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APRIL 15, 2020 -- Cardiac troponins by high-sensitivity assays (hs-cTn) should be considered "an ally and a crucial diagnostic and prognostic aid" during the COVID-19 pandemic, cardiologists in the United Kingdom advise in a recently published viewpoint.
The tests can be used to "inform the triage of patients to critical care, guide the use of supportive treatments, and facilitate targeted cardiac investigations in those most likely to benefit, Nicholas Mills, MD, PhD, University of Edinburgh, United Kingdom, told theheart.org | Medscape Cardiology. He is senior author on the viewpoint published online April 6 in the journal Circulation.
Older adults and those with a history of underlying cardiovascular disease appear to be at greatest risk of dying from COVID-19. "From early reports it is clear that elevated cardiac troponin concentrations predict in-hospital mortality," said Mills.
In a recent report on hospitalized patients with COVID-19 in Wuhan, China, for example, cardiac injury (hs-cTn above the 99th-percentile upper reference limit) was seen in 1 in 5 patients and was an independent predictor of dying in the hospital. Mortality was 10-fold higher in those with cardiac injury on presentation.
Elevated cardiac troponin in the setting of COVID-19, Mills said, "may reflect illness severity with myocardial injury arising due to myocardial oxygen supply–demand imbalance. Or it may be due to direct cardiac involvement through viral myocarditis or stress cardiomyopathy, or where the prothrombotic and proinflammatory state is precipitating acute coronary syndromes."
In their viewpoint, the authors note that circulating cTn is a marker of myocardial injury, "including but not limited to myocardial infarction or myocarditis, and the clinical relevance of this distinction has never been so clear."
Therefore, the consequence of not measuring cardiac troponin may be to "ignore the plethora of ischemic and nonischemic causes" of myocardial injury related to COVID-19. "Clinicians who have used troponin measurement as a binary test for myocardial infarction independent of clinical context and those who consider an elevated cardiac troponin concentration to be a mandate for invasive coronary angiography must recalibrate," they write.
"Rather than encouraging avoidance of troponin testing, we must harness the unheralded engagement from the cardiovascular community due to COVID-19 to better understand the utility of this essential biomarker and to educate clinicians on its interpretation and implications for prognosis and clinical decision making.
Based on "Same Logic" as Recent ACC Guidance
The viewpoint was to some extent a response to a recent informal guidance from the American College of Cardiology (ACC) that advised caution in use of troponin and natriuretic peptide tests in patients with COVID-19.
Even so, that ACC guidance and the new viewpoint in Circulation are based on the "same logic," James Januzzi Jr, MD, Massachusetts General Hospital, Boston, told theheart.org | Medscape Cardiology . Januzzi was the the author of the ACC article. Both documents:
Point out that troponins are frequently abnormal in patients with severe cases of COVID-19
Caution that clinicians should not equate an abnormal hs-cTn with acute myocardial infarction
Note that, in most cases, hs-cTn elevations are a result of noncoronary mechanisms
Recognize the potential risk to caregivers and the continued unchecked spread of SARS-CoV-2 related to downstream testing that might not be needed
"The Circulation opinion piece states that clinicians often use troponin as a binary test for myocardial infarction and a mandate for downstream testing, suggesting clinicians will need to recalibrate that approach, something I agree with and which is the central message of the ACC position," Januzzi said.
Probably the biggest difference between the two documents, he said, is in the Circulation authors' apparent enthusiasm to use hs-cTn as a tool to judge disease severity in patients with COVID-19.
It's been known for more than a decade that myocardial injury is "an important risk predictor" in critical illness, Januzzi explained. "So the link between cardiac injury and outcomes in critical illness is nothing new. The difference is the fact we are seeing so many patients with COVID-19 all at once, and the authors suggest that using troponin might help in triage decision making."
"There may be [such] a role here, but the data have not been systematically collected, and whether troponin truly adds something beyond information already available at the bedside — for example, does it add anything not already obvious at the bedside? — has not yet been conclusively proven." Januzzi cautioned.
"As well, there are no prospective data supporting troponin as a trigger for ICU triage or for deciding on specific treatments."
Positive cTn Status "Common" in COVID Patients
In his experience, Barry Cohen, MD, Morristown Medical Center, New Jersey, told theheart.org | Medscape Cardiology, that positive cTn status is "common in COVID-19 patients and appears to have prognostic value, not only in type 1 MI due to atherothrombotic disease (related to a proinflammatory and prothrombotic state), but more frequently type 2 MI (supply–demand mismatch), viral myocarditis, coronary microvascular ischemia, stress cardiomyopathy or tachyarrhythmias."
Moreover, Cohen said, hs-cTn "has identified patients at increased risk for ventilation support (invasive and noninvasive), acute respiratory distress syndrome, acute kidney injury, and mortality."
Echoing both the ACC document and the Circulation report, Cohen also said hs-cTn measurements "appear to help risk stratify COVID-19 patients, but clearly do not mean that a troponin-positive patient needs to go to the cath lab and be treated as having acute coronary syndrome. Only a minority of these patients require this intervention."
Mills discloses receiving honoraria from Abbott Diagnostics, Roche Diagnostics, Siemens Healthineers, and LumiraDx. Januzzi has previously disclosed receiving personal fees from the American College of Cardiology, Pfizer, Merck, AbbVie, Amgen, Boehringer Ingelheim, and Takeda; grants and personal fees from Novartis, Roche, Abbott, and Janssen; and grants from Singulex and Prevencio. Cohen has disclosed no relevant financial relationships.
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