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

• Authors: Ayman Samman Tahhan, Emory University; Pratik Sandesara, Emory University; Salim S. Hayek, Emory University; Muhammad Hammadah, Emory University; Ayman Alkhoder, Emory University; Heval M. Kelli, Emory University; Matthew Topel, Emory University; Wesley T. O'Neal, Emory University; Nima Ghasemzadeh, Emory University; Yi-An Ko, Emory University; Mohamad Mazen Gafeer, Emory University; Naser Abdelhadi, Emory University; Fahad Choudhary, Emory University; Keyur Patel, Emory University; Agim Beshiri, Abbott Laboratories; Gillian Murtagh, Abbott Laboratories; Jonathan Ho-Youn Kim, Emory University; Peter W Wilson, Emory University; Leslee J Shaw, Emory University; Viola Vaccarino, Emory University; Stephen E. Epstein, Washington Hospital Center; Laurence S Sperling, Emory University; Arshed Ali Quyyumi, Emory University
• Journal Title: Journal of the American Heart Association
• Volume: Volume 7, Number 5
• Publisher: Wiley Open Access: Creative Commons Attribution Non-Commercial | 2018-03-06
• Type of Work: Article | Final Publisher PDF
• Publisher DOI: http://doi.org/10.1161/JAHA.117.007914
• Subjects: Biology, Biostatistics; Biology, Bioinformatics; Health Sciences, Medicine and Surgery
• Keywords: atherosclerosis; coronary angiography; coronary artery disease; troponin

Abstract

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.