COVID-19 and risk of arrhythmia?

To the Editor

Coronavirus disease-2019 (COVID-19) is an infectious disease caused by severe acute respiratory coronavirus 2 (SARS-CoV-2) with a wide range of clinical manifestations, mainly dominated by respiratory symptoms.[1] With the growing number of infected patients, major cardiac complications have been reported[2,3] with higher risk of in-hospital mortality.[4]

An 85-year-old male with a history of hypertension, type 2 diabetes and junctional rhythm (Fig. 1A) presented to the ED due to progressive dyspnea and dry cough in the previous week and paroxysmal nocturnal dyspnea on the previous day. The physical examination revealed a blood pressure of 118/45 mm Hg, heart rate of 36 bpm, O2 saturation of 90% on room air and an axillary temperature of 37.7°C. The patient had bilateral crackles on lung auscultation. Arterial blood gas analysis showed type 1 respiratory failure. A 12-lead electrocardiogram (EKG) showed junctional rhythm with left bundle branch block (Fig. 1B). Blood-work revealed an elevated C-reactive protein (83.8 mg/dL; normal ≤7.5 mg/L), D-dimer (2095 ng/mL; normal <243 ng/mL), N-terminal pro-brain natriuretic peptide (5360 pg/mL; normal ≤133 pg/mL), creatinine phosphokinase (760 UI/L; normal 10–72 UI/L) and high sensitivity troponin (139 pg/mL; normal <19.8 pg/mL). The chest x-ray showed an enlarged cardiothoracic ratio. The patient's nasopharyngeal swab was positive for SARS-CoV-2 PCR. The patient had a favorable chronotropic response to inhaled salbutamol and was admitted to the COVID ward under cardiac telemetry monitoring. On the first day of admission, a new episode of bradycardia was observed. The EKG showed a complete left bundle branch block and a permanent pacemaker was placed. The remainder of his hospital stay was uneventful with resolution of heart failure symptoms, respiratory failure and progressive decrease of the inflammatory markers and troponin levels.

Figure 1

A, Previous 12-lead electrocardiogram (2015)—junctional rhythm. B, 12-Lead electrocardiogram on admission (May 2020)—junctional rhythm, enlargement of QRS complex on D1, aVL, V5 and V6 leads.

Although the pathophysiology underlying COVID-19 remains poorly understood, SARS-CoV-2 may directly injure the heart leading to higher risk of in-hospital mortality.[4]

Some theories have been postulated to explain the myocardial injury and the damage to the conduction system.[2] One explanation suggests that patients with chronic cardiovascular diseases may become unstable due to the imbalance between metabolic demand and reduced cardiac reserve, intensified by the inflammatory response and disturbance of autonomic tone.[2] This injurious effect could be perpetuated by the prompt and severe downregulation of myocardial and pulmonary ACE2 pathways.[2]

Another matter of debate has been the use of drugs that have been tested in patients with COVID-19 that predispose to arrythmias, such as hydroxychloroquine and azithromycin.[5] This was not the case since this patient was treated with supportive care alone without any antiviral or immunomodulatory therapies.

In conclusion, we present the case of an elderly man with a predisposition to arrhythmia in whom SARS-CoV-2 infection was diagnosed when he presented to the ED with severe bradycardia. Could the conduction abnormality described in this patient (who already had a predisposition to arrhythmia) be interpreted as a result of the disfunction of the electrical conduction system induced by SARS-CoV-2? Or could it merely reflect the impact of a systemic illness like many others?[6] Our knowledge regarding the cardiovascular involvement of SARS-CoV-2 infection is still limited. In these patients, one should remain on high alert for cardiovascular complications.

Acknowledgments

We acknowledge Mari Mesquita MD MSc and Mariana Meireles MD MSc for their helpful comments regarding this patient's case.

Conflicts of interest

MMB, DP, SG, BS, HV and LN declares no conflicts of interest, real or perceived, financial or nonfinancial