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High‐Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long‐Term Outcomes

BACKGROUND: The associations between high‐sensitivity troponin I (hsTnI) levels and coronary artery disease (CAD) severity and progression remain unclear. We investigated whether there is an association between hsTnI and angiographic severity and progression of CAD and whether the predictive value o...

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Autores principales: Samman Tahhan, Ayman, Sandesara, Pratik, Hayek, Salim S., Hammadah, Muhammad, Alkhoder, Ayman, Kelli, Heval M., Topel, Matthew, O'Neal, Wesley T., Ghasemzadeh, Nima, Ko, Yi‐An, Gafeer, Mohamad Mazen, Abdelhadi, Naser, Choudhary, Fahad, Patel, Keyur, Beshiri, Agim, Murtagh, Gillian, Kim, Jonathan, Wilson, Peter, Shaw, Leslee, Vaccarino, Viola, Epstein, Stephen E., Sperling, Laurence, Quyyumi, Arshed A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5866331/
https://www.ncbi.nlm.nih.gov/pubmed/29467150
http://dx.doi.org/10.1161/JAHA.117.007914
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author Samman Tahhan, Ayman
Sandesara, Pratik
Hayek, Salim S.
Hammadah, Muhammad
Alkhoder, Ayman
Kelli, Heval M.
Topel, Matthew
O'Neal, Wesley T.
Ghasemzadeh, Nima
Ko, Yi‐An
Gafeer, Mohamad Mazen
Abdelhadi, Naser
Choudhary, Fahad
Patel, Keyur
Beshiri, Agim
Murtagh, Gillian
Kim, Jonathan
Wilson, Peter
Shaw, Leslee
Vaccarino, Viola
Epstein, Stephen E.
Sperling, Laurence
Quyyumi, Arshed A.
author_facet Samman Tahhan, Ayman
Sandesara, Pratik
Hayek, Salim S.
Hammadah, Muhammad
Alkhoder, Ayman
Kelli, Heval M.
Topel, Matthew
O'Neal, Wesley T.
Ghasemzadeh, Nima
Ko, Yi‐An
Gafeer, Mohamad Mazen
Abdelhadi, Naser
Choudhary, Fahad
Patel, Keyur
Beshiri, Agim
Murtagh, Gillian
Kim, Jonathan
Wilson, Peter
Shaw, Leslee
Vaccarino, Viola
Epstein, Stephen E.
Sperling, Laurence
Quyyumi, Arshed A.
author_sort Samman Tahhan, Ayman
collection PubMed
description BACKGROUND: The associations between high‐sensitivity troponin I (hsTnI) levels and coronary artery disease (CAD) severity and progression remain unclear. We investigated whether there is an association between hsTnI and angiographic severity and progression of CAD and whether the predictive value of hsTnI level for incident cardiovascular outcomes is independent of CAD severity. METHODS AND RESULTS: In 3087 patients (aged 63±12 years, 64% men) undergoing cardiac catheterization without evidence of acute myocardial infarction, the severity of CAD was calculated by the number of major coronary arteries with ≥50% stenosis and the Gensini score. CAD progression was assessed in a subset of 717 patients who had undergone ≥2 coronary angiograms >3 months before enrollment. Patients were followed up for incident all‐cause mortality and incident cardiovascular events. Of the total population, 11% had normal angiograms, 23% had nonobstructive CAD, 20% had 1‐vessel CAD, 20% had 2‐vessel CAD, and 26% had 3‐vessel CAD. After adjusting for age, sex, race, body mass index, smoking, hypertension, diabetes mellitus history, and renal function, hsTnI levels were independently associated with the severity of CAD measured by the Gensini score (log 2 ß=0.31; 95% confidence interval, 0.18–0.44; P<0.001) and with CAD progression (log 2 ß=0.36; 95% confidence interval, 0.14–0.58; P=0.001). hsTnI level was also a significant predictor of incident death, cardiovascular death, myocardial infarction, revascularization, and cardiac hospitalizations, independent of the aforementioned covariates and CAD severity. CONCLUSIONS: Higher hsTnI levels are associated with the underlying burden of coronary atherosclerosis, more rapid progression of CAD, and higher risk of all‐cause mortality and incident cardiovascular events. Whether more aggressive treatment aimed at reducing hsTnI levels can modulate disease progression requires further investigation.
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spelling pubmed-58663312018-03-28 High‐Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long‐Term Outcomes Samman Tahhan, Ayman Sandesara, Pratik Hayek, Salim S. Hammadah, Muhammad Alkhoder, Ayman Kelli, Heval M. Topel, Matthew O'Neal, Wesley T. Ghasemzadeh, Nima Ko, Yi‐An Gafeer, Mohamad Mazen Abdelhadi, Naser Choudhary, Fahad Patel, Keyur Beshiri, Agim Murtagh, Gillian Kim, Jonathan Wilson, Peter Shaw, Leslee Vaccarino, Viola Epstein, Stephen E. Sperling, Laurence Quyyumi, Arshed A. J Am Heart Assoc Original Research BACKGROUND: The associations between high‐sensitivity troponin I (hsTnI) levels and coronary artery disease (CAD) severity and progression remain unclear. We investigated whether there is an association between hsTnI and angiographic severity and progression of CAD and whether the predictive value of hsTnI level for incident cardiovascular outcomes is independent of CAD severity. METHODS AND RESULTS: In 3087 patients (aged 63±12 years, 64% men) undergoing cardiac catheterization without evidence of acute myocardial infarction, the severity of CAD was calculated by the number of major coronary arteries with ≥50% stenosis and the Gensini score. CAD progression was assessed in a subset of 717 patients who had undergone ≥2 coronary angiograms >3 months before enrollment. Patients were followed up for incident all‐cause mortality and incident cardiovascular events. Of the total population, 11% had normal angiograms, 23% had nonobstructive CAD, 20% had 1‐vessel CAD, 20% had 2‐vessel CAD, and 26% had 3‐vessel CAD. After adjusting for age, sex, race, body mass index, smoking, hypertension, diabetes mellitus history, and renal function, hsTnI levels were independently associated with the severity of CAD measured by the Gensini score (log 2 ß=0.31; 95% confidence interval, 0.18–0.44; P<0.001) and with CAD progression (log 2 ß=0.36; 95% confidence interval, 0.14–0.58; P=0.001). hsTnI level was also a significant predictor of incident death, cardiovascular death, myocardial infarction, revascularization, and cardiac hospitalizations, independent of the aforementioned covariates and CAD severity. CONCLUSIONS: Higher hsTnI levels are associated with the underlying burden of coronary atherosclerosis, more rapid progression of CAD, and higher risk of all‐cause mortality and incident cardiovascular events. Whether more aggressive treatment aimed at reducing hsTnI levels can modulate disease progression requires further investigation. John Wiley and Sons Inc. 2018-02-21 /pmc/articles/PMC5866331/ /pubmed/29467150 http://dx.doi.org/10.1161/JAHA.117.007914 Text en © 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial (http://creativecommons.org/licenses/by-nc/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Original Research
Samman Tahhan, Ayman
Sandesara, Pratik
Hayek, Salim S.
Hammadah, Muhammad
Alkhoder, Ayman
Kelli, Heval M.
Topel, Matthew
O'Neal, Wesley T.
Ghasemzadeh, Nima
Ko, Yi‐An
Gafeer, Mohamad Mazen
Abdelhadi, Naser
Choudhary, Fahad
Patel, Keyur
Beshiri, Agim
Murtagh, Gillian
Kim, Jonathan
Wilson, Peter
Shaw, Leslee
Vaccarino, Viola
Epstein, Stephen E.
Sperling, Laurence
Quyyumi, Arshed A.
High‐Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long‐Term Outcomes
title High‐Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long‐Term Outcomes
title_full High‐Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long‐Term Outcomes
title_fullStr High‐Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long‐Term Outcomes
title_full_unstemmed High‐Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long‐Term Outcomes
title_short High‐Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long‐Term Outcomes
title_sort high‐sensitivity troponin i levels and coronary artery disease severity, progression, and long‐term outcomes
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5866331/
https://www.ncbi.nlm.nih.gov/pubmed/29467150
http://dx.doi.org/10.1161/JAHA.117.007914
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