Electrocardiographic abnormalities in COVID-19 patients visiting the emergency department: a multicenter retrospective study

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can be associated with myocardial injury, which have been described in various case reports, from acute myocarditis to pseudo acute myocardial infarction [1‐4]. Emergency departments (EDs) worldwide have been at the epicenter of COVID-19 pandemic [5]. Early identification of cardiac involvement in COVID-19 in patients presenting to the Emergency Department (ED) is crucial. Electrocardiogram (ECG), widely performed in the ED and costless, could be a useful tool. Bertini et al. analysed COVID-19 patients who died or were treated with invasive mechanical ventilation, and found that electrocardiogram (ECG) recorded at hospital admission was abnormal in 93% of the patients, with signs of acute right ventricular pressure overload (RVPO) in 30% of the patients [6]. However, they did not compare these ECG findings to those from patients with mild to moderate forms of COVID-19. Mccullough and al. performed a retrospective cohort study in patients with COVID-19 who had an ECG at or near hospital admission in a large New York City teaching hospital. Using a multivariable logistic regression model that included age, ECG, and clinical characteristics, they found that the presence of one or more atrial premature contractions, a right bundle branch block or intraventricular block, ischemic T-wave inversion and nonspecific repolarization increased the odds of death [7]. However, these findings from a population with high incidence of cardiovascular conditions may be of limited external validity. Thus, the aim of our study was to assess if specific ECGs patterns could be related to in-hospital mortality in COVID-19 patients presenting to the ED in a European country.

Our multicenter study of the ECGs performed at ED admission in 275 COVID-19 patients found that repolarization abnormities were frequent, whereas ST segment elevation was rare, as previously reported [7]. In our cohort, the patients were older than in another Asian cohort [9], and our patients had lower prevalence rates of cardiovascular comorbidities than the North American cohorts [8, 10]. However, the baseline characteristics of COVID-19 patients reported here were consistent with those observed in French EDs during the first wave of COVID-19 pandemic [11]. Compared to a cohort of patients with community-acquired pneumonia (CAP), our population had similar age but with less cardiovascular risk factors [12]. Nonetheless, the comparison should be made with caution, regarding the impact of cardiovascular comorbidities in both COVID-19 and CAP.

In our multivariable logistic regression model, the presence of abnormal axis and LBBB were associated with in-hospital mortality. Finding early signs of cardiac impairment is extremely valuable in prioritizing ED patients, and our results suggest that ECG, widely performed in the ED and at no cost, is a useful tool in the ED assessment of COVID-19 patients. Mccullough and al. previously reported that ischemic T-wave inversion was associated with an increased risk of death in patients with COVID-19 who had a ECG at or near hospital admission [7]. Moreover, Lombardi et al. reported that elevated troponin was an independent variable associated with in-hospital mortality and a greater risk of complications during hospitalization for COVID-19 [13]. Myocardial involvement in COVID-19 is supported by pathological finding of interstitial inflammatory mononuclear cells in heart tissue during autopsy [14]. But the specific involvement of SARS-CoV2 is unclear in the underlying cardiac pathogenicity. Importantly, similar patterns have been found in CAP, where cardiovascular disease (CVD) events have been reported to be frequent [15‐17] and ECG changes are often seen, with frequent ST segment or T-wave abnormalities [18]. Hypoxia, hypotension or decreased cardiac output could be one of the non-specific explanotary factors. Animal models have previously suggested that bacterial infections may lead to apoptosis of cardiomyocytes through direct and indirect toxicity of S. pneumoniae [19]. Violi et al. suggested that Nox2 related oxidative stress could explain myocardial damage [20]. Complex interactions through direct cardiomyocyte invasion and indirect inflammatory-mediated damage could explain cardiac involvement in COVID-19 [21]. Myocardial injuries have been described in various case reports, from acute myocarditis to pseudo acute myocardial infarction [1‐4, 22], and several studies highlight an association between cardiac injuries and mortality [23‐26]. Other studies suggested that abnormal heart rhythms are common [7, 13, 27]. But relationship between these findings and COVID-19 infection should be made with caution, as in an unselected population of healthy adults, inverted T waves in the anterior and lateral leads have been shown to be associated with long-term risk of mortality from CVD event [28]. A prospective cohort of patients with COVID-19 infection and ECG abnormalites should assess long-term cardiovascular consequences of COVID-19.

Our study has some limitations. First, because of its retrospective design, data were missing in both biological data and comorbidities, especially regarding troponin level which was available in only 171 patients. As symptoms onset was also unknown, this prevented us from doing any survival curve analysis. Since ECGs were not performed in every patient, it is possible that more severe patients had ECG analyses, therefore inducing a selection bias explaining the high mortality rate in our patients. Second, when the ECG was abnormal, it was not possible to determine if those abnormalities were related to the COVID-19 infection or to a previous unknown cardiopathy. Third, the ECG were interpreted by two emergency physicians or an emergency physician and a cardiologist, it is possible that some subtle ECG findings have been missed. However, previous studies suggested that most ED misinterpretations were determined unlikely to have clinical significance [29, 30]. Moreover, centralized ECG reading by cardiologists is not feasible in most hospitals. Fourth, echocardiography or cardiovascular magnetic resonance were not performed in all included patients for evaluation of heart involvement.

In a multicenter study, we reported that ECG performed at ED admission may be useful to predict severity and death in COVID-19 patients. Our data suggest that the presence of abnormal axis and LBBB on ECG at ED admission indicated a higher risk of death. We also confirmed that ST segment elevation at ED presentation was rare in COVID-19 patients. A prospective study should be performed to evaluate the monitoring of ECG in COVID-19 prognosis, and if ECG abnormalities detected during COVID-19 infection is a risk factor for subsequent CVD event.