Q&A: COVID-19 with elevated troponins

Q: I have a patient admitted with COVID-19 pneumonia and acute on chronic respiratory failure with hypoxia. The patient denied any chest pain. Routine chemistries revealed an elevated troponin level of 0.09; on repeat the level was 0.21 (reference range <0.10). The electrocardiogram (EKG) revealed sinus tachycardia with frequent premature atrial complexes (PAC) and nonspecific ST abnormality. Repeat EKGs revealed normal sinus rhythm (NSR), normal EKG. Subsequent troponin levels of 0.14 and 0.14.

The patient was seen by a cardiologist who documented, “Elevated troponin levels are frequent in patients with COVID-19 and significantly associated with fatal outcomes. Several mechanisms are associated with elevated troponin including viral myocarditis, cytokine driven myocardial damage, microangiopathy, and coronary artery disease [CAD]. Fortunately, the patient’s troponin level is declining. The EKG does not show a new wall motion abnormality.”

As there is a rise and fall in the troponin, should I query for the clinical significance of the elevated troponin offering Type 2 MI, demand ischemia without MI, other or clinically unable to determine? Or should I code this to elevated troponin (R77.8)?

A: What I recommend based on the information you’ve provided is to query to see if there’s a more specific diagnosis that can explain the clinical scenario. Let’s discuss the possible choices though. 

The first thing that I notice is that the patient did not demonstrate any signs of ischemia as evidenced by the cardiologist’s statement of “The echocardiogram does not show a new wall motion abnormality” along with your statement that “the patient denied any chest pain.”

With that said, let’s look at myocardial injury versus myocardial infarction as a possible diagnosis. Myocardial injury is discussed in the Fourth Universal Definitions of Myocardial Infarctions and states (emphasis added):

The term acute myocardial infarction should be used when there is acute myocardial injury with clinical evidence of acute myocardial ischemia and with detection of a rise and/or fall of cTn values with at least one value above the 99th percentile and at least one of the following:

• Symptoms of myocardial ischemia;
• New ischemic ECG changes;
• Development of pathological Q waves;
• Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology;
• Identification of a coronary thrombus by angiography or autopsy (not for type 2 or 3 MIs)

The Fourth Universal Definition for Myocardial Infarctions further states (emphasis added): “Criteria for myocardial injury: Detection of an elevated cTn value above the 99th percentile is defined as myocardial injury. The injury is considered acute if there is a rise and/or fall of cTn values.”

Lastly, regarding your suggestion of Type 2 MI, the Fourth Universal Definition for Myocardial Infarctions also states: “Type 2 MI and non-ischemic myocardial injury may coexist,” but goes on to further clarify that “few studies have compared the incidence and clinical features of type 2 MI versus myocardial injury without acute myocardial ischemia.”

Let’s switch over to the cardiologist’s comment regarding viral myocarditis. According to an article published in Heart Rhythm (emphasis added), “myocarditis is an inflammatory disease of the heart characterized by inflammatory infiltrates and myocardial injury without an ischemic cause. The most commonly identifiable cause of myocarditis in the United States and other developed countries is viral.”

The article continues saying,

Esfandiarei and McManus proposed that the pathophysiology of viral myocarditis is a combination of direct cell injury and T-lymphocyte–mediated cytotoxicity, which can be augmented by the cytokine storm syndrome. […] Despite being a minor cause of all viral myocarditis cases, human coronaviruses have been linked to myocarditis in patients of all age groups.

Treatment for myocarditis depends on the underlying cause.

With that said, I feel that it is prudent for you to present all the possible options and allow the physician to decide which, if any, are applicable. Based on the clinical scenario provided, possible choices are as follows:

• Acute myocardial injury secondary to: COVID-19, pneumonia, and acute on chronic respiratory failure
• Acute myocardial injury secondary to: Other; please specify in the progress notes
• Demand ischemia only secondary to: COVID-19, pneumonia, and acute on chronic respiratory failure
• Type 2 MI secondary to: COVID-19, pneumonia, and acute on chronic respiratory failure
• Cytokine release syndrome secondary to COVID-19, pneumonia, and acute on chronic respiratory failure
• Viral myocarditis secondary to COVID-19
• Other: Please specify in the progress notes
• Clinically unable to determine

Editor’s Note: Dawn Valdez, RN, LNC, CDIP, CCDS, CDI education specialist and CDI Boot Camp instructor for HCPro in Middleton, Massachusetts, answered this question. For information, contact her at dvaldez@hcpro.com. For information regarding CDI Boot Camps, click here.