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| LETTER TO EDITOR |
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| Year : 2022 | Volume
: 2
| Issue : 1 | Page : 43-44 |
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Coronavirus disease 2019 and atrial fibrillation: A dreadful yet not uncommon association
Mansi Gupta1, Nitesh Gupta2, AJ Mahendran2, Pranav Ish2
1 Department of Pulmonary, Critical Care and Sleep Medicine, SGPGI, Lucknow, Uttar Pradesh, India
2 Department of Pulmonary, Critical Care and Sleep Medicine, VMMC and Safdarjung Hospital, New Delhi, India
| Date of Submission | 17-Sep-2021 |
| Date of Decision | 03-Oct-2021 |
| Date of Acceptance | 03-Oct-2021 |
| Date of Web Publication | 17-Jan-2022 |
Correspondence Address:
Dr. Pranav Ish
B1, Green Park Extension, New Delhi - 110 016
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/jalh.jalh_21_21
How to cite this article:
Gupta M, Gupta N, Mahendran A J, Ish P. Coronavirus disease 2019 and atrial fibrillation: A dreadful yet not uncommon association. J Adv Lung Health 2022;2:43-4 |
How to cite this URL:
Gupta M, Gupta N, Mahendran A J, Ish P. Coronavirus disease 2019 and atrial fibrillation: A dreadful yet not uncommon association. J Adv Lung Health [serial online] 2022 [cited 2022 May 16];2:43-4. Available from: http://www.jalh.com/text.asp?2022/2/1/43/335924 |
To the Editor,
A 43-year-old male was admitted to the emergency department with complaints of fever, cough with worsening shortness of breath for 3 days. He was prediabetic and hypertensive, on enalapril 5 mg twice a day, metoprolol succinate 50 mg once a day, but did not have any other comorbidity. At presentation, the patient was tachypneic with heart rate of 100 beats/min, blood pressure of 138/88 mmHg, respiratory rate of 24/min, and saturation of 88% on room air. Reverse transcriptase-polymerase chain reaction for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was positive and chest X-ray showed the presence of bilateral lower lobe pneumonia. Laboratory investigations revealed normal hemoglobin (13.6g/dL), total leukocyte count (4100/mm3), platelet counts (184,000/mm3) along with normal electrolytes, liver, and renal function tests. Inflammatory markers were raised with Interleukin 6 (IL-6) levels- 34 pg/mL (range, 0–10) and C-reactive protein- 67 mg/dl (range, 0–10). The patient was diagnosed with severe Coronavirus disease 2019 (COVID-19) and admitted to the intensive care unit. He was started on hydroxychloroquine 400 mg twice daily for 1 day followed by 400 mg daily, injection methylprednisolone 80 mg twice daily, proton-pump inhibitor, low-molecular-weight heparin 0.6 mg subcutaneous once a day, regular insulin, and oxygen at 4 l/min by nasal prongs.
On day 2 of presentation, the patient complained of sudden-onset palpitations. A 12 lead electrocardiogram (EKG) showed atrial fibrillation (AF) with fast ventricular rate of 140/min [Figure 1]a. Cardiac biomarkers (troponin I, myoglobin) were not raised. He had a blood pressure of 128/78 mmHg. The patient was given intravenous diltiazem 12.5 mg bolus for rate control and started on oral amiodarone 400 mg twice daily. His heart rate reduced to 93/min along with reduction of his symptoms. Oxygen was tapered to 2 l/min on day 4 and stopped on day 6 of presentation. EKG on day 7 [Figure 1]b showed normal sinus rhythm with heart rate of 100/min and blood pressure of 148/92 mmHg. The dose of metoprolol succinate was increased to 50 mg twice a day and amiodarone was reduced to 200 mg twice a day. The patient was discharged after 20 days of admission and is doing well on follow-up. An echocardiogram was done on day 10 of discharge which was reported normal. | Figure 1: (a) (Day 3) - 12 lead electrocardiogram (EKG) showing the irregular narrow complex tachycardia, loss of P waves with heart rate of 140/min, suggestive of atrial fibrillation, (b) (day 7) - EKG showed normal sinus rhythm (P wave precedes every QRS complex) with heart rate of 100/min
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COVID-19 is caused by the SARS-CoV-2 virus with predominant pulmonary manifestation. However, the extrapulmonary manifestations often contribute significantly to the morbidity and mortality in COVID-19. The predominant cardiovascular manifestations of COVID-19 are myocardial infarction, myocarditis presenting as heart failure, pulmonary embolism, and arrhythmias. Initial literature had focused predominantly on the QT prolongation and arrhythmias associated with hydroxychloroquine; subsequently, the malignant arrhythmias associated with COVID-19 were recognized.[1]
It is proposed that the mechanism of AF in COVID-19-infected patients may be multifactorial. The most common factors triggering arrhythmia in COVID-19 patients, as specified in many studies, are hypoxia and arrhythmogenic drugs, especially hydroxychloroquine. Both the factors were present in the index case. However, these factors are not seen in many cases, hence a direct viral activity is also suspected. The following are few mechanisms proposed for direct viral activity leading to arrhythmia.[1]
- The virus gains entry through angiotensin-converting enzyme 2 receptor facilitated by transmembrane serine protease 2. Once inside, the viral particle induces NF-kB which in turn induces the mRNA of pore-forming proteins. These pores promote outward potassium current inducing arrhythmia
- In bile-duct cells, COVID-19 virus induces expression of genes for proteins such as CD40, caspase recruitment domain family member 8 (CARD8), and serine/threonine kinase 4 which induce cell death. If such a mechanism is possible in cardiomyocytes, the death of cardiac cells may lead to the generation of abnormal currents, leading to arrhythmia
- Pro-inflammatory cytokine storm-induced high IL-6 levels-down regulate SERCA (Ca2+ ATPase) leading to alteration in intracellular calcium levels causing arrhythmia.
Nevertheless, some studies question the above-mentioned mechanisms as the disease severity directly correlates with the incidence of AF in patients, proposing the possibility of hypoxia, cytokine storm, and drug activity to contribute to AF rather than direct involvement.[2] Moreover, postmortem evidence show no viral involvement or typical features of myocarditis.[3] Further research is needed to clarify the exact electrophysiological mechanism.
The recent online survey from the Heart Rhythm Society among 915 hospitalized COVID-19 positive patients from 76 countries and 6 continents showed the AF was the most common sinus tachyarrhythmia (19.6%), followed by paroxysmal supraventricular tachycardia, sustained monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, and sustained atrial tachycardia. Sinus bradycardia (8%) and complete heart block (8%) were the most common bradyarrhythmia, followed by the first- or second-degree atrioventricular block, and bundle branch block.[4]
We do not have any evidence-based guidelines to treat a case of AF in the presence of COVID-19.[5] However, the European society of cardiology proposes that in hospitalized COVID-19 patients with AF/atrial flutter without hemodynamic instability; initiation of rate control therapy [Figure 2] is a reasonable therapeutic option.[6] | Figure 2: Mechanism and management of atrial fibrillation in coronavirus disease 2019
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Thus, it is imperative for all treating physicians including pulmonologists to monitor all severe COVID-19 patients for various arrhythmias; especially AF and start early appropriate therapy for a favorable outcome.
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 his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
| 1. | Wang Y, Wang Z, Tse G, Zhang L, Wan EY, Guo Y, et al. Cardiac arrhythmias in patients with COVID-19. J Arrhythm 2020;36:827-36.  |
| 2. | Bhatla A, Mayer MM, Adusumalli S, Hyman MC, Oh E, Tierney A, et al. COVID-19 and cardiac arrhythmias. Heart Rhythm 2020;17:1439-44. |
| 3. | Schaller T, Hirschbühl K, Burkhardt K, Braun G, Trepel M, Märkl B, et al. Postmortem examination of patients with COVID-19. JAMA 2020;323:2518-20. |
| 4. | Gopinathannair R, Merchant FM, Lakkireddy DR, Etheridge SP, Feigofsky S, Han JK, et al. COVID-19 and cardiac arrhythmias: A global perspective on arrhythmia characteristics and management strategies. J Interv Card Electrophysiol 2020;59:1-8. |
| 5. | Kumar R, Yadav SR, Goel A, Kumar A, Ish P, Gupta N. Cardiology and COVID: A bidirectional association! Adv Respir Med 2021;89:86-9. |
| 6. | |
[Figure 1], [Figure 2]
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