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 Table of Contents  
Year : 2020  |  Volume : 6  |  Issue : 1  |  Page : 2-3

Corona virus disease and the heart

Department of Cardiology, AIIMS, New Delhi, India

Date of Submission20-Mar-2020
Date of Decision21-Mar-2020
Date of Acceptance25-Mar-2020
Date of Web Publication15-Apr-2020

Correspondence Address:
Satyavir Yadav
Room No. 32 7th Floor Cardioneuro Center, Department of Cardiology, AIIMS, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpcs.jpcs_20_20

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The world is in the midst of a corona virus disease (COVID-19) pandemic. We review a case of COVID-19 myocarditis which was successfully managed and reported and also comment on the connection of COVID-19 and the heart.

Keywords: Corona virus, COVID-19, heart, myocarditis, troponin

How to cite this article:
Yadav S, Vashista S, Bhardwaj P. Corona virus disease and the heart. J Pract Cardiovasc Sci 2020;6:2-3

How to cite this URL:
Yadav S, Vashista S, Bhardwaj P. Corona virus disease and the heart. J Pract Cardiovasc Sci [serial online] 2020 [cited 2023 Feb 2];6:2-3. Available from: https://www.j-pcs.org/text.asp?2020/6/1/2/282563

  Introduction Top

Coronavirus disease (COVID-19) is an infectious disease caused by a newly discovered coronavirus. The COVID-19 virus spreads primarily through droplets of saliva or discharge from the nose when an infected person coughs or sneezes. At this time, there are no specific vaccines or treatments for COVID-19. However, there are many ongoing clinical trials evaluating potential treatments.

Hu et al. reported a male patient of 37 years who was admitted to the hospital with a history of complaints of chest pain, dyspnea, and diarrhea for 3 days. On examination, blood pressure was noted as 80/50 mmHg. During investigations, there was a significant enlargement of the heart on chest X-ray and pulmonary infection, enlarged heart, and pulmonary effusion on computed tomography. The levels of cardiac biomarkers were increased with troponin T >10,000 ng/L, creatine phosphokinase muscle-brain (CKMB) = 112.9 ng/L, and N-terminal prohormone of brain natriuretic peptide (NT-proBNP) = 21025 ng/L. Echo scans revealed an enlarged heart and a marked decrease in ventricular systolic function, left ventricular ejection fraction = 27%. Sputum test for corona virus nucleic acid tested positive, whereas tests for other viruses' tests were negative. The diagnosis of the patient was made as coronavirus fulminant myocarditis with cardiogenic shock and pulmonary infection. The treatment given included methyl prednisolone – 200 mg/day for 4 days, immunoglobulin – 20 gm/day for 4 days, norepinephrine, diuretics, milrinone, piperacillin, salbactam, and pantoprazole. After 1 week of treatment, the patient conditions improved, chest X-ray showed normal heart size, and echo was normal. Cardiac biomarker levels were decreased: troponin T – 220.5 ng/L, CKMB – 9.14mg/dl, and NTproBNP – 1587ng/L. After 3 weeks of treatment, troponin T reduced to 21.4ng/L, CKMB – 2.25ng/L, and NTproBNP – 139ng/L.[1]

  Discussion Top

This is a useful report to show that treatment may work in corona myocarditis. There are some reports also though that steroids may do harm, especially with lung injury, other reports suggest that high-dose steroids may not be beneficial, particularly with lung injury.[2],[3],[4],[5],[6]


Acute effect of corona on the heart includes arrhythmia – 16.7% and acute cardiac injury − 7.2%, and there are anecdotal reports of acute-onset heart failure, myocardial infarction (MI), myocarditis, and cardiac arrest.

Cardiac complications of coronavirus disease (COVID-19) are approximately commensurate with severe acute respiratory syndrome (SARS), middle east respiratory syndrome (MERS), and influenza.

Coronavirus disease implications for patients with underlying cardiovascular conditions

  1. Identify and isolate cardiovascular patients with COVID-19 symptoms from other patients, including in the ambulatory setting
  2. Patients with underlying cardiovascular disease are at higher risk of contracting COVID-19 and have a worse prognosis

  3. It is important for patients with CVD to remain current with vaccinations, including the pneumococcal and influenza vaccine given the increased risk of secondary bacterial infection

  4. It may be reasonable to substitute telephonic or telehealth visits for in-person routine visits for stable CVD patients to avoid possible nosocomial COVID-19 infection
  5. Triage COVID-19 patients according to the underlying cardiovascular, diabetic, respiratory, renal, oncological, or other comorbid conditions for prioritized treatment
  6. For patients with heart failure or volume overload conditions, copious fluid administration for viral infection should be used cautiously and carefully monitored
  7. General immunological health remains important for both providers and patients, including eating well, sleeping, and managing stress.

Coronavirus disease and interventional cardiology

The Wuhan protocol for patients diagnosed with or highly suspected to have COVID-19 infection recommended thrombolytics rather than primary percutaneous coronary intervention, because health-care professionals are faced with multiple management issues, including resource utilization and nonavailability of equipment and potential risks of exposure for staff and other patients.

Troponin and brain natriuretic peptide use in coronavirus disease

Given the frequency and nonspecific nature of abnormal troponin or natriuretic peptide results among patients with COVID-19 infection, clinicians are advised to only measure troponin or natriuretic peptides if the diagnosis of acute MI or heart failure is being considered on clinical grounds. An abnormal troponin or natriuretic peptide result should not be considered evidence for an acute MI or heart failure without corroborating evidence.[5],[6]

ACE I or ARB use in hypertension

There has been a lot of talk about the molecular and pathophysiology basis of the virus being mediated by the angiotensin-converting enzyme II (ACE-II) receptors. However, the mechanisms behind the interactions of ACE-II and the angiotensin converting enzyme (ACE) inhibitor and angiotensin receptor blockers ARBs are very complex and there is no clear evidence that these drugs help inhibit or aid the disease. They are primarily in the lung and that is why many people obviously have the pulmonary symptoms that are showing, but we know they are in the heart and intestine as well.

European society of cardiology (ESC) strongly recommends that physicians and patients should continue treatment with their usual antihypertensive therapy because there is no clinical or scientific evidence to suggest they cause any harm in COVID-19 infections.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Hu H, Ma F, Wei X, Fang Y. Coronavirus fulminant myocarditis saved with glucocorticoid and human immunoglobulin. Eur Heart 2020. Available from: https://doi.org/10.1093/eurheartj/ehaa190. [Last accessed on 2020 Mar 16].  Back to cited text no. 1
Wang D, Hu B, Hu C, Zhu F1, Liu X, Zhang J, et al. Clinical characteristics of 138 Hospitalized Patients with 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China. JAMA 2020;323:1061-9. [doi: 10.1001/jama. 2020].  Back to cited text no. 2
Alhogbani T. Acute myocarditis associated with novel Middle East respiratory syndrome coronavirus. Ann Saudi Med 2016;36:78-80.  Back to cited text no. 3
Zaki AM, van Boheemen S, Bestebroer TM, Osterhaus AD, Fouchier RA. Isolation of a novel coronavirus from a man with pneumonia in Saudi Arabia. N Engl J Med 2012;367:1814-20.  Back to cited text no. 4
Zhou F, Yu T, Du R, Fan G, Liu Y, Liiu Z, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: A retrospective cohort study. Lancet 2020. Available from: https://doi.org/10.1016/S0140-6736(20)30566-3. [Last accessed on 2020 Mar 11].  Back to cited text no. 5
Russell CD, Millar JE, Baillie JK. Clinical evidence does not support corticosteroid treatment for 2019-nCoV lung injury. Lancet 2020;395:473-5.  Back to cited text no. 6


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