The Impact of Troponin Levels on the Care of COVID-19 Patients

In this Q&A, James L. Januzzi, Jr, MD, director of the Dennis and Marilyn Barry Fellowship in Cardiology Research at Massachusetts General Hospital Corrigan Minehan Heart Center, discusses cardiac injury in COVID-19 patients and what elevated troponin and other biomarker levels can tell providers about the prognosis of and care for their patients.

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Q: What trends have you seen in troponin levels of COVID-19 patients?

Januzzi: Cardiac injury—reflected in abnormal troponin concentrations—is seen in some patients with COVID-19. Determining the level of cardiac injury relates to the severity of illness. Overall, about 20% of patients with COVID-19 have evidence of cardiac injury, but if you look at sicker patients in the ICU, this number rises to nearly all patients.

Why this occurs is not entirely clear, and is probably multifactorial. Respiratory illnesses besides COVID-19, including seasonal influenza, have also been shown to cause cardiac injury in severe cases, so it may be a non-specific indicator of disease severity. After all, if the lungs and kidneys are injured, shouldn't the heart be allowed to express its suffering?

That said, there may be other reasons why injury occurs. For example, direct myocardial infection by the SARS-CoV-2 virus might lead to this finding. Additionally, since COVID-19 has been linked to a risk of clot formations, perhaps a small percentage of patients may have in situ thrombosis involving their coronary vessels leading to an acute myocardial infarction (MI).

Notably, an elevated troponin level and a related cardiac biomarker NT-proBNP, which detects heart muscle stress and is also abnormal in COVID-19, is an independent predictor of worse outcomes in COVID-19.

Regardless of the mixed-bag of reasons why myocardial injury may be occurring, one thing is clear: most of these patients do not have an acute MI. Thus, we need to be very cautious about how we interpret troponin concentrations in patients with COVID-19, since a mistaken diagnosis of acute MI is not something anyone wants in this setting.

Q: What impact does COVID-19 have on the cardiovascular system in general?

Januzzi: The primary effect on the myocardium has to do with multiorgan system stress that severe COVID-19 may cause. This may be so severe that it causes cardiomyopathy with accompanying heart failure.

Additionally, direct injury to the myocardium related to myocarditis might occur in some patients with COVID-19, as might so-called "stress cardiomyopathy," an unusual and reversible weakening of the heart muscle. A small number of patients may develop an MI, but the true number of patients suffering from MI remains unclear.

In some patients, irregular heart rhythms may occur. These include atrial fibrillation and more worrisome arrhythmias such as ventricular tachycardia. The latter may be exacerbated by the use of hydroxychloroquine, one of the therapies used in an effort to treat COVID-19.

Lastly, and of particular concern, we simply don't know the chronic, long-lasting effects of recovered COVID-19 on the heart. Will this lead to longer-term increases in heart failure or other cardiovascular diagnoses? Right now, no one can say.

Q: Do elevated troponin levels have an impact on their prognosis and likelihood of survival?

Januzzi: Yes, elevated troponin and NT-proBNP concentrations both predict a worse prognosis. Higher values for either suggests a lower likelihood for survival. Of course, this is not an all-or-nothing finding, and many patients with abnormal cardiac biomarker levels recover, but measurement of troponin and NT-proBNP have become part of our routine risk stratification profile for patients we evaluate with COVID-19. These data are interpreted within the full context of the clinical picture, and not used as a stand-alone test.

Q: Has the link between positive troponin and mortality in COVID-19 patients led to any changes in how Mass General tests and treats those patients?

Januzzi: We do use troponin and NT-proBNP to evaluate our patients with COVID-19 and to judge their risk, however, it is critical to point out we use them as part of a complete clinical evaluation strategy. Also, there is not a single therapy that has been shown to specifically benefit patients based on their troponin or NT-proBNP, so we do not alter therapy solely on the basis of these biomarkers.

Q: Is there anything else on this topic that you'd like to add?

Januzzi: In my capacity as a Trustee of the American College of Cardiology, I was responsible for the writing of the early position of the College regarding the use of biomarker measurements in patients with COVID-19. Our early position, as it remains today, is that clinicians must be aware that COVID-19 is associated with myocardial injury, and that the vast majority of this injury is not related to acute MI. We emphasize while troponin (and NT-proBNP) measurement may be useful as tools to inform prognosis among patients with the diagnosis of COVID-19, they are to be used with the knowledge that these patients do not necessarily need to be taken urgently to the cath lab as a patient with an acute MI might be treated.

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