TY - JOUR
T1 - High-sensitivity troponin I levels and coronary artery disease severity, progression, and long-term outcomes
AU - Tahhan, Ayman Samman
AU - Sandesara, Pratik
AU - Hayek, Salim S.
AU - Hammadah, Muhammad
AU - Alkhoder, Ayman
AU - Kelli, Heval M.
AU - Topel, Matthew
AU - O'Neal, Wesley T.
AU - Ghasemzadeh, Nima
AU - Ko, Yi An
AU - Gafeer, Mohamad Mazen
AU - Abdelhadi, Naser
AU - Choudhary, Fahad
AU - Patel, Keyur
AU - Beshiri, Agim
AU - Murtagh, Gillian
AU - Kim, Jonathan
AU - Wilson, Peter
AU - Shaw, Leslee
AU - Vaccarino, Viola
AU - Epstein, Stephen E.
AU - Sperling, Laurence
AU - Quyyumi, Arshed A.
N1 - Funding Information:
This work was supported partially by Abbott. Quyyumi is supported by National Institutes of Health (NIH) grants 5P01HL101398-02, 1P20HL113451-01, 1R56HL126558-01, 1RF1AG051633-01, R01 NS064162-01, R01 HL89650-01, HL095479-01, 1U10HL110302-01, 1DP3DK094346-01, and 2P01HL086773-06A1. Samman Tahhan is supported by the Abraham J. & Phyllis Katz Foundation grant (Atlanta, GA) and NIH/National Institute on Aging grant AG051633.
Publisher Copyright:
© 2018 The Authors.
PY - 2018/3/6
Y1 - 2018/3/6
N2 - 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 β=0.31; 95% confidence interval, 0.18-0.44; P < 0.001) and with CAD progression (log 2 β=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.
AB - 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 β=0.31; 95% confidence interval, 0.18-0.44; P < 0.001) and with CAD progression (log 2 β=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.
KW - Atherosclerosis
KW - Coronary angiography
KW - Coronary artery disease
KW - Troponin
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U2 - 10.1161/JAHA.117.007914
DO - 10.1161/JAHA.117.007914
M3 - Article
C2 - 29467150
AN - SCOPUS:85042731344
SN - 2047-9980
VL - 7
JO - Journal of the American Heart Association
JF - Journal of the American Heart Association
IS - 5
M1 - e007914
ER -