Already established for the assessment of people with suspected acute coronary syndrome (ACS), cardiac troponin also predicted coronary events in people with symptoms suggestive of stable angina, the MICA group showed.
Sampled just before diagnostic outpatient angiography, high-sensitivity cardiac troponin I (hs-cTnI) results tracked with the presence of angiographically proven coronary artery disease (CAD) and subsequent myocardial infarction (MI) or cardiovascular death:
No CAD: troponin 1.9 ng/LCAD with no event: 3.3 ng/LCAD with an event: 6.7 ng/L
Troponin concentrations were associated with the primary outcome after adjusting for cardiovascular risk factors and CAD severity (adjusted HR 2.3, 95% CI 1.7-3.0), reported Nicholas Mills, MD, PhD, of University of Edinburgh and the Royal Infirmary of Edinburgh in Scotland.
Moreover, troponin>10 ng/L was the threshold that identified patients with a 50% increase in the risk of MI or cardiovascular death over a median follow-up of 2.4 years, the authors showed in the Journal of the American College of Cardiology.
“Together these findings suggest that routine cardiac troponin testing could provide important additional information to guide the management of patients with chronic CAD,” they wrote, noting that the role of troponin testing in diagnosing chronic disease itself is “likely to be limited.”
It is possible that routine testing could inform the selection of high-risk patients for treatment intensification, such revascularization or a short period of dual antiplatelet therapy, Mill’s group suggested. “Randomized trials are needed to evaluate whether routine cardiac troponin testing to guide the management of patients with chronic CAD can reduce major adverse cardiovascular events.”
For now, routine troponin testing is not recommended for people with chronic CAD despite studies showing its prognostic value in some people with asymptomatic heart disease or heart attack survivors.
Recently updated American recommendations give a class I endorsement for revascularization to improve symptoms in patients with lifestyle-limiting angina despite guideline-directed medical therapy and with coronary stenoses amenable to revascularization.
“Current risk stratification strategies for patients with chronic CAD primarily focus on the identification of obstructive disease and revascularization targets using anatomical and functional imaging. However, one-half of all MIs occur in patients with nonobstructive coronary disease who typically do not have the ischemic substrate on functional testing to effectively guide risk stratification,” Mills and colleagues argued.
In their report, angiography revealed CAD in 92% of the symptomatic cohort: 32% with nonobstructive disease and 68% with obstructive disease.
“The role of cTn continues to evolve beyond ACS, with emerging data such as in MICA supporting its application as a risk-stratification tool in patients with CCS [chronic coronary syndrome]. Although more data are needed to understand how to use this prognostic information to improve outcomes, the measurement of hs-cTn in patients with chronic CAD may serve multiple functions,” agreed Yader Sandoval, MD, of Minneapolis Heart Institute, Abbott Northwestern Hospital, and Allan Jaffe, MD, of Mayo Clinic in Rochester, Minnesota.
“Recognizing that increasing severity of angina is associated with worse outcomes because of more adverse anatomy, it may be that hs-cTn is beneficial in higher-risk patients with more symptoms rather than in those with mild or no symptoms,” they noted in an accompanying editorial.
For the study, the MICA investigators had prospectively enrolled a cohort of consecutive patients with suspected stable angina who were scheduled for outpatient coronary angiography from 2016 to 2021. They had hs-cTnI measured, but their clinicians were blinded to the results so as not to alter the course of subsequent clinical care.
Participants were 4,240 individuals averaging age 66, with one in three being women. Most were already on lipid-lowering and antiplatelet therapy.
Ultimately, 6% had primary outcome events over follow-up.
This study cohort may not represent the full spectrum of chronic CAD, the investigators cautioned. They added that external validation of the results is needed in other settings, and that they did not evaluate changes in cardiac troponin over time.
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Nicole Lou is a reporter for MedPage Today, where she covers cardiology news and other developments in medicine. Follow
Disclosures
The study was funded by a grant from the British Heart Foundation and supported by DataLoch, which is funded by the Data Driven Innovation programme within the Edinburgh and South East Scotland City Region Deal.
Mills was supported by awards from the British Heart Foundation and has received honoraria from Abbott Diagnostics, Siemens Healthineers, Roche Diagnostics, and LumiraDx; and institutional research grants from Abbott Diagnostics and Siemens Healthineers.
Sandoval has been on advisory boards for Abbott Diagnostics, Roche Diagnostics, Philips, and Zoll; and holds patent 20210401347 (for machine learning models for ECG-based troponin assessment) along with others.
Jaffe has consulted for Abbott, Roche, Siemens, Beckman-Coulter, Ortho, Radiometer, Astellas, SpinChip, LumiraDx, and RCE Technologies; and holds patent 20210401347 along with others.
Primary Source
Journal of the American College of Cardiology
Source Reference: Wereski R, et al “High-sensitivity cardiac troponin for risk assessment in patients with chronic coronary artery disease” J Am Coll Cardiol 2023; DOI: 10.1016/j.jacc.2023.05.046.
Secondary Source
Journal of the American College of Cardiology
Source Reference: Sandoval Y and Jaffe AS “The evolving role of cardiac troponin: from acute to chronic coronary syndromes” J Am Coll Cardiol 2023; DOI: 10.1016/j.jacc.2023.05.047
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