Myocardial injury during COVID-19 hospitalization tied to mortality, long-term symptoms
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Among patients hospitalized with COVID-19, myocardial injury as determined by high-sensitivity cardiac troponin T was linked to mortality and ongoing COVID-19 symptoms, researchers reported.
Brittany Weber, MD, PhD, cardiologist at Brigham and Women’s Hospital and instructor in medicine at Harvard Medical School, and colleagues conducted a prospective analysis of 483 patients (median age, 63 years; 51% women) who were admitted to Brigham and Women’s Hospital for COVID-19 and had high-sensitivity cardiac troponin T measured (Elecsys 2010 system, Roche Diagnostics) at admission from March to May 2020.
During the index hospitalization, 18.8% of patients died, 14.4% had thrombotic complications and 25.6% had CV complications, whereas at 1 year, 22.2% died, Weber and colleagues found.
Cardiac injury, defined as high-sensitivity cardiac troponin T of at least 14 ng/L, occurred in 62.3% of the cohort during index hospitalization, according to the researchers.
Cardiac injury and mortality
Patients with cardiac injury had higher rates of mortality at index hospitalization (28.6%) compared with those with low-level positive troponin (4.1%) and those with undetectable troponin (0%), Weber and colleagues wrote.
Similar mortality rates were observed at 6 months (cardiac injury, 32.2%; low-level positive troponin, 4.9%; undetectable troponin, 0%) and at 12 months (cardiac injury, 33.2%; low-level positive troponin, 4.9%; undetectable troponin, 0%), according to the researchers.
After adjustment for age, sex, CAD, hypertension, hyperlipidemia, HF and diabetes, cardiac injury was associated with elevated risk for mortality compared with undetectable troponin (HR = 13.76; 95% CI, 1.85-102.3; P = .01), but there was no difference in mortality risk between low-level positive troponin and undetectable troponin (HR = 2.31; 95% CI, 0.27-19.48; P = .44).
During index hospitalization, those who had 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 with those who did not, according to the researchers.
Among the 392 patients who survived their index hospitalization, 24% were readmitted at least once within 1 year and 65% of those patients had myocardial injury during index hospitalization, Weber and colleagues found.
Readmission within 1 year was more common in patients with cardiac injury compared with low-level positive troponin and undetectable troponin (64.9% vs. 21.3% vs. 13.8%, respectively; P = .01), but the difference was not significant after multivariable adjustment (HR = 1.5; 95% CI, 0.8-2.5; P = .23).
Ongoing symptoms
Among the 211 patients who were alive at 6 months and had a detailed clinical assessment at that time, 37% had ongoing COVID-19-related symptoms, 16.1% had neurocognitive decline, 3.8% required increased supplemental oxygen and 19.9% had worsening functional status, according to the researchers.
The presence of ongoing COVID-19-related symptoms at 6 months was more common in patients with cardiac injury compared with low-level positive troponin and undetectable troponin (56.4% vs. 30.7% vs. 12.8%, respectively), but the difference did not reach statistical significance, Weber and colleagues wrote.
“This study provides unique insights into the relationship between cardiovascular injury during the index hospitalization for patients with COVID-19 and longer-term outcomes,” Weber and colleagues wrote. “Patients with evidence of myocardial injury during index hospitalization had an increased risk of cardiac, thrombotic and infectious complications during the hospitalization and all-cause mortality. Furthermore, these patients had higher rates of hospital readmissions and post-acute sequelae of COVID-19 at 6 months, although this was not statistically significant. An additional unique aspect of our cohort findings is that even among those patients with positive troponins during their index hospitalization, the incremental mortality at 6 months and 1 year among COVID-19 survivors was low. These data suggest that patients who are hospitalized with COVID-19, even if critically ill, but survive the index hospitalization are likely to survive up to 1 year. Whether this trend is observed longer-term is not known and will be an important question to investigate as we gather longer-term data.”
Perspective
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Allan S. Jaffe, MD
There is a ton of information already out there confirming that patients with COVID-19 and elevated troponin indicative of myocardial injury have a prognosis that is substantially worse.
The potential benefit of this study, which was unfortunately not leveraged in the publication, is that it had serial samples. However, the analysis was performed using just the highest troponin value, which could be at admission, early on or later on. The ability to know when that value occurred is key. If there was a signal on day 1 that could be mined, that is very different from a signal late in the course when people are critically ill. In addition, it is very likely that many of these patients, because they had underlying CVD, had troponin increases on admission as a manifestation of their underlying CVD, which may have nothing to do with COVID-19.
This timing issue is nontrivial, but in fairness to the authors, it has been an issue with many such studies, and is one of the reasons why many have usually focused on just the admission samples, and why these authors may have decided to just use the maximum value. That maximum value in a group of patients who are apt to get sick can get very complicated. A study published in February (Metkus TS, et al. Circulation. 2021;doi:10.1161/CIRCULATIONAHA.120.050543) suggested that if you compare patients with COVID-19 to a group of individuals who are critically ill with acute respiratory failure of another etiology, they look remarkably similar. We know that critically ill people end up getting troponin elevations indicating myocardial injury. There may not be much difference between COVID-19 and some of these other disease entities because both concern critical illness, which seems more apt to occur in patients with underlying CVD for reasons we are not really sure about, one of which may be related to the ACE2 receptor. Critical illness could exaggerate the role troponin might play. There is a signal that has been observed in many studies. The question is, can you use that signal? If it was on day 1, maybe you can. The key question is whether the change in troponin came before any of the clinical events occurred, so troponin could be used to guide management of the patient.
My suspicion is that the troponin changes did come before clinical events in this study. But we do not know for sure because that sort of analysis was not included. My group has advocated for measuring troponin serially, and when there is a change, anticipating that it is likely that something bad is happening to your patient, and to be on alert for that whether it is clinically manifest or not. We have not proven that yet, unfortunately. But we think this is the best way to use troponin to manage patients with COVID-19. Low troponin values identify a low-risk group, which is probably helpful in a different sense. The high-risk group is likely to get in trouble if they have an elevated troponin level on admission. One could argue that their serial troponin measurements will likely track with the clinical disease, in particular if it is earlier in the clinical disease, which means it would be very valuable in anticipating that there might be a problem, and one could surveil those individuals more closely and potentially intervene when one identifies the problem that is being marked. But this point is not yet clear from any of the literature that we have.
It is also not surprising that those with increases in cardiac troponin had more downstream admissions; it is likely they had more severe CVD. How much COVID-19 contributed is unclear.
What would be helpful would be to analyze serial samples. We know having an elevated troponin on admission is a risk factor. The question is what is the incremental value of measuring troponin more comprehensively throughout the hospitalization — do increases really presage subsequent complications, as I hypothesized? If they do, as is our bias, serial troponin measurements become very valuable. These patients are often left alone because they are in quarantine of some sort, so having a leg up in terms of the timing of complications because of information from troponin testing would be very important. The authors know troponin, so my guess is that since it was not mentioned in the publication, they did not see that.
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