Subject(s)
Heart Valve Prosthesis Implantation , Heart Valve Prosthesis , Pulmonary Valve Insufficiency , Pulmonary Valve , Tetralogy of Fallot , Cardiac Catheterization/adverse effects , Cardiac Catheterization/methods , Heart Valve Prosthesis Implantation/adverse effects , Heart Valve Prosthesis Implantation/methods , Humans , Pulmonary Valve/diagnostic imaging , Pulmonary Valve/surgery , Pulmonary Valve Insufficiency/diagnostic imaging , Pulmonary Valve Insufficiency/etiology , Pulmonary Valve Insufficiency/surgery , Tetralogy of Fallot/surgery , Treatment OutcomeABSTRACT
Pulmonary valve endocarditis after transcatheter pulmonary valve implantation has been an emerging concern due to the increasing prevalence of transcatheter placement of pulmonary valve in the treatment of residual right ventricular outflow tract stenosis or regurgitation. Pulmonary valve endocarditis is a dreadful complication of transcatheter pulmonary valve implantation that have been reported with Melody valve (Medtronic, Inc., Minneapolis, MN) and Edward Sapien valve (Edwards Life Sciences, Irvine, CA) till date. There are scanty available literatures for pulmonary valve endocarditis with Venus P valve (Venus Medtech, Hangzhou, China) implantation. Furthermore, cardiovascular comorbidity is common in COVID-19 infection with limited evidence of COVID-19 infection concomitant with infective endocarditis. This case happens to be the first reported case of infective endocarditis of pulmonary valve with concomitant COVID-19 infection and also delayed presentation of pulmonary valve endocarditis with Venus P valve implantation.
Subject(s)
COVID-19 , Endocarditis , Heart Valve Prosthesis Implantation , Heart Valve Prosthesis , Pulmonary Valve Insufficiency , Pulmonary Valve , Cardiac Catheterization , Endocarditis/diagnosis , Endocarditis/etiology , Endocarditis/surgery , Heart Valve Prosthesis/adverse effects , Heart Valve Prosthesis Implantation/adverse effects , Humans , Prosthesis Design , Pulmonary Valve/diagnostic imaging , Pulmonary Valve/surgery , Pulmonary Valve Insufficiency/etiology , Pulmonary Valve Insufficiency/surgery , SARS-CoV-2 , Treatment OutcomeABSTRACT
COVID-19, caused by SARS-CoV-2 involves multiple organs including cardiovascular, pulmonary and central nervous system. Understanding how SARS-CoV-2 infection afflicts diverse organ systems remains challenging. Particularly vexing has been the problem posed by persistent organ dysfunction known as "long COVID", which includes cognitive impairment. Here we provide evidence linking SARS-CoV-2 infection to activation of TGF beta signaling and oxidative overload. One consequence is oxidation of the ryanodine receptor/calcium (Ca2+) release channels (RyR) on the endo/sarcoplasmic (ER/SR) reticuli in heart, lung and brains of patients who succumbed to COVID-19. This depletes the channels of the stabilizing subunit calstabin2 causing them to leak Ca2+ which can promote heart failure, pulmonary insufficiency and cognitive and behavioral defects. Ex-vivo treatment of heart, lung, and brain tissues from COVID-19 patients using a Rycal drug (ARM210) prevented calstabin2 loss and fixed the channel leak. Of particular interest is that neuropathological pathways activated downstream of leaky RyR2 channels in Alzheimer's Disease (AD) patients were activated in COVID-19 patients. Thus, leaky RyR2 Ca2+ channels may play a role in COVID-19 pathophysiology and could be a therapeutic target for amelioration of some comorbidities associated with SARS-CoV-2 infection.