, additional, Ambrosini, Samuele, additional, Gorica, Era, additional, Karsai, Gergely, additional, Caravaggi, Carlo M., additional, Masi, Stefano, additional, Camici, Giovanni G., additional, Wenzl, Florian A., additional, Calderone, Vincenzo, additional, Madeddu, Paolo, additional, Sciarretta, Sebastiano, additional, Matter, Christian M., additional, Spinetti, Gaia, additional, Lüscher, Thomas F., additional, Ruschitzka, Frank, additional, Costantino, Sarah, additional, Fadini, Gian Paolo, additional, and Paneni, Francesco, additional

Published
2022
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39. Soluble lectin-like oxidized low-density lipoprotein receptor-1 predicts premature death in acute coronary syndromes

Author

Kraler, Simon, primary, Wenzl, Florian A, additional, Georgiopoulos, Georgios, additional, Obeid, Slayman, additional, Liberale, Luca, additional, von Eckardstein, Arnold, additional, Muller, Olivier, additional, Mach, François, additional, Räber, Lorenz, additional, Losdat, Sylvain, additional, Schmiady, Martin O, additional, Stellos, Konstantinos, additional, Stamatelopoulos, Kimon, additional, Camici, Giovanni G, additional, Srdic, Annie, additional, Paneni, Francesco, additional, Akhmedov, Alexander, additional, and Lüscher, Thomas F, additional

Published
2022
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40. Inflammation in Metabolic Cardiomyopathy

Author

Wenzl, Florian A., Ambrosini, Samuele, Mohammed, Shafeeq A., Kraler, Simon, Lüscher, Thomas F., Costantino, Sarah, Paneni, Francesco, University of Zurich, and Paneni, Francesco

Subjects
obesity, cardiometabolic disease, inflammation, 10209 Clinic for Cardiology, 610 Medicine & health, Review, Cardiovascular Medicine, lipotoxicity, HFpEF, Cardiology and Cardiovascular Medicine, 2705 Cardiology and Cardiovascular Medicine
Abstract

Overlapping pandemics of lifestyle-related diseases pose a substantial threat to cardiovascular health. Apart from coronary artery disease, metabolic disturbances linked to obesity, insulin resistance and diabetes directly compromise myocardial structure and function through independent and shared mechanisms heavily involving inflammatory signals. Accumulating evidence indicates that metabolic dysregulation causes systemic inflammation, which in turn aggravates cardiovascular disease. Indeed, elevated systemic levels of pro-inflammatory cytokines and metabolic substrates induce an inflammatory state in different cardiac cells and lead to subcellular alterations thereby promoting maladaptive myocardial remodeling. At the cellular level, inflammation-induced oxidative stress, mitochondrial dysfunction, impaired calcium handling, and lipotoxicity contribute to cardiomyocyte hypertrophy and dysfunction, extracellular matrix accumulation and microvascular disease. In cardiometabolic patients, myocardial inflammation is maintained by innate immune cell activation mediated by pattern recognition receptors such as Toll-like receptor 4 (TLR4) and downstream activation of the NLRP3 inflammasome and NF-κB-dependent pathways. Chronic low-grade inflammation progressively alters metabolic processes in the heart, leading to a metabolic cardiomyopathy (MC) phenotype and eventually to heart failure with preserved ejection fraction (HFpEF). In accordance with preclinical data, observational studies consistently showed increased inflammatory markers and cardiometabolic features in patients with HFpEF. Future treatment approaches of MC may target inflammatory mediators as they are closely intertwined with cardiac nutrient metabolism. Here, we review current evidence on inflammatory processes involved in the development of MC and provide an overview of nutrient and cytokine-driven pro-inflammatory effects stratified by cell type.

Published
2021
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41. Abstract 10474: The Bet Protein Inhibitor Apabetalone Rescues Diabetes Induced Impairment of Angiogenic Response

Author

Mohammed, Shafeeq Ahmed A, primary, Albiero, Mattia, additional, Ambrosini, Samuele, additional, Gergely, Karsai, additional, Wenzl, Florian, additional, Gorica, Era, additional, Calderone, Vincenzo, additional, Madeddu, Paolo, additional, Spinetti, Gaia, additional, Luscher, Thomas F, additional, Costantino, Sarah, additional, Fadini, Gian P, additional, and Paneni, Francesco, additional

Published
2021
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48. The cardiologist in the age of artificial intelligence: what is left for us?

Author

Lüscher TF and Wenzl FA

Abstract

Competing Interests: Conflict of interest: T.F.L. and F.W. have no conflicts of interest related to this manuscript. Outside this work. T.F.L. has received educational and research grants to the institution from Abbott, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Daichi-Sankyo, Eli Lilly, Novartis, Novo Nordisk, Sanofi, Vifor.

Published
2024
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49. Proenkephalin Improves Cardio-Renal Risk Prediction in Acute Coronary Syndromes: The KID-ACS Score.

Author

Wenzl FA, Wang P, Arrigo M, Parenica J, Jones DJL, Bruno F, Tarnwski D, Hartmann O, Boucek L, Lang F, Obeid S, Schober A, Kraler S, Akhmedov A, Kahles F, Schober A, Ow KW, Ministrini S, Camici GG, Bergmann A, Liberale L, Jarkovsky J, Schweiger V, Sandhu JK, von Eckardstein A, Templin C, Muller O, Ondrus T, Olic JJ, Roffi M, Räber L, Cao TH, Jungbauer CG, Ng LL, Mebazaa A, and Lüscher TF

Abstract

Background and Aims: Circulating proenkephalin (PENK) is a stable endogenous polypeptide with fast response to glomerular dysfunction and tubular damage. This study examined the predictive value of PENK for renal outcomes and mortality in patients with acute coronary syndromes (ACS)., Methods: Proenkephalin was measured in plasma in a prospective multicentre ACS cohort from Switzerland (n=4787) and in validation cohorts from the UK (n=1141), Czechia (n=927), and Germany (n=220). A biomarker-enhanced risk score (KID-ACS score) for simultaneous prediction of in-hospital acute kidney injury (AKI) and 30-day mortality was derived and externally validated., Results: On multivariable adjustment for established risk factors, circulating PENK remained associated with in-hospital AKI (per log2 increase: adjusted odds ratio [OR] 1.53, 95% confidence interval [CI] 1.13-2.09, P=0.007) and 30-day mortality (adjusted hazard ratio [HR] 2.73, 95% CI 1.85-4.02, P<0.001). The KID-ACS score integrates PENK and showed an area under the receiver operating characteristic curve (AUC) of 0.72 (95% CI 0.68-0.76) for in-hospital AKI, and of 0.91 (95% CI 0.87-0.95) for 30-day mortality in the derivation cohort. Upon external validation, KID-ACS achieved similarly high performance for in-hospital AKI (Zurich: AUC 0.73, 95% CI 0.70-0.77; Czechia: AUC 0.75, 95% CI 0.68-0.81; Germany: AUC 0.71, 95% CI 0.55-0.87) and 30-day mortality (UK: AUC 0.87, 95% CI 0.83-0.91; Czechia: AUC 0.91, 95% CI 0.87-0.94; Germany: AUC 0.96, 95% CI 0.92-1.00) outperforming the CA-AKI score and the GRACE 2.0 score, respectively., Conclusions: Circulating PENK offers incremental value for predicting in-hospital AKI and mortality in ACS. The simple 6-item KID-ACS risk score integrates PENK and provides a novel tool for simultaneous assessment of renal and mortality risk in patients with ACS., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Published
2024
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50. Trajectories of cardiovascular ageing - from molecular mechanisms to clinical implementation.

Author

Ministrini S, Wenzl FA, Lüscher TF, and Camici GG

Abstract

Due to its peculiar structure and function, the cardiovascular system is particularly vulnerable to the detrimental effects of ageing. Current knowledge about the molecular mechanisms of ageing revealed the processes actively promoting ageing, e.g. progressive telomeres shortening, and the mechanisms opposing it, e.g. endogenous production of antioxidant substances. This knowledge can be used to measure biological age at a cellular and molecular level and to interfere with it by pharmacological or non-pharmacological interventions. Biological ageing is determined by the simultaneous occurrence of independent hallmarks, which encompass a wide range of biological processes, from genomic changes to systemic inflammation and dysbiosis. This narrative review will summarize the role of ageing hallmarks in the cardiovascular system, how they can be measured and what are the possible interventions to counteract their effects., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Published
2024
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