Myocardial injury was common but mild and likely non-ischemic among hospitalized COVID-19 patients in New York City, researchers said.
Troponin elevations were observed in approximately 40% of 2,736 patients with lab-confirmed SARS-CoV-2 infection who had been admitted to one of five hospitals in the Mount Sinai Health System, according to the group led by Anuradha Lala, MD, of Icahn School of Medicine there in New York City.
Fewer than 20% of hospitalized COVID-19 patients had troponin over 0.09 ng/mL, but even people with such elevations had significantly higher mortality risk compared with those whose troponin results were within the reference range (adjusted HR 3.23, 95% CI 2.59-4.02). Only 2% of patients showed troponin levels exceeding 2 ng/mL, indicating severe injury.
The paper was released as a preprint on medRxiv and therefore has not undergone peer review.
“This is the first report to describe the prevalence of myocardial injury in COVID-19 in the USA. The findings are consistent with many reports from the Hubei province in China, and our observations from clinical practice in Europe,” according to Nicholas Mills, MD, PhD, of the University of Edinburgh in Scotland. Mills was not involved with the study.
“These results suggest abnormal troponin concentrations might be helpful with regard to triage decision-making. However, whether treatment strategies based on troponin concentrations would be expected to improve outcomes remains a testable hypothesis,” Lala’s team suggested.
“The take home from their findings is that although often the troponin elevation is mild, it is certainly a marker for an increased risk of mortality: here it seems to triple the risk of mortality with any troponin elevation, no matter how minor,” commented Martha Gulati, MD, MS, of the University of Arizona College of Medicine-Phoenix, in an email.
Based on the limited, observational data, she suggested that troponin be used as a marker of risk and that clinicians do whatever they can to reduce myocardial damage.
“Practitioners must be made aware of these findings,” said Robert Christenson, PhD, of the University of Maryland School of Medicine in Baltimore.
“In fact, they may wish to check their COVID-19 patientâs cardiac troponin levels, especially if the patient has comorbidities such as hypertension, diabetes or renal insufficiency,” he continued.
Similar to those reports, however, the investigators found COVID-19 patients with myocardial injury to be older and to have a history of cardiovascular disease, lower hemoglobin values, higher inflammatory markers, and more frequent rates of tachycardia, hypotension, or hypertension.
“This observation tends to support a theory that troponin elevation associated with COVID-19 is more likely to be consistent with non-ischemic myocardial injury as opposed to dramatic acute coronary syndrome or myocarditis,” study authors wrote.
“Possible mechanisms by which COVID-19 leads to cardiovascular morbidity include direct myocardial injury as a result of the inflammatory cascade or cytokine release, acute coronary syndrome from acute inflammation-triggered destabilization of atheromas, microvascular damage due to disseminated intravascular coagulation and thrombosis, direct entry of SARS-CoV-2 into myocardial cells by binding to ACE2 receptors, and hypoxemia combined with increased metabolic demands of acute illness leading to myocardial injury akin to Type 2 MI,” they added.
For their retrospective cohort study, the investigators analyzed the EHR records of COVID-19 patients who had been admitted from Feb. 27 to April 12 of this year. All had at least one troponin I measurement within 24 hours of admission.
Median age was 66.4 years, with 40.7% of patients over age 70. Men accounted for approximately 60% of the cohort.
Besides the lack of peer review, the study was limited by the fact that some patients were still in the hospital at the time of data collection.
“Many questions remain unresolved. In this series, cardiac troponin was measured on clinical indication, and therefore this cohort represents a selected group of higher-risk patients. The true prevalence of myocardial injury is likely to be substantially lower,” according to Mills.
He added that the mechanism of myocardial injury is still unknown.
“The authors suggest it largely reflects pre-existing cardiovascular disease or non-ischemic injury. Whilst that may well be the case, two-thirds of patients with more substantial troponin elevations did not have known heart disease and the authors did not report even the most basic of cardiac investigations, the 12-lead electrocardiogram, in support of this hypothesis,” Mills told MedPage Today.
Mild elevations in cardiac troponin are, in most cases, the result of the combination of pre-existing cardiac disease and acute myocardial injury or stress related to severe illness among patients hospitalized with COVID-19 or other pneumonias, according to Christian Mueller, MD, PhD, of University Hospital Basel, Switzerland.
“In patients with COVID-19 or other pneumonias who are not critically ill, cardiac troponin concentrations maintain high diagnostic accuracy for acute MI, as most patients with acute MI show higher cardiac troponin concentrations at presentation versus those concentrations observed with COVID-19,” Mueller noted.
“Although it is early, the cardiac troponin evidence presented in this manuscript strongly suggests that COVID-19 patients are likely at particularly high risk for cardiac and cardiovascular sequelae. More work, including a properly designed clinical trial in this area should be conducted in my opinion,” Christenson said.
Last Updated April 29, 2020
The study was supported by a grant from the National Center for Advancing Translational Sciences.
Lala reported no conflicts of interest.
Several co-authors disclosed ties to industry.