|Year : 2021 | Volume
| Issue : 4 | Page : 227-232
Electrocardiographic findings in Coronavirus Disease-19 and its correlation with clinical severity of disease
Mumtaz Ali Khan, Anindita Menon, BS Nagaraja
Department of General Medicine, Bangalore Medical College and Research Institute, Bengaluru, Karnataka, India
|Date of Submission||04-Mar-2021|
|Date of Decision||19-Jun-2021|
|Date of Acceptance||26-Jul-2021|
|Date of Web Publication||20-Oct-2021|
Dr. Anindita Menon
001, Ansal Krsna 2, Hosur Road, Adugodi, Bengaluru - 560 030, Karnataka
Source of Support: None, Conflict of Interest: None
Background and Aims: Most data on electrocardiographic (ECG) changes in patients with coronavirus disease-19 (COVID-19) have been presented without comparison to patients with other acute respiratory illnesses. The correlation of ECG changes with disease severity has also not been studied. Subjects and Methods: We compared forty COVID-19-positive and forty COVID-19-negative patients in terms of clinical presentation, ECG at admission, and cardiac biomarkers. Statistical analysis was presented as frequency (percentage) and continuous as mean ± standard deviation. Chi-square test/Fischer's exact test was used. Results: Mean age overall in the study was 52.4 ± 16 years, 67.5% data were males. About 87.5% of the COVID-positive patients and 70% of the COVID-negative patients had ECG changes at baseline. Sinus tachycardia was seen in 45% (18/40) of COVID-positive patients. About 95% (38/40) of COVID-19 positive patients had normal axis, 5% (2/40) had supraventricular tachycardia, 2.5% (1/40) had premature atrial contractions (PACs), and 7.5% (3/40) had premature ventricular contractions. One patient had ventricular bigeminy. About 7.5% (3/40) of COVID-positive cases had complete right bundle branch block (RBBB), one had complete left bundle branch block (LBBB), whereas one had incomplete LBBB. About 7.5% (3/40) of COVID-positive cases had ST-segment elevation, one of whom also developed postmyocardial infarction left ventricular thrombus. About 15% (6/40) had nonST-segment elevation acute coronary syndrome. Conclusions: COVID-19 patients have ECG changes of left-sided heart disease (PACs and LBBB) and right-sided disease (RBBB, right axis deviation, and right ventricular strain pattern) at presentation, however, right heart changes predominate. COVID-19 patients had a higher occurrence and a wider variety of ECG changes at presentation than other acute respiratory illnesses and these changes correlate well with clinical disease severity as does troponin I level.
Keywords: Coronavirus disease-19, severe acute respiratory syndrome, coronavirus 2, electrocardiography, troponin
|How to cite this article:|
Khan MA, Menon A, Nagaraja B S. Electrocardiographic findings in Coronavirus Disease-19 and its correlation with clinical severity of disease. APIK J Int Med 2021;9:227-32
|How to cite this URL:|
Khan MA, Menon A, Nagaraja B S. Electrocardiographic findings in Coronavirus Disease-19 and its correlation with clinical severity of disease. APIK J Int Med [serial online] 2021 [cited 2021 Nov 29];9:227-32. Available from: https://www.ajim.in/text.asp?2021/9/4/227/328672
| Introduction|| |
Coronavirus disease-19 (COVID-19) can result in many cardiovascular complications including acute myocardial injury, myocarditis, arrhythmias, and venous thromboembolism.
The virus has a tropism for the angiotensin-converting enzyme 2 receptor, found in the heart and lungs. Hypoxemia, a surge of cytokine levels, and myocardial oxygen demand-supply mismatch may injure myocardial cells., Acute plaque rupture can occur due to the increased plaque vulnerability resulting in acute coronary syndrome.
The case fatality rate for COVID-19 patients is 2.3%, while for individuals with cardiovascular disease, the risk is 10.5%.
There is a need for markers to help clinicians prognosticate the disease. Most reports have not described the presentation of patients with acute respiratory illness who tested negative for COVID-19. Without control patients, it is uncertain whether electrocardiographic (ECG) changes in COVID-19 presents differently from other respiratory infections.
| Subjects and Methods|| |
The source population was in-patients of the General Medicine Department.
This study was a retrospective cohort study.
The study period was March 2020–November 2020.
The sample size was a minimum of 80 patients.
- Patient/attender willing to give informed consent
- Patient of either sex with age ≥18 years
- Patients having acute respiratory illness diagnosed with influenzas such as illness or severe acute respiratory illness either COVID-19 positive or negative
- Patients with COVID-19 reverse transcriptase-polymerase chain reaction (RTPCR) (oropharyngeal or nasopharyngeal swabs) positive or negative report.
- Patients not willing to give informed consent
- Age <18 years
- Patients with known ischemic heart disease or other significant cardiac disease
- Patients with preexisting arrhythmias and those with electrolyte abnormalities at presentation
- Pregnant patients
- Patients not willing to undergo RTPCR testing for COVID-19 disease.
Ethical clearance has been obtained from the Institutional Ethics Committee and the procedures followed were in accordance with the ethical standards of the committee and with the Helsinki Declaration of 1975 (as revised in 2000). We conducted the RTPCR test on patients who presented to the hospital and included the first forty patients testing positive and the first forty patients testing negative in our study. All the participants in the study had an ECG at presentation to the hospital. Patients with known ischemic heart disease or other significant cardiac disease, those with preexisting arrhythmias, and those with electrolyte abnormalities at presentation were excluded from the study.
At admission, a detailed history was obtained, clinical examination was performed, 12-lead ECG and laboratory tests which included troponin I and CKMB levels (Creatine kinase MB) were obtained. History of patients' comorbidities was obtained. The severity of infection was determined by respiratory rate and oxygen saturation. Infection is classified as:
- Mild infection if the saturation and respiratory rate are normal
- Moderate infection if saturation is 90 to ≤93% on room air and respiratory rate ≥24/min
- Severe infection if respiratory rate >30 breaths/min with severe respiratory distress and saturation is <90% on room air.
The following ECG parameters were measured: Heart rate (HR), rhythm, axis, corrected QT interval, ST-T changes, PR interval, and QRS complex duration. The presence and type of arrhythmias were also noted.
Descriptive and inferential analysis has been carried out in the present study. The results were analyzed using SPSS version 18 (IBM Corporation, SPSS Inc., Chicago, IL, USA).
We have presented data as mean ± standard deviation (SD) for continuous variables and frequency (percentage) for categorical variables. Inferential statistics such as
- Chi-square test
- Fischer's exact test was used.
P < 0.05 was considered to be statistically significant.
Statistical power for intragroup comparison (mild vs. moderate vs. severe COVID-19 infection) was 80%.
| Results|| |
Overall, we studied eighty patients of whom 40 tested RTPCR positive for severe acute respiratory syndrome coronavirus 2 and forty patients tested negative.
Mean age overall in the study population was 52.4 ± 16 years, 67.5% (54/80) were males.
Overall, 32.5% (26/80) of the study population had Type 2 diabetes mellitus and 32.5% (26/80) had hypertension [Table 1] and [Table 2].
Sinus tachycardia was seen in 45% (18/40) of COVID-positive patients and 55% (22/40) of COVID-negative patients in our study.
Only three patients had bradycardia which was in sinus rhythm and all the three patients had tested positive for COVID-19.
The majority of the population had a normal axis (83.8–67/80). Out of the 12 patients who had left axis deviation, 11 were COVID-19 negative, whereas one was COVID-19 positive. Only one patient had right axis deviation and this patient had tested positive for COVID-19 [Figure 1].
|Figure 1: Axis in electrocardiographic and coronavirus disease status of patients|
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About 95% (76/80) of the population had normal sinus rhythm. Three patients had supraventricular tachycardia (SVT) (Two COVID-19-positive patients and one COVID-19-negative patient) [Figure 2]. Premature atrial contractions (PAC) was present in one COVID-positive patient's ECG, while premature ventricular contractions (PVCs) were found in three COVID-positive patients' ECG (7.5% – 3/40 of COVID-19 positive cases). One of the COVID--positive patients also had ventricular bigeminy.
|Figure 2: A 58-year-old male with no known comorbidities, presented with a short history of fever, cough, and breathlessness. He tested positive for severe acute respiratory syndrome coronavirus 2. His baseline electrocardiographic showed right axis deviation with supraventricular tachycardia. Baseline d-dimer level was 1050|
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The mean overall Bazett-corrected QT interval was 0.406 ± 0.03769 s, which did not vary much between the two study groups.
About 7.5% (3/40) of COVID-positive cases had complete right bundle branch block (RBBB), while one COVID negative had incomplete RBBB. One COVID patient had complete left bundle branch block (LBBB), while one had incomplete LBBB.
Three COVID-positive cases (7.5%-3/40) had significant ST-segment elevation (2 had anterior wall myocardial infarction [MI] and one had anterolateral wall MI) which was associated with raised troponin I values [Table 3].
We had one patient with anterior wall MI and one with anterolateral wall MI who were siblings. They were young, nonsmokers with no comorbidities, or underlying cardiac conditions, who had tested positive for COVID-19. They presented to the hospital on the 2nd day of their symptom onset. Left ventricular (LV) segmental hypokinesia was seen in both the cases on echocardiography [Figure 3].
|Figure 3: A 29-year-old male, coronavirus disease positive, nonsmoker, with no known comorbidities, presented with breathlessness, and chest pain for 2 days. Electrocardiographic- significant ST-segment elevation in leads V2–V5 with raised troponin I value of 340. Echocardiography showed left ventricular segmental hypokinesia|
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The patient with anteroseptal wall MI had also no known comorbidities. Echocardiography done showed LV global hypokinesia and the presence of clot at the LV apex [Figure 4].
|Figure 4: 45-year-old male, no known comorbidities, presented with 4 days of cough, and breathlessness. electrocardiographic showed evolved anterior wall myocardial infarction. Troponin I value was 220 and Creatine kinase MB value was 2.7. Echocardiography showed hypokinetic anteroseptal wall of left ventricle with a left ventricular apical clot|
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About 15% (6/40) of COVID-positive patients had nonST-segment elevation acute coronary syndrome (NSTE-ACS) with raised troponin I values. Five COVID-positive patients had nonspecific ST-T changes.
The COVID-19 negative patients had neither STEMI nor NSTEMI. Only one patient in this group had nonspecific ST-T changes.
S1Q3T3 pattern with right axis deviation, and sinus tachycardia was seen in one patient's ECG suggestive of pulmonary embolism in COVID-19 [Table 3].
Baseline mean HR on ECG increased with disease severity (109.12 [±27.85] in severe disease vs. 94.5 [±25.87] in moderate disease) [Table 4].
|Table 4: Comparison of electrocardiographic characteristics and biomarkers across disease severity|
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Rhythm abnormalities such as SVT and ventricular bigeminy were also seen only in the severe disease category, as was ST elevation and ST depression. Ectopic beats were also noted in severe disease cases. About 87.5% (35/40) of the COVID-positive patients and 70% (28/40) of the COVID-negative patients had ECG changes at baseline.
The mean troponin I value in the COVID-19 positive group was 44.35 ± 18.35, while in the COVID-19 negative group was 10.76 ± 5.41. Troponin I level correlated with clinical severity of COVID-19 infection [Table 4].
| Discussion|| |
COVID-19 infection can result in many cardiovascular complications.
At present, there are no studies comparing ECG changes in COVID-19 cases and other acute respiratory illness. Hence, it is uncertain whether ECG changes in COVID-19 presents differently from other respiratory infections.
In this regard, we analyzed data consecutively from forty COVID-positive and forty COVID-negative patients admitted to our hospital with acute respiratory illness. Both groups were comparable in terms of age and sex distribution as well as the presence of comorbidities.
We set out to find a correlation between clinical severity of infection and ECG changes and whether an ECG could be used as a tool to predict the prognosis of patients. We also sought to evaluate the role of troponin I in the detection of cardiac events.
In our study, the most common arrhythmia overall was sinus tachycardia. Sinus bradycardia was less common and there were no other cases of bradyarrhythmia in our study. This is consistent with many studies published so far.
We also had patients presenting with PVCs, PACs, SVT, and ventricular bigeminy.
PACs have been attributed to increased LV filling pressures, particularly after acute MI.
Hypoxemia caused by respiratory failure creates a hypoxic environment surrounding the myocardium. Hypoxia causes cardiac myocyte cell death and affects the functioning of ion channels, thereby leading to arrhythmias.
In our study, RBBB was more common than LBBB in the COVID--positive group showing a higher incidence of RV dysfunction in this group probably secondary to respiratory failure.
We also had a patient with S1Q3T3 pattern on ECG with right axis deviation, sinus tachycardia, hypoxia on ABG, and raised D-dimer levels suggestive of pulmonary embolism.
Multiple studies in acute pulmonary embolism have attributed RBBB to acute right ventricular overload and distention. RBBB could also be due to right ventricular dysfunction secondary to acute cor pulmonale in the background of acute respiratory distress syndrome.
The pathogenesis of pulmonary vascular disease in COVID-19 is not completely understood and thus ECGs may be an early indicator for an “RV at risk.”
We also had patients in our study presenting with ST-segment elevation MI and non-ST-segment elevation MI. One of the patients who presented with an evolved ST-segment elevation MI also had a clot in the LV apex, suggesting that MI in COVID-19 cases may precipitate LV thrombus formation earlier than expected due to the hypercoagulable state induced in this disease [Figure 4].
There were several strengths to our study. Clinical data extraction and ECG interpretation were manually performed which has many advantages over automated processes such as being more comprehensive and accurate.
We also conducted echocardiographic evaluation of all patients by an experienced professional which lends credibility to our results.
We encountered a few limitations while carrying out our study. We could not assess other cardiac biomarkers such as high sensitivity C-reactive protein, aspartate transaminase, and lactate dehydrogenase as these were obtained if required by the clinician; and hence, were not conducted for all patients in our study. As we did not have ECGs before admission in all patients, we could not compare the ECG on presentation with before ECGs to confirm the presence of new findings.
| Conclusions|| |
Our findings highlight the impact of COVID-19 on the right chambers of the heart (RBBB, RAD, and RV strain) and the significant incidence of arrhythmias in COVID-19 patients versus other acute respiratory illnesses. Troponin I levels were found to correlate well with disease severity in COVID-19. We also reported cases of ST-segment elevation MI, nonST-segment elevation MI, pulmonary thromboembolism, and a post-MI LV thrombus formation. We would like to recommend routine early screening of postMI COVID-19 patients for LV thrombus.
Our study shows that the ECG may be a good prognostic tool in COVID-19, aiding in timely intervention before the onset of clinical deterioration.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3], [Table 4]