Cardiac troponin elevation and mortality in takotsubo syndrome: New insights from the international takotsubo registry

IF 4.4 3区 医学 Q1 MEDICINE, GENERAL & INTERNAL
Barbara E. Stähli, Matthias Schindler, Victor Schweiger, Victoria L. Cammann, Konrad A. Szawan, David Niederseer, Michael Würdinger, Alexander Schönberger, Maximilian Schönberger, Iva Koleva, Julien C. Mercier, Vanya Petkova, Silvia Mayer, Rodolfo Citro, Carmine Vecchione, Eduardo Bossone, Sebastiano Gili, Michael Neuhaus, Jennifer Franke, Benjamin Meder, Miłosz Jaguszewski, Michel Noutsias, Maike Knorr, Thomas Jansen, Fabrizio D’Ascenzo, Wolfgang Dichtl, Dirk von Lewinski, Christof Burgdorf, Behrouz Kherad, Carsten Tschöpe, Annahita Sarcon, Jerold Shinbane, Lawrence Rajan, Guido Michels, Roman Pfister, Alessandro Cuneo, Claudius Jacobshagen, Mahir Karakas, Wolfgang Koenig, Alexander Pott, Philippe Meyer, Marco Roffi, Adrian Banning, Mathias Wolfrum, Florim Cuculi, Richard Kobza, Thomas A. Fischer, Tuija Vasankari, K. E. Juhani Airaksinen, L. Christian Napp, Rafal Dworakowski, Philip MacCarthy, Christoph Kaiser, Stefan Osswald, Leonarda Galiuto, Christina Chan, Paul Bridgman, Daniel Beug, Clément Delmas, Olivier Lairez, Ekaterina Gilyarova, Alexandra Shilova, Mikhail Gilyarov, Ibrahim El-Battrawy, Ibrahim Akin, Karolina Poledniková, Petr Toušek, David E. Winchester, Michael Massoomi, Jan Galuszka, Christian Ukena, Gregor Poglajen, Pedro Carrilho-Ferreira, Christian Hauck, Carla Paolini, Claudio Bilato, Yoshio Kobayashi, Ken Kato, Iwao Ishibashi, Toshiharu Himi, Jehangir Din, Ali Al-Shammari, Abhiram Prasad, Charanjit S. Rihal, Kan Liu, P. Christian Schulze, Matteo Bianco, Lucas Jörg, Hans Rickli, Gonçalo Pestana, Thanh H. Nguyen, Michael Böhm, Lars S. Maier, Fausto J. Pinto, Petr Widimský, Stephan B. Felix, Ruediger C. Braun-Dullaeus, Wolfgang Rottbauer, Gerd Hasenfuß, Burkert M. Pieske, Heribert Schunkert, Monika Budnik, Grzegorz Opolski, Holger Thiele, Johann Bauersachs, John D. Horowitz, Carlo Di Mario, William Kong, Mayank Dalakoti, Yoichi Imori, Luca Liberale, Fabrizio Montecucco, Thomas Münzel, Filippo Crea, Thomas F. Lüscher, Jeroen J. Bax, Frank Ruschitzka, Jelena R. Ghadri, Davide Di Vece, Christian Templin
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Mercier,&nbsp;Vanya Petkova,&nbsp;Silvia Mayer,&nbsp;Rodolfo Citro,&nbsp;Carmine Vecchione,&nbsp;Eduardo Bossone,&nbsp;Sebastiano Gili,&nbsp;Michael Neuhaus,&nbsp;Jennifer Franke,&nbsp;Benjamin Meder,&nbsp;Miłosz Jaguszewski,&nbsp;Michel Noutsias,&nbsp;Maike Knorr,&nbsp;Thomas Jansen,&nbsp;Fabrizio D’Ascenzo,&nbsp;Wolfgang Dichtl,&nbsp;Dirk von Lewinski,&nbsp;Christof Burgdorf,&nbsp;Behrouz Kherad,&nbsp;Carsten Tschöpe,&nbsp;Annahita Sarcon,&nbsp;Jerold Shinbane,&nbsp;Lawrence Rajan,&nbsp;Guido Michels,&nbsp;Roman Pfister,&nbsp;Alessandro Cuneo,&nbsp;Claudius Jacobshagen,&nbsp;Mahir Karakas,&nbsp;Wolfgang Koenig,&nbsp;Alexander Pott,&nbsp;Philippe Meyer,&nbsp;Marco Roffi,&nbsp;Adrian Banning,&nbsp;Mathias Wolfrum,&nbsp;Florim Cuculi,&nbsp;Richard Kobza,&nbsp;Thomas A. Fischer,&nbsp;Tuija Vasankari,&nbsp;K. E. Juhani Airaksinen,&nbsp;L. Christian Napp,&nbsp;Rafal Dworakowski,&nbsp;Philip MacCarthy,&nbsp;Christoph Kaiser,&nbsp;Stefan Osswald,&nbsp;Leonarda Galiuto,&nbsp;Christina Chan,&nbsp;Paul Bridgman,&nbsp;Daniel Beug,&nbsp;Clément Delmas,&nbsp;Olivier Lairez,&nbsp;Ekaterina Gilyarova,&nbsp;Alexandra Shilova,&nbsp;Mikhail Gilyarov,&nbsp;Ibrahim El-Battrawy,&nbsp;Ibrahim Akin,&nbsp;Karolina Poledniková,&nbsp;Petr Toušek,&nbsp;David E. Winchester,&nbsp;Michael Massoomi,&nbsp;Jan Galuszka,&nbsp;Christian Ukena,&nbsp;Gregor Poglajen,&nbsp;Pedro Carrilho-Ferreira,&nbsp;Christian Hauck,&nbsp;Carla Paolini,&nbsp;Claudio Bilato,&nbsp;Yoshio Kobayashi,&nbsp;Ken Kato,&nbsp;Iwao Ishibashi,&nbsp;Toshiharu Himi,&nbsp;Jehangir Din,&nbsp;Ali Al-Shammari,&nbsp;Abhiram Prasad,&nbsp;Charanjit S. Rihal,&nbsp;Kan Liu,&nbsp;P. Christian Schulze,&nbsp;Matteo Bianco,&nbsp;Lucas Jörg,&nbsp;Hans Rickli,&nbsp;Gonçalo Pestana,&nbsp;Thanh H. Nguyen,&nbsp;Michael Böhm,&nbsp;Lars S. Maier,&nbsp;Fausto J. 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The present study sought to investigate the role of cardiac troponin (cTn) elevations in mortality prediction of patients with Takotsubo syndrome (TTS).</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>Patients enrolled in the International Takotsubo (InterTAK) Registry from January 2011 to February 2020 with available data on peak cTn levels were included in the analysis. Peak cTn levels during the index hospitalization were used to define clinically relevant myocardial injury. The threshold at which clinically relevant myocardial injury drives mortality at 1 year was identified using restricted cubic spline analysis.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>Out of 2′938 patients, 222 (7.6%) patients died during 1-year follow-up. A more than 28.8-fold increase of cTn above the upper reference limit was identified as threshold for clinically relevant myocardial injury. 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引用次数: 0

Abstract

Background

The clinical relevance of cardiac troponin (cTn) elevation in takotsubo syndrome (TTS) remains uncertain. The present study sought to investigate the role of cardiac troponin (cTn) elevations in mortality prediction of patients with Takotsubo syndrome (TTS).

Methods

Patients enrolled in the International Takotsubo (InterTAK) Registry from January 2011 to February 2020 with available data on peak cTn levels were included in the analysis. Peak cTn levels during the index hospitalization were used to define clinically relevant myocardial injury. The threshold at which clinically relevant myocardial injury drives mortality at 1 year was identified using restricted cubic spline analysis.

Results

Out of 2′938 patients, 222 (7.6%) patients died during 1-year follow-up. A more than 28.8-fold increase of cTn above the upper reference limit was identified as threshold for clinically relevant myocardial injury. The presence of clinically relevant myocardial injury was significantly associated with an increased risk of mortality at 5 years (adjusted HR 1.58, 95% CI 1.18–2.12, p =.002). Clinically relevant myocardial injury was related to an increased 5-year mortality risk in patients with apical TTS (adjusted HR 1.57, 95% CI 1.21–2.03, p =.001), in presence of physical stressors (adjusted HR 1.60, 95% CI 1.22–2.11, p =.001), and in absence of emotional stressors (adjusted HR 1.49, 95% CI, 1.17–1.89, p =.001).

Conclusion

This study for the first time determined a troponin threshold for the identification of TTS patients at excess risk of mortality. These findings advance risk stratification in TTS and assist in identifying patients in need for close monitoring and follow-up.

Abstract Image

心肌肌钙蛋白升高与塔可洼氏综合征的死亡率:国际塔库洼登记处的新见解。
背景:心肌肌钙蛋白(cTn)升高在高钾综合征(TTS)中的临床意义仍不确定。本研究旨在探讨心肌肌钙蛋白(cTn)升高在预测塔克次氏综合征(TTS)患者死亡率中的作用:方法:分析对象包括 2011 年 1 月至 2020 年 2 月期间加入国际塔克次氏综合征(InterTAK)登记处并提供 cTn 峰值数据的患者。指标住院期间的 cTn 峰值用于定义临床相关心肌损伤。通过限制性三次样条分析确定了临床相关心肌损伤导致 1 年死亡率的阈值:在 2938 名患者中,有 222 名(7.6%)患者在 1 年随访期间死亡。临床相关心肌损伤的阈值是 cTn 升高超过参考上限 28.8 倍。临床相关心肌损伤的存在与 5 年后死亡风险的增加显著相关(调整后 HR 1.58,95% CI 1.18-2.12,p =.002)。临床相关心肌损伤与心尖TTS患者的5年死亡风险增加有关(调整后HR为1.57,95% CI为1.21-2.03,P =.001),与存在身体应激因素有关(调整后HR为1.60,95% CI为1.22-2.11,P =.001),与不存在情绪应激因素有关(调整后HR为1.49,95% CI为1.17-1.89,P =.001):本研究首次确定了肌钙蛋白阈值,用于识别有超额死亡风险的 TTS 患者。这些发现推进了对 TTS 的风险分层,有助于识别需要密切监测和随访的患者。
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来源期刊
CiteScore
9.50
自引率
3.60%
发文量
192
审稿时长
1 months
期刊介绍: EJCI considers any original contribution from the most sophisticated basic molecular sciences to applied clinical and translational research and evidence-based medicine across a broad range of subspecialties. The EJCI publishes reports of high-quality research that pertain to the genetic, molecular, cellular, or physiological basis of human biology and disease, as well as research that addresses prevalence, diagnosis, course, treatment, and prevention of disease. We are primarily interested in studies directly pertinent to humans, but submission of robust in vitro and animal work is also encouraged. Interdisciplinary work and research using innovative methods and combinations of laboratory, clinical, and epidemiological methodologies and techniques is of great interest to the journal. Several categories of manuscripts (for detailed description see below) are considered: editorials, original articles (also including randomized clinical trials, systematic reviews and meta-analyses), reviews (narrative reviews), opinion articles (including debates, perspectives and commentaries); and letters to the Editor.
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