Electrophysiology in the time of coronavirus: coping with the great wave.

Jia Li; Patrizio Mazzone; Lisa Leung; Weiqian Lin; Giuseppe D'Angelo; Jun Ma; Jin Li; Zaki Akhtar; Yuechun Li; Paolo E Della Bella; Jiafeng Lin; Mark M Gallagher

The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/2020.03.30.20044776 doi: medRxiv preprint A history of ischaemic heart disease also predicts mortality in COVID-19. Any acute inflammatory condition can destabilise coronary plaque and triger acute coronary syndromes. A minority of patients with COVID-19 may present acutely with cardiac sounding symptoms. 13 It is not clear whether the apparent high mortality in patients with ischaemic heart disease represents an effect on ACE2 receptor expression, a vulnerability to ischaemic complications of the systemic illness or a bias against such patients when ventilatiors must be rationed. The pathophysiology of COVID-19 and its routes of systemic transmission remain incompletely understood. Observations had been noted of its neuroinvasive potential via peripheral neuronal trans-synaptic route and viral preponderance in organs with low expression of ACE2. 15 Brugada syndrome is a concern as the prolonged febrile illness characteristic of COVID-19 has the propensity to trigger arrhythmias. No such case has been reported, but like patients with heart failure and ischaemic heart disease, those with Brugada syndrome should take particular care to isolate themselves from likely sources of infection.