In response to a recent American College of Cardiology (ACC) review that advocated that troponin should only be measured when a diagnosis of acute myocardial infarction is being considered, Andrew R Chapman (BHF Centre for Cardiovascular Science, Royal Infirmary of Edinburgh, Edinburgh, UK) and colleagues argue in Circulation that high-sensitivity cardiac troponin “could actually be an ally in the fight against COVID-19”. They add that the biomarker is a “crucial diagnostic and prognostic aid in what will become even more challenging times for healthcare provision worldwide”.
Chapman et al note that the rationale for the ACC’s recommendation to not use troponin testing unless an acute myocardial infarction is suspected is on the “basis that troponin elevation in patients with COVID-19 is likely to be multifactorial and less likely to be due to atherothrombotic coronary occlusion”. However, commenting that circulating cardiac troponin is a marker of myocardial injury,
the authors state: “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 for prognosis and clinical decision making.”
According to Chapman et al, recent studies have indicated that troponin is elevated in one in five patients who have (confirmed) COVID-19 and that the presence of elevated troponin in COVID-19 may be associated with a higher mortality risk. COVID-19 patients with elevated troponin may also be more likely to require ventilation (non-invasive or invasive) and develop acute respiratory distress syndrome. “The observed rate of mortality was 10-fold higher in those with myocardial injury on presentation [and who had elevated troponin],” the authors report. They add: “If clinicians are reluctant to measure cardiac troponin in these patients, the consequences may be to ignore the plethora of ischaemic and non-ischaemic causes of myocardial injury related to COVID-19, which may be directly or indirectly associated with poor outcomes.”
Another benefit of troponin testing, Chapman et al say, is that it is “one of the earliest and most precise indicators of end-organ dysfunction”. “Here, cardiac troponin testing could prompt early initiation of measures to improve tissue oxygenation and perfusion,” they explain.
The authors do acknowledge testing troponin in COVID patients “could increase the need for cardiology consultation and downstream testing, including bedside echocardiography and angiography”. However, they comment: “The recognition of a normal or modestly elevated troponin could conversely reduce the need for cardiac imaging and minimise the risk of exposure to cardiac physiology staff. The role of further investigation must be carefully considered and based on risk to the individual performing the test and the likelihood of informing clinical management.”
Summing up their case for increasing, rather than decreasing, the use of troponin testing, Chapman et al comment that “clinicians must recognise that troponin is not a test for myocardial infarction, and it never was”. They add that the “myth” that it had the ability to detect an acute atherothrombotic occlusion in a coronary artery is limiting physicians’ ability to “evaluate and triage care in critically unwell patients” and argue “we need more, rather than, less information to guide the international response to the COVID-19 patients”. They conclude: “Troponin should be considered an ally and a crucial diagnostic and prognostic aid in what will become even more challenging times for healthcare professionals worldwide.”
Study author Nicholas Mills (BHF Centre for Cardiovascular Science, Royal Infirmary of Edinburgh, Edinburgh, UK), who is an interventional cardiologist and a British Heart Foundation (BHF) funded professor of cardiology, told Cardiovascular News: “Cardiologists around the world are having to rapidly learn how to assess patients with COVID-19, either because they are being drafted into the general medical service or because these patients are also presenting directly to the coronary care unit with cardiac complications of the condition. Cardiac troponin is the most sensitive and most widely available test to determine whether there is cardiac involvement or not. It does not tell us the mechanism of injury, but it is a good place to start and can help 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.”