PropertyValue
?:abstract
  • Abstract In December 2019, a new type of coronavirus emerged in the city of Wuhan, China This novel virus has unleashed a pandemic that has inflicted a considerable impact on public health and the economy and has therefore become a severe concern worldwide This new virus -named SARS-CoV-2has been rapidly investigated in order to create knowledge aimed at achieving its control Comparative studies with SARS-CoV virus, responsible for the 2002-2003 pandemic, suggest that SARS-CoV-2 requires the same receptor to bind and infect cells: angiotensin converting enzyme 2 (ACE-2) This hypothesis has been thoroughly supported by a variety of in vitro research and is currently considered a potential therapeutic target ACE-2 is part of the counter-regulatory renin-angiotensin system, exerting effects in pulmonary, renal and cardiovascular systems In this context, concerns have arisen in regards to the vulnerability of hypertensive patients against COVID-19, given that there is evidence that may suggest that polymorphisms associated to hypertension may increase the expression of ACE-2 Moreover, preclinical studies have shown that antihypertensive drugs may increase the expression of this enzyme In this review article, we present the current state of the art on this polemic topic Our critical analysis suggest that there is no robust clinical evidence supporting the hypothesis that the use of antihypertensive drugs can increase vulnerability to infection with SARS-CoV-2 Therefore, we recommend that the use of these therapeutic agents should not be discontinued in hypertensive patients in risk to or suffering COVID-19
is ?:annotates of
?:creator
?:journal
  • Revista_chilena_de_cardiología
?:license
  • unk
?:publication_isRelatedTo_Disease
is ?:relation_isRelatedTo_publication of
?:source
  • WHO
?:title
  • Anti hypertensive agents in patients with COVID-19 Antihipertensivos en pacientes con COVID-19/ Anti hypertensive agents in patients with COVID-19
?:type
?:who_covidence_id
  • #635041
?:year
  • 2020

Metadata

Anon_0  
expand all