Stripe B, Rechenmacher S, Jurewitz D, Lee C, Schaefer S. The Diagnostic Yield of Cardiac Catheterization in Low-Risk Troponinemia. JAMA Intern Med. 2013;173(22):2088-2090. doi:10.1001/jamainternmed.2013.11109
Serum cardiac troponin I (cTnI) is a sensitive indicator of myocardial necrosis.1 However, many disease states can result in an elevated cTnI level without clinical evidence of myocardial infarction,2 resulting in possible misdiagnosis of epicardial coronary artery disease (CAD).3 In the present study, we investigated the prevalence of CAD and associated patient characteristics in patients with mildly elevated cTnI levels without clinical evidence of acute coronary syndrome.
This study was approved by the institutional review board of the University of California, Davis. All patients had agreed to the use of their medical records for research purposes.
This was a single center, retrospective cohort study that examined patients 18 years or older who presented with a peak cTnI level between 0.05 ng/mL (>99th percentile of normal population) and 2 ng/mL (nanograms per milliliter to micrograms per liter is a 1-to1 conversion)within 30 days prior to coronary angiography. Patients were excluded if they had chest pain with cardiac features, a history of known CAD, or ischemic changes on electrocardiography or stress test.
Baseline characteristics recorded included age, sex, history of heart failure, diabetes, dyslipidemia, peripheral vascular disease, lung disease, smoking, kidney disease, hypertension, and pulmonary hypertension, as well as data related to the index episode such as level of peak troponin, B-type natriuretic peptide (BNP) level, left ventricular ejection fraction, and hemoglobin and serum creatinine levels.
The primary end point was the presence of significant CAD, defined as 50% or greater left main stenosis, 70% or greater stenosis of another epicardial coronary artery, or fractional flow reserve of less than 0.8. Secondary end points were revascularization by percutaneous coronary intervention or coronary artery bypass grafting. The final presumed cause of elevated troponin level was also assessed.
Of 140 patients, 16 (11%) were found to have significant CAD. Of these patients, 12 underwent revascularization, 10 with percutaneous coronary intervention and 2 via coronary artery bypass grafting. Patients with CAD were older (P = .006), with none younger than 49 years. Patients with CAD were more likely to have a presenting symptom of syncope (P = .02) or have evidence of a new arrhythmia (P = .003 by univariate analysis and P = .03 after multiple regression analysis) (Table 1). Patients with diabetes were more likely to have CAD (P = .01) by univariate analysis. A history of stroke was associated with CAD, but only after multiple regression analysis (P = .04). Notably, factors such as sex, smoking history, heart failure, dyslipidemia, and hypertension were not associated with CAD.
The majority of patients (58.9%) without significant CAD had an elevated troponin level associated with heart failure (Table 2). Fluid or pressure overload states—including heart failure, hypertensive emergency, pulmonary hypertension, hypertrophic cardiomyopathy, or significant aortic valve disease—accounted for 81.5% of the patients without CAD. Other causes of “troponinemia” included increased oxygen demand due to infection, tachycardia, or sympathomimetic abuse such as cocaine or methamphetamine.
The use of sensitive biomarkers such as cTnI is becoming more widespread, with as many as 50% of hospitalized patients having a troponin test ordered during their hospitalization.4 Given the need to limit ineffective medical testing and associated costs and risks of cardiac catheterization (estimated at a complication rate of approximately 1.7%5 and $5000 for an outpatient procedure6), it is imperative to appropriately triage patients with low-level elevations of troponin in the absence of clinical acute coronary syndrome. Some of the risk factors identified by this study were diabetes, age, chronic kidney disease, and disease of other vascular beds; however, in this population, other risk factors such as syncope and supraventricular tachyarrhythmia appear to confer increased risk as well. Appropriate management of patients with low-level elevations of troponin should consider the pretest probability of CAD and the likelihood that most patients in this population do not have significant CAD.
Corresponding Author: Saul Schaefer, MD, Division of Cardiovascular Medicine and Cardiology Section, Department of Internal Medicine, University of California Davis, One Shields Ave, Davis, CA 95616 (email@example.com).
Published Online: October 7, 2013. doi:10.1001/jamainternmed.2013.11109.
Author Contributions: Dr Schaefer had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Rechenmacher, Jurewitz, Schaefer.
Acquisition of data: Stripe, Rechenmacher, Jurewitz, Lee, Schaefer.
Analysis and interpretation of data: Stripe, Rechenmacher, Schaefer.
Drafting of the manuscript: Stripe, Rechenmacher, Schaefer.
Critical revision of the manuscript for important intellectual content: Stripe, Rechenmacher, Jurewitz, Lee, Schaefer.
Statistical analysis: Stripe, Rechenmacher, Lee.
Administrative, technical, or material support: Rechenmacher, Schaefer.
Study supervision: Rechenmacher, Jurewitz, Schaefer.
Funding/Support: The project described was supported by the National Center for Advancing Translational Sciences, National Institutes of Health, through grant #UL1 TR000002.
Role of the Sponsor: The funding agency had no role in design and conduct of the study; in the collection, analysis, and interpretation of the data; or in the preparation, review, or approval of the manuscript.
Additional Contributions: Blythe Durbin-Johnson, PhD, provided statistical analysis. Ayan Patel, MS, performed set up of the REDCap database. Neither was compensated for their work on this project, but they were paid by the sponsor to provide statistical support.