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. 2020 Dec:229:102734.
doi: 10.1016/j.autneu.2020.102734. Epub 2020 Sep 21.

Syncope at SARS-CoV-2 onset

Ciro Canetta  1 , Silvia Accordino  1 , Elisabetta Buscarini  2 , Gianpaolo Benelli  3 , Giuseppe La Piana  4 , Alessandro Scartabellati  5 , Giovanni Viganò  6 , Roberto Assandri  7 , Alberto Astengo  8 , Chiara Benzoni  8 , Gianfranco Gaudiano  8 , Daniele Cazzato  9 , Davide Sebastiano Rossi  9 , Susanna Usai  10 , Irene Tramacere  11 , Giuseppe Lauria  12
Affiliations

Syncope at SARS-CoV-2 onset

Ciro Canetta et al. Auton Neurosci. 2020 Dec.

Abstract

We describe clinical and laboratory findings in 35 patients tested positive for SARS-CoV-2 by reverse transcriptase-polymerase chain reaction on nasopharyngeal swab experiencing one or multiple syncope at disease onset. Clinical neurologic and cardiologic examination, and electrocardiographic findings were normal. Chest computed tomography showed findings consistent with interstitial pneumonia. Arterial blood gas analysis showed low pO2, pCO2, and ratio of arterial oxygen partial pressure to fractional inspired oxygen (PaO2/FiO2) indicating hypocapnic hypoxemia. Patients who presented with syncope showed significantly lower heart rate as compared to 68 SARS-CoV-2 positive that did not. Such poorer than expected compensatory heart rate increase may have led to syncope based on individual susceptibility. We speculate that SARS-CoV-2 could have caused angiotensin-converting enzyme-2 (ACE2) receptor internalization in the nucleus of the solitary tract and other midbrain nuclei, impairing baroreflex and chemoreceptor response, and inhibiting the compensatory tachycardia during acute hypocapnic hypoxemia.

Keywords: Angiotensin-converting enzyme-2 (ACE2) receptor; Baroreceptor reflex; Central chemoreceptors; Hypocapnic hypoxemia; SARS-CoV-2; Syncope.

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