|Ahead of print publication
Sudden onset of chest pain in SARS-CoV-2 patients: Myocarditis or acute coronary syndrome? A case series
Sangeeta Dhanger, Pratheeba Natrajan, Bhavani Vaidhiyanathan, Idhuyya Rajesh Joseph
Department of Anaesthesia and Critical Care, Indira Gandhi Medical College and Research Institute, Puducherry, India
|Date of Submission||12-Feb-2022|
|Date of Decision||21-May-2022|
|Date of Acceptance||14-Jun-2022|
|Date of Web Publication||17-Sep-2022|
Department of Anaesthesia and Critical Care, Indira Gandhi Medical College and Research Institute, Puducherry
Source of Support: None, Conflict of Interest: None
The most common symptoms of severe acute respiratory syndrome–COVID-19 (SARS-CoV-2) infection are fever and cough, followed by headache, fatigue, or shortness of breath. The most severe presentations include pneumonia (91.1%) and acute respiratory distress syndrome (67%). In this case series, we report the evidence of cardiac tissue inflammation as a possible sequela of the respiratory infection. In May 2021, 16 patients (median age: 43 years, 10 males and 6 females) out of 95 patients, between the 6th and 10th days following admission in the intensive care unit, complained of sudden onset of excruciating chest pain. Changes in electrocardiography rhythm with evidence for diffuse ischemia were supported by positive Trop-T and echo findings in most of the patients. In this case series, we report the evidence of cardiac tissue inflammation as a possible sequel of the respiratory infection.
Keywords: Chest pain, COVID-19, myocardial infarction, myocarditis, pneumonia
|How to cite this URL:|
Dhanger S, Natrajan P, Vaidhiyanathan B, Joseph IR. Sudden onset of chest pain in SARS-CoV-2 patients: Myocarditis or acute coronary syndrome? A case series. J Curr Res Sci Med [Epub ahead of print] [cited 2022 Oct 6]. Available from: https://www.jcrsmed.org/preprintarticle.asp?id=356209
| Introduction|| |
The most common symptoms of severe acute respiratory syndrome–COVID-19 (SARS-CoV-2) infections are fever (in up to 88.7% of patients during hospitalization) and cough (in 67.8% of patients), followed by headache, fatigue, or shortness of breath, as reported by the China Medical Treatment Expert Group for COVID-19., More severe presentations include pneumonia and acute respiratory distress syndrome and are most often associated with the inflammatory process of the respiratory tract which may have a significant impact on the cardiovascular system too. In this case series, we report the evidence of cardiac tissue inflammation as a possible sequel of the respiratory infection.
| Case series|| |
In May 2021, 95 patients with SARS-CoV-2 infection with severe COVID pneumonia with SARS-CoV-2 infection were admitted and managed in our COVID intensive care unit (ICU) with a bed occupancy rate of 87.1%. All the patients were managed according to the Indian Council of Medical Research and the Ministry of Health and Family Welfare guidelines. Between the 6th and 10th days following admission to ICU, 16 patients (mean age: 43 years, 10 males and 6 females) complained of sudden onset of excruciating chest pain, along with changes in electrocardiography (ECG) rhythm with evidence for diffuse ischemia [Table 1]. Troponin T was positive in ten patients whereas in six patients test was negative. A bedside echocardiography revealed diffuse hyperkinesis with an estimated LV ejection fraction of 30%–40% in the majority of patients. The details of the patients are tabulated in [Table 2].
|Table 1: Demographic profiles, clinical features, treatments, investigation and outcome of 95 patients with severe acute respiratory syndrome–COVID-19 (SARS-CoV-2)|
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After primary care, eight patients progressed to pulseless electrical activity within hours of developing chest pain and expired despite cardiopulmonary resuscitation. The remaining six patients had contraindications for percutaneous transluminal coronary angioplasty (PTCA) (four had left main vessel block and two had proximal blockade) and hence were managed with pharmacological methods. Despite our best efforts, five of them developed cardiogenic shock and expired within 2–5 days. Of the total 16 patients, only 2 patients survived – one after PTCA and another after pharmacological treatment. The patients mentioned above initially presented with weakness and hypoxia, with no signs of any cardiac or renal disease.
| Discussion|| |
Fulminant myocarditis is an acute, diffuse cardiac inflammation, which leads to cardiogenic shock, ventricular arrhythmias, multi-organ failure, and cardiac arrest. It presents a wide range of changes in ECG, as seen in our patients, and none of which was specific to its diagnosis. Most often, the presentation includes the presence of PR-segment depression in the precordial and limb leads, reciprocal ST elevation in aVR, the presence of pathologic Q waves, and intraventricular conduction delay or bundle branch block. In most of our patients, ECG showed the presence of Q waves, broad QRS, and ST-segment elevation in the inferolateral leads.
Myocarditis associated with influenza and parvovirus B19 infection has been widely described. The pathogenesis of myocarditis associated with SARS-CoV-2 may reflect a process of replication and dissemination of the virus through the blood from the respiratory tract. However, there are no such reports available to support this theory. It is quite possible that SARS-CoV-2 could trigger an exaggerated inflammatory response that can cause myocardial injury. Evidence of significant inflammatory cell infiltration has been reported in the alveoli of patients with acute respiratory distress syndrome associated with SARS-CoV-2 infection. Although ultrastructural mechanisms are not certain, a potential binding to a viral receptor of the myocyte can favor the internalization and subsequent replication of the capsid proteins and the viral genome. In addition, the onset of symptoms several days after the respiratory symptoms may reflect these proposed mechanisms with potential myocyte dissemination of the virus, the activation of the immune system, and, ultimately, the clinical onset of heart failure.
All our 16 patients had elevated D-dimer levels (2500–5000) and were administered intravenous heparin infusion to maintain activated partial thromboplastin time to two times the normal value. However, a few authors recently in their study reported that the dimer level seemed normal in 64% of the patients who presented with ST-segment elevation MI. Therefore, the possibility that myocardial injury in patients with COVID-19 could be due to plaque rupture, cytokine storm, hypoxic injury, coronary spasm, microthrombi, or direct endothelial or vascular injury should be contemplated. Myocardial interstitial edema has been shown on magnetic resonance imaging in such patients. However, we were not able to perform MRIs for our patients due to complications associated with the shifting of sick patients.
Coronary thrombosis and ST-elevation myocardial infarction (STEMI) have also been described in COVID-19 patients by Shi et al. They have shown that the mortality rate was much higher in a patient with evident MI (ST elevation) with SARS-CoV-2 (42/82, 51.2%). In addition to that, the degree of ST elevation is directly correlated with the mortality rate.
The prognosis also depends upon the time interval between the onset of MI (ECG changes) and coronary intervention. Bangalore et al. reported the data of 18 COVID-19 patients with STEMI, of which 8 patients presented with STEMI within 24 h of admission and did not survive even after primary percutaneous intervention (PCI).
A significant number of patients with STEMI had only nonobstructive lesions. Stefanini et al. reported that 40% of the patients who underwent emergency PCI did not have obstructive coronary artery disease. Therefore, it becomes difficult to predict whether the clinical presentation was due to myocardial infarction, myocarditis, or cytokine storm.
One another causative factor of ECG changes in these patients could be oral azithromycin as all our patients received tablet azithromycin for the first 5 days. Azithromycin per se is known to increase QT interval in the ECG in the presence of hypoxia. All our patients received azithromycin orally for the first 5 days as our treatment protocol. However, only 16 patients showed the ECG changes whereas the rest had normal ECG.
Hence, myocardial infarction may be associated with severe inflammation or fulminant myocarditis, as seen in patients with ST elevation in ECG, as well as it could be associated with increased leukocytosis, inflammatory markers (C-reactive protein and interleukin-6), and pro-brain natriuretic peptide. The only laboratory value that portended the event was the increasing percentage of immature granulocytes. The effect of SARS-CoV-2 on the heart can be better understood with an autopsy. However, this was not possible, as the family members did not consent to an autopsy.
The nonavailability of cardiac biomarker assay, brain natriuretic peptide (BNP), and the endomyocardial biopsy in our institute to histologically demonstrate myocarditis and the absence of viral genome search in the heart are the limitations.
| Conclusions|| |
We believe that recognition of acute myocarditis, as a possible complication associated with COVID-19, will be helpful for patients. This report highlights the importance of clinical surveillance and basic laboratory testing, including troponin levels, in individuals with recent symptoms of an acute illness to guarantee appropriate identification of cardiac complications.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients/family members have given their consent for their images and other clinical information to be reported in the journal. The patients/family members understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2]