Infectious Disease

Myocardial injury during COVID-19 hospitalization associated with mortality, long-term symptoms

January 13, 2022

3 min read


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Weber does not report relevant financial information. The relevant financial information of all other authors can be found in the study.


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In patients hospitalized with COVID-19, myocardial injury, as determined by highly sensitive cardiac troponin T, was associated with mortality and persistent COVID-19 symptoms, the researchers reported.

Brittany Weber, MD, PhD, Cardiologist at Brigham and Women’s Hospital and Associate Professor of Medicine at Harvard Medical School and colleagues conducted a prospective analysis of 483 patients (mean age 63 years; 51% women) admitted to Brigham and Women’s Hospital for COVID-19 and at High suffering sensitivity of cardiac troponin T measured (Elecsys 2010 System, Roche Diagnostics) on admission from March to May 2020.

Graphical representation of the data presented in the article

Data were adapted from Weber B, et al. J Am Heart Assoc. 2021;doi:10.1161/JAHA.121.022010.

During the index hospitalization, 18.8% of patients died, 14.4% had thrombotic complications, and 25.6% had cardiovascular complications, while at 1 year 22.2% died, Weber and colleagues found.

Cardiac injury, defined as a high-sensitivity cardiac troponin T of at least 14 ng/L, occurred in 62.3% of the cohort during the index hospitalization, according to the researchers.

cardiac injury and mortality

Patients with cardiac injury had higher index hospitalization mortality rates (28.6%) compared to patients with weakly positive troponin (4.1%) and patients with undetectable troponin (0%), Weber and colleagues wrote.

Similar mortality rates were observed at 6 months (cardiac injury, 32.2%; low troponin positive, 4.9%; undetectable troponin, 0%) and 12 months (cardiac injury, 33.2%; low troponin positive, 4.9% ; low positive troponin, 4.9%; undetectable troponin, 0%) observed. undetectable troponin, 0%), the researchers said.

After adjusting for age, gender, CHD, hypertension, hyperlipidemia, heart failure, and diabetes, cardiac injury was associated with an increased risk of mortality compared to undetectable troponin (HR = 13.76; 95% CI, 1.85-102.3; p = 0.01). there was no difference in mortality risk between low positive troponin and undetectable troponin (HR=2.31; 95% CI, 0.27-19.48; p=0.44).

During the index hospitalization, those with cardiac injury were more likely to have infectious complications (adjusted OR = 7.6; 95% CI, 3.6-15.8), cardiac complications (aOR = 15.3; 95% CI, 6, 3-37.1) and thrombotic complications (aOR = 6; 95% CI, 2.8-13.2) compared to those who did not, the researchers said.

Of the 392 patients who survived their index hospitalization, 24% were readmitted at least once within a year, and 65% of these patients suffered myocardial injury during the index hospitalization, Weber and colleagues found.

Readmission within one year was more common in patients with cardiac injury than in those with low positive troponin and undetectable troponin (64.9% vs. 21.3% vs. 13.8%; p=0.01), but the difference was not significant adjustment after multivariable analysis (HR = 1.5; 95% CI, 0.8-2.5; P = 0.23).

Ongoing Symptoms

Of the 211 patients who were alive at 6 months and had a detailed clinical examination at that time, 37% had ongoing COVID-19-related symptoms, 16.1% had neurocognitive decline, 3.8% needed more supplemental oxygen, and 19.9% ​​had deteriorating functional status, the researchers said.

The presence of persistent COVID-19-related symptoms at 6 months was more common in patients with cardiac injury than in those with low positive troponin and undetectable troponin (56.4% vs 30.7% vs 12.8%), but the difference did it does not reach statistical significance, Weber and colleagues wrote.

“This study provides unique insights into the relationship between cardiovascular injury during index hospitalization for patients with COVID-19 and longer-term outcomes,” Weber and colleagues wrote. “Patients with evidence of myocardial injury during the index hospitalization had an increased risk of cardiac, thrombotic and infectious complications during the hospitalization and all-cause mortality. In addition, these patients had a higher rate of hospitalizations and post-acute episodes of COVID-19 at 6 months, although this was not statistically significant. Another unique aspect of our cohort results is that even for those patients with positive troponins during their index hospitalization, incremental mortality at 6 months and 1 year was low among COVID-19 survivors. These data suggest that patients hospitalized with COVID-19, even if critically ill, but survive the index hospitalization are likely to survive up to 1 year. Whether this trend persists over the longer term is unknown and will be an important question to investigate as we collect longer term data.”


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Allan S Jaffe, MD)

Allan S Jaffe, MD

There is already a body of information confirming that patients with COVID-19 and elevated troponin, indicative of myocardial injury, have a significantly poorer prognosis.

The potential advantage of this study, which unfortunately was not considered in the publication, is that there were serial samples. However, the analysis was performed only with the highest troponin level that could be present at admission, early, or late. The ability to know when that value occurred is key. If there was a signal on day 1 that could be dismantled, that’s very different than a signal late in the course when people are critically ill. In addition, it is highly likely that because many of these patients had underlying cardiovascular disease, they had troponin elevations on admission as a manifestation of their underlying cardiovascular disease, which may be unrelated to COVID-19.

This timing issue is not trivial, but to be fair to the authors, it has been an issue in many such studies and is one of the reasons many have typically focused only on the admissions samples and why these authors may have chosen only to use the maximum value. This maximum value in a group of patients who are prone to get sick can become very complicated. A study published in February (Metkus TS, et al. Circulation. 2021;doi:10.1161/CIRCULATIONAHA.120.050543) suggested that patients with COVID-19 be compared to a group of people who are critically ill and have acute respiratory failure suffering from a different etiology, they look remarkably similar. We know that seriously ill people end up with troponin elevations that indicate myocardial damage. There may not be much difference between COVID-19 and some of these other disease entities, as both affect critical illnesses that are more likely to occur in patients with underlying cardiovascular disease, for reasons we’re not really sure about, one of which is related could be the ACE2 receptor. Critical illness might exaggerate the role troponin might play. There is a signal that has been observed in many studies. The question is, can you use this signal? If it was on day 1, maybe you can. The key question is whether the troponin change occurred before any of the clinical events occurred such that troponin could be used to guide patient management.

My suspicion is that the troponin changes in this study preceded the clinical events. But we don’t know for sure because that kind of analysis wasn’t included. My group has advocated measuring troponin regularly and, if there is a change, assuming something bad is likely to happen to your patient and noting whether or not it is clinically manifested. Unfortunately, we haven’t proven that yet. However, we believe this is the best way to use troponin to treat patients with COVID-19. Low troponin levels identify a low-risk group, which is probably helpful in another sense. The high-risk group will likely run into trouble if they have elevated troponin levels upon admission. One could argue that their serial troponin measurements are likely to be consistent with clinical disease, especially if it occurs earlier in clinical disease, meaning it would be very valuable in anticipating that there might be a problem and one could better understand these individuals monitor closely and may intervene upon identifying the flagged issue. But this point has not yet become clear from the literature that we have.

It is also not surprising that those with increases in cardiac troponin had more downstream admissions; it is likely that they had more severe CVD. How much COVID-19 has contributed to this is unclear.

The analysis of serial samples would be helpful. We know that elevated troponin levels upon admission is a risk factor. The question is what is the incremental value of a more comprehensive troponin measurement throughout the hospital stay – do increases really indicate later complications, as I assumed? When this is the case, serial troponin measurements become very valuable, consistent with our bias. These patients are often left alone because they are in some form of quarantine, so having a head start on the timing of complications based on information from troponin tests would be very important. The authors know about troponin, so I’m guessing they haven’t seen it since it wasn’t mentioned in the publication.

Allan S Jaffe, MD

Member of the Editorial Board of Cardiology Today

Mayo Clinic, Rochester, Minnesota

Disclosure: Jaffe advises most troponin test manufacturers, including Roche Diagnostics.


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