January 06, 2020
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High-sensitivity cardiac troponin may not exclude myocardial ischemia

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Joan Walter

Very low concentrations of high-sensitivity cardiac troponin did not allow the safe exclusion of inducible myocardial ischemia, according to a study published in the Annals of Internal Medicine.

“While being integral to the diagnosis of acute myocardial infarction, circulating cardiac troponin I or T concentrations, even when measured with the most sensitive assays, cannot be used to exclude the presence of inducible myocardial ischemia in symptomatic patients with known coronary artery disease,” Joan Walter, MD, PhD, resident at the Cardiovascular Research Institute at University Hospital Basel in Switzerland, told Healio. “Contrary to acute myocardial infarction, we have to face the reality that in the clinically much more common phenotype of stable coronary artery disease, a single marker strategy is not and might never be available to aid clinical decision-making.”

CAD with potential myocardial ischemia

Researchers analyzed data from 1,896 patients (median age, 69 years; 19% women) with CAD who had symptoms potentially related to inducible myocardial ischemia. Typical symptoms were defined as thoracic chest discomfort or pain provoked by emotional stress or exertion that can be relieved by nitroglycerin or rest.

Patients were referred for rest and stress myocardial perfusion imaging. Questionnaires were also completed by patients to collect information on medications, characteristics, CV history and symptoms. Blood samples were taken to measure high-sensitivity cardiac troponin I and T assays.

Researchers decided upon predefined target performance criteria of at least 90% for negative predictive value and at least 90% for sensitivity to exclude inducible myocardial ischemia.

Follow-up was conducted by phone or in writing after 1 year, 2 years and 5 years, during which major adverse cardiac events were documented including nonfatal acute MI, CV death and coronary revascularization.

Of the patients in the study, 46% had inducible myocardial ischemia. A predefined high-sensitivity cardiac troponin I cutoff of 2.5 ng/L resulted in a negative predictive value of 70% (95% CI, 64-75) and a sensitivity of 90% (95% CI, 88-92) to exclude inducible myocardial ischemia.

Target performance was not achieved when alternative assays for high-sensitivity cardiac troponin I and T were used. A high-sensitivity cardiac troponin T concentration less than 5 ng/L led to a negative predictive value of 66% (95% CI, 59-72). A concentration less than 2 ng/L for high-sensitivity cardiac troponin I resulted in a negative predictive value of 68% (95% CI, 62-74).

“To address the major unmet clinical need of a safe, easy and affordable risk stratification strategy for patients with suspected inducible myocardial ischemia, multi-marker strategies should be further explored,” Walter said in an interview. “A single marker, including cardiac troponin or brain natriuretic peptide, seems to be unable to provide sufficient objective information concerning the potential presence of inducible ischemia.”

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Remaining questions

In a related editorial, Katy J.L. Bell, MBChB, MMed(Clin Epi), PhD, senior research fellow at the University of Sydney, and colleagues wrote: “Walter and colleagues conclude that high-sensitivity cardiac troponin concentrations cannot safely exclude inducible myocardial ischemia, and by implication stable obstructive CAD, but the bigger question is whether it needs to be excluded in the first place. Rather, should the focus of testing in patients with stable CAD be on safely ruling out significant pathology, such as left main artery disease (revascularization likely to have net benefit), while preventing unnecessary invasive tests and interventions (likely to have net harm) in most patients? Whether high-sensitivity cardiac troponin has a role in such a triage process remains unclear.” – by Darlene Dobkowski

For more information:
Joan Walter, MD, PhD, can be reached at joanelias.walter@usb.ch.

Disclosures: Walter reports he received grants from the Swiss Academy of Medical Sciences and the Swiss Heart Foundation. The authors of the editorial report no relevant financial disclosures. Please see the study for all other authors’ relevant financial disclosures.