|Year : 2020 | Volume
| Issue : 4 | Page : 223-226
Shock and diffuse ST-elevation in a patient with coronavirus disease-2019 disease
Maria Cristina Vedovati1, Michela Giustozzi1, Serenella Conti2, Cecilia Becattini1
1 Department of Medicine, Vascular and Emergency Medicine - Stroke Unit, University of Perugia, Perugia, Italy
2 Department of Cardiology, San Matteo Degli Infermi Hospital, Spoleto, Italy
|Date of Submission||30-Jun-2020|
|Date of Decision||06-Sep-2020|
|Date of Acceptance||12-Sep-2020|
|Date of Web Publication||20-Jan-2021|
Maria Cristina Vedovati
Vascular and Emergency Medicine . Stroke Unit, University of Perugia, Via G. Dottori, 1, 06129 Perugia
Source of Support: None, Conflict of Interest: None
The infection by the novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is associated with significant cardiovascular morbidity and mortality. Cardiac events require prompt diagnosis and management, also in the SARS-CoV-2 era. A 58-year-old male, heavy smoker and with known SARS-CoV-2 infection, abruptly developed severe hypotension and asthenia. At patients' home, emergency physicians found hemodynamic compromise with diffuse ST-elevation at electrocardiography. The patient was rapidly moved to the cardiac catheterization laboratory, and any contact with other health-care workers was avoided. Coronary angiography excluded coronary artery disease. At admission to the coronavirus disease-2019 unit, an increase in inflammatory markers and liver enzymes with normal troponin levels were observed. Bedside lung ultrasonography showed interstitial syndrome and bilateral pleural effusion, whereas echocardiography showed large and diffuse pericardial effusion with a swinging heart. The hemodynamic status improved after gentle fluid therapy such suggesting potential concomitant sepsis and pericardiocentesis was not performed. At this time, a computed tomography scan showed a widespread neoplasm in the right lung involving the subclavian artery and vein and the thoracic lymph nodes. The histology confirmed the diagnosis of a locally advanced pulmonary adenocarcinoma. One week after admission, the patient died for worsening respiratory failure. Not delayed primary PCI remains the standard of care for patients with suspected ST-elevation myocardial infarction (STEMI) in the SARS-CoV-2 era. A diagnostic deepening for potential STEMI-mimicker (known to be associated with SARS-CoV-2 infection and to patients' comorbidities) should be considered, and a multidisciplinary approach is needed in these patients.
Keywords: Cardiovascular disease, case report, coronavirus disease-19, severe acute respiratory syndrome coronavirus 2
|How to cite this article:|
Vedovati MC, Giustozzi M, Conti S, Becattini C. Shock and diffuse ST-elevation in a patient with coronavirus disease-2019 disease. J Cardiovasc Echography 2020;30:223-6
|How to cite this URL:|
Vedovati MC, Giustozzi M, Conti S, Becattini C. Shock and diffuse ST-elevation in a patient with coronavirus disease-2019 disease. J Cardiovasc Echography [serial online] 2020 [cited 2021 Feb 24];30:223-6. Available from: https://www.jcecho.org/text.asp?2020/30/4/223/307377
| Introduction|| |
Cardiac involvement is a prominent feature in the novel coronavirus disease-2019 (COVID-19), a clinical syndrome caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection., Myocardial injury and heart failure contributed to 40% of COVID-19 deaths, either in conjunction or not with respiratory failure., However, little is currently known about the incidence, clinical manifestations, and management of heart disease in patients with COVID-19. Here, we describe a case of a patient with COVID-19 disease admitted with shock and diffuse ST-elevation at the electrocardiogram.
| Case Report|| |
A 58-year-old Caucasian male was admitted to the hospital for shock and diffuse ST-elevation at the electrocardiogram. He had been complaining fever and persistent cough for 7–10 days. The first nasopharyngeal swab test performed 2 days before admission resulted positive for SARS-CoV-2 infection on the real-time reverse transcriptase-polymerase chain reaction assay. The fever decreased after 5 days of levofloxacin.
The patient was a current smoker (20/30 cigarettes a day for 40 years), and he was also affected by hypothyroidism. Because of persistent cough, the patient had performed a chest X-ray and pneumological consultant 3 months before. A diagnosis of interstitial lung disease was assumed, and a high-resolution lung computed tomography (CT) scan was performed showing a mass in the right lung suspected for cancer. Subsequently, an endobronchial ultrasound-guided transbronchial needle aspiration was planned.
On April 2, for the occurrence of severe hypotension and asthenia, the emergency service was called. At patients' home, he was found in shock, and the electrocardiogram revealed a diffuse ST-elevation [Figure 1]a. Blood pressure was 80/40 mmHg, heart rate 110 bpm, oxygen saturation 88% on room air, and body temperature 37.5°C. He was directly moved to the catheterization laboratory, and any contact with other health-care workers was avoided. An emergency coronary angiography showed the absence of a coronary artery disease as well as a normal left ventricular function.
|Figure 1: Electrocardiogram A (emergency setting) showed ST-elevation from V4 to V6 and in DII and DIII, with a ST-down elevation in aVR strongly suspected for proximal coronary occlusion. Electrocardiogram B (coronavirus disease unit) better underlined the PR depression and the morphology of the diffuse ST-elevation suggesting a probable diagnosis of acute pericarditis|
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Afterward, the patient was admitted to the COVID-19 ward. At blood samples, high inflammatory markers, increased liver enzymes, and normal troponin values were observed (peak HS-troponin value 10.5 ng/L); arterial blood gas analysis showed respiratory alkalosis with hyperlactatemia (pH 7.5, paCO2 27.1 mmHg, HCO3-24.1 mmol/dL, and lactates 5.5 mmol/dL). [Table 1] shows the results of the blood samples and [Figure 1]b a control electrocardiogram. A bedside focused ultrasound was performed. The lung ultrasound showed an interstitial syndrome with bilateral B lines, small sub-pleural consolidations, and bilateral pleural effusion. The echocardiography highlighted the presence of diffuse pericardial effusion of 2.5 cm and a swinging heart, inferior caval vein of 2.2 cm with no respiratory excursion, and global left ventricular ejection fraction of 50% [Figure 2]. Blood pressure values increased after fluid therapy, and pericardiocentesis was not performed due to the improved patient's hemodynamic conditions, instead oxygen saturation rapidly deteriorated with the need of high flow oxygen therapy. A diagnosis of pericarditis was made; corticosteroids and colchicine were started. Heparin prophylaxis was started, and high dose aspirin was avoided. Empiric antibiotic therapy was administrated as a concomitant lung infection was suspected. A second and third (2 days after) nasopharyngeal swab tested negative for SARS-CoV-2 infection, whereas an enzyme-linked immunosorbent assay based test resulted positive for IgM and IgG antibodies for SARS-CoV-2.
|Figure 2: Diffuse pericardial effusion and dilated inferior vena cava at the focused cardiac ultrasound|
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In the next days, the patient remained hemodynamically stable but severe respiratory failure persisted. At this time, a total body CT was performed and confirmed the presence of a locally advanced lung cancer of 8.5 cm with subclavian artery and vein and thoracic lymph nodes involvement and confirmed the pleural and pericardial effusion [Figure 3]. The histological examination confirmed the diagnosis of lung adenocarcinoma. Indeed, after oncologic evaluation, the patient was moved to the oncologic clinic, but 1 week later, he died for rapidly worsening of the respiratory failure.
|Figure 3: Large mass in the right upper lung, pleural and pericardial effusion at the computed tomography thoracic scan|
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| Discussion|| |
We report on the management of a man with shock, diffuse ST-elevation at the electrocardiogram, pericardial effusion, and concomitant SARS-CoV-2 infection. A diagnosis of locally advanced lung adenocarcinoma was done.
During COVID-19, a considerable proportion of patients may develop cardiac events with a subsequently increased risk of in-hospital mortality.,,, Those include acute coronary syndrome or venous thromboembolism but also pericarditis or myocarditis. Cardiac events require a quick diagnosis and management and should not be overlooked due to the presence of SARS-CoV-2 infection. In this view, a correct triage of the patient is essential for the right in-hospital allocation according to the infective state and allows the prompt adoption of protective measures. At the emergency service arrival, our patient had hemodynamic deterioration and electrocardiographic findings compatible with an ST-elevation myocardial infarction (STEMI). According to the triage protocol, an emergency angiography was immediately performed, and a myocardial ischemia was excluded. Emergency coronary angiography is recommended in patients with heart failure or shock (Class I, Level A) irrespective of COVID-19 status., In our patient, the bedside echocardiogram was performed after the coronary angiography. Recent guidance suggests that focused cardiac ultrasound study and critical care echocardiography should be performed and focused only to answer clinical questions to reduce patient contact during COVID-19 pandemic., Indeed, a differential diagnosis with “STEMI-mimicker” such as focal myocarditis or stress cardiomyopathy known to be associated with COVID-19 should be considered in these patients since the prehospital setting. However, in this case, a focused cardiac ultrasound study performed before moving the patient to the catheterization laboratory would have led to a quicker correct diagnosis of pericardial effusion.
A second electrocardiogram better underlined the PR depression and the diffuse concave upward ST-segment elevation suggesting a probable diagnosis of acute pericarditis ultimately confirmed by focus echocardiography. Thus, a multidisciplinary evaluation is essential in these patients.
The hemodynamic deterioration in our patient should be related to both a cardiogenic and a septic component. Since pericardiocentesis was not performed, the etiology of the pericardial effusion remains to be defined (infective or neoplastic). Finally, the diagnostic tests for SARS-CoV-2 infection should be correctly interpreted. In our patient, the infection of SARS-CoV-2 was confirmed by the positive of nasopharyngeal swab on the real-time reverse transcriptase-polymerase chain reaction assay before admission. However, while the patient had positive IgM and IgG antibodies for SARS-CoV-2 infection, a second and a third, at 48 hours nasopharyngeal swabs during hospital stay were negative. This suggests even according to symptoms onset, that SARS-CoV-2 infection occurred 2 weeks before.
In conclusion, our case highlights a complex diagnostic and therapeutic management in a patient with SARS-CoV-2 infection, hemodynamic compromise, and important comorbidities (locally advanced lung cancer). In this view, not delayed primary PCI remains the standard of care for patients with suspected STEMI in the COVID-19 era. The use of the established management protocols and multidisciplinary approach is essential in daily clinical practice, especially in critically ill patients with SARS-CoV-2 infection.
Statement of consent
The authors confirm that consent for submission and publication of this case report, including images, has been obtained according to the Local Institutional Review board.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]