Relative bradycardia as a clinical feature in patients with coronavirus disease 2019 (COVID-19): A report of two cases

Abstract

We treated two patients with COVID-19 pneumonia requiring mechanical ventilation. Case 1 was a 73-year-old Japanese man. Computed tomography (CT) revealed ground-glass opacities in both lungs. He had severe respiratory failure with a partial pressure of oxygen in arterial blood/fraction of inspiratory oxygen ratio (P/F ratio) of 203. Electrocardiogram showed a heart rate (HR) of 56 beats/min, slight ST depression in leads II, III, and aVF, and mild saddle-back type ST elevation in leads V1 and V2. High-sensitivity cardiac troponin T (cTnT) level was slightly elevated. Despite a high fever and hypoxemia, his HR remained within 50–70 beats/min. Case 2 was a 52-year-old Japanese woman. CT revealed ground-glass opacities in the lower left lung. Electrocardiogram showed a HR of only 81 beats/min, despite a body temperature of 39.2 °C, slight ST depression in leads V4, V5, V6, and a prominent U wave in multiple leads. She had an elevated cTnT and a P/F ratio of 165. Despite a high fever and hypoxemia, her HR remained within 50–70 beats/min. Both patients had a poor compensatory increase in their HR, despite their critical status. Relative bradycardia could be a cardiovascular complication and is an important clinical finding in patients with COVID-19. < Learning objective: We report two Japanese cases of COVID-19 pneumonia with relative bradycardia as a condition and no significant compensatory increase in heart rate despite high fever and severe hypoxemia. Relative bradycardia in COVID-19 might be associated with myocardial injury due to not only direct viral involvement but also systemic inflammation. We should carefully observe the occurrence of relative bradycardia because it could potentially be a clinical sign of COVID-19.>

Sinus bradycardia in a toddler with multisystem inflammatory syndrome in children (MIS-C) related to COVID-19

“…[4][5][6][7][8][9][10] Two papers speak specifically to associations between COVID-19 and relative bradycardia in adults, seen in states of high metabolic demand such as increased body temperature during which tachycardia would be expected. [11][12][13] One study found that one-third of adult patients with severe COVID-19 infection but overall stable vital signs developed sinus bradycardia at some point during the course of their illness. 4 Additionally, there are reports of adult patients infected with COVID-19 who develop bradycardia related to medications such as lopinavir-ritonavir, 14 hydroxychloroquine and other QT-interval-prolonging medications 15 and of course sedating medications.…”

“… 4–10 Two papers speak specifically to associations between COVID-19 and relative bradycardia in adults, seen in states of high metabolic demand such as increased body temperature during which tachycardia would be expected. 11–13 One study found that one-third of adult patients with severe COVID-19 infection but overall stable vital signs developed sinus bradycardia at some point during the course of their illness. 4 …”

A novel study on SARS‐COV‐2 virus associated bradycardia as a predictor of mortality‐retrospective multicenter analysis

“…3 Bradycardia in COVID-19 appears to be an important cardiac manifestation that has a multifactorial etiology and is increasingly becoming a characteristic clinical finding in patients with COVID-19. It has been described in isolated case reports, 4,5 a limited case series 6 defined as relative bradycardia with heart rate (HR) < 90 beats per minute (BPM) 7 and through a survey sent among cardiac electrophysiologists. 3 In Southern California, there have been a multitude of patients with COVID-19 with variable presentations.…”

Clarifying Terminology of Signs in COVID-19

“…Relative bradycardia is considered the most reliable and sensitive parameter when applied to cases where the body temperature is >38.9°C (102°F). Faget sign was named in honor of Jean Charles Faget (1818-1884) and initially reported in cases of yellow fever (42)(43)(44). Relative bradycardia has been described in a variety of infectious and noninfectious conditions, including a host of viral illness.…”

“…Relative bradycardia has been described in a variety of infectious and noninfectious conditions, including a host of viral illness. Although the mechanism is unknown, it has been hypothesized that it may be caused by a direct pathogenic effect on the myocardium or nodal tissue, inflammatory cytokines increasing the vagal tone and decreasing the heart rate variability or systemic autonomic dysregulation, or a possible link between angiotensin-converting enzyme 2 (ACE2), the receptor for COVID-19, and its expression on cardiac cells regulating autonomic heart rate control (44)(45)(46).…”