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 Table of Contents  
Year : 2022  |  Volume : 8  |  Issue : 2  |  Page : 182-185

Sudden onset of chest pain in SARS-CoV-2 patients: Myocarditis or acute coronary syndrome? A case series

Department of Anaesthesia and Critical Care, Indira Gandhi Medical College and Research Institute, Puducherry, India

Date of Submission12-Feb-2022
Date of Decision21-May-2022
Date of Acceptance14-Jun-2022
Date of Web Publication17-Sep-2022

Correspondence Address:
Pratheeba Natrajan
Department of Anaesthesia and Critical Care, Indira Gandhi Medical College and Research Institute, Puducherry
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jcrsm.jcrsm_13_22

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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 article:
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 2022;8:182-5

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 [serial online] 2022 [cited 2023 Mar 21];8:182-5. Available from: https://www.jcrsmed.org/text.asp?2022/8/2/182/356209

  Introduction Top

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.[1],[2] More severe presentations include pneumonia and acute respiratory distress syndrome[3] and are most often associated with the inflammatory process of the respiratory tract which may have a significant impact on the cardiovascular system too.[4] In this case series, we report the evidence of cardiac tissue inflammation as a possible sequel of the respiratory infection.

  Case series Top

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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Table 2: Patient characteristics who developed chest pain

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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 Top

Fulminant myocarditis is an acute, diffuse cardiac inflammation, which leads to cardiogenic shock, ventricular arrhythmias, multi-organ failure, and cardiac arrest.[5] 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.[6]

Myocarditis associated with influenza and parvovirus B19 infection has been widely described.[7] 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.[2] 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.[2] 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.[8] 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.[9] 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.[10] Myocardial interstitial edema has been shown on magnetic resonance imaging in such patients.[11] 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.[12] 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.[13] 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.[14] 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.[11] 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.[15] 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 Top

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.

  References Top

Wu Z, McGoogan JM. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: Summary of a report of 72 314 cases from the Chinese Center for Disease Control and Prevention. JAMA 2020;323:1239-42.  Back to cited text no. 1
Inciardi RM, Lupi L, Zaccone G, Italia L, Raffo M, Tomasoni D, et al. Cardiac involvement in a patient with coronavirus disease 2019 (COVID-19). JAMA Cardiol 2020;5:819-24.  Back to cited text no. 2
Yang X, Yu Y, Xu J, Shu H, Xia J, Liu H, et al. Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: A single-centered, retrospective, observational study. Lancet Respir Med 2020;8:475-81.  Back to cited text no. 3
Yu CM, Wong RS, Wu EB, Kong SL, Wong J, Yip GW, et al. Cardiovascular complications of severe acute respiratory syndrome. Postgrad Med J 2006;82:140-4.  Back to cited text no. 4
Chen C, Zhou Y, Wang DW. SARS-CoV-2: A potential novel etiology of fulminant myocarditis. Herz 2020;45:230-2.  Back to cited text no. 5
Madjid M, Safavi-Naeini P, Solomon SD, Vardeny O. Potential effects of coronaviruses on the cardiovascular system: A review. JAMA Cardiol 2020;5:831-40.  Back to cited text no. 6
Fung G, Luo H, Qiu Y, Yang D, McManus B. Myocarditis. Circ Res 2016;118:496-514.  Back to cited text no. 7
Rahman JE, Helou EF, Gelzer-Bell R, Thompson RE, Kuo C, Rodriguez ER, et al. Noninvasive diagnosis of biopsy-proven cardiac amyloidosis. J Am Coll Cardiol 2004;43:410-5.  Back to cited text no. 8
Choi S, Jang WJ, Song YB, Lima JA, Guallar E, Choe YH, et al. D-dimer levels predict myocardial injury in ST-segment elevation myocardial infarction: A cardiac magnetic resonance imaging study. PLoS One 2016;11:e0160955.  Back to cited text no. 9
Tavazzi G, Pellegrini C, Maurelli M, Belliato M, Sciutti F, Bottazzi A, et al. Myocardial localization of coronavirus in COVID-19 cardiogenic shock. Eur J Heart Fail 2020;22:911-5.  Back to cited text no. 10
Saleh M, Gabriels J, Chang D, Soo Kim B, Mansoor A, Mahmood E, et al. Effect of chloroquine, hydroxychloroquine, and azithromycin on the corrected QT interval in patients with SARS-CoV-2 infection. Circ Arrhythm Electrophysiol 2020;13:e008662.  Back to cited text no. 11
Shi S, Qin M, Shen B, Cai Y, Liu T, Yang F, et al. Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China. JAMA Cardiol 2020;5:802-10.  Back to cited text no. 12
Bangalore S, Sharma A, Slotwiner A, Yatskar L, Harari R, Shah B, et al. ST-segment elevation in patients with covid-19 – A case series. N Engl J Med 2020;382:2478-80.  Back to cited text no. 13
Stefanini GG, Montorfano M, Trabattoni D, Andreini D, Ferrante G, Ancona M, et al. ST-elevation myocardial infarction in patients with COVID-19: Clinical and angiographic outcomes. Circulation 2020;141:2113-6.  Back to cited text no. 14
Mitra A, Dwyre DM, Schivo M, Thompson GR 3rd, Cohen SH, Ku N, et al. Leukoerythroblastic reaction in a patient with COVID-19 infection. Am J Hematol 2020;95:999-1000.  Back to cited text no. 15


  [Table 1], [Table 2]


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