About: Hypertension, the renin–angiotensin system, and the risk of lower respiratory tract infections and lung injury: implications for COVID-19: European Society of Hypertension COVID-19 Task Force Review of Evidence

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About: Hypertension, the renin–angiotensin system, and the risk of lower respiratory tract infections and lung injury: implications for COVID-19: European Society of Hypertension COVID-19 Task Force Review of Evidence Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Hypertension, the renin–angiotensin system, and the risk of lower respiratory tract infections and lung injury: implications for COVID-19: European Society of Hypertension COVID-19 Task Force Review of Evidence
Creator	Abd, Engi Algharably, El-Hady Angiotensin, Hypertension Azizi, Michel Burnier, Michel Cardiovascular, • Covid-19, • Dobrowolski, Piotr Guzik, Tomasz Gü Nther Riemer, Thomas Januszewicz, Andrzej Kreutz, Reinhold Lung, • Persu, Alexandre Prejbisz, Aleksander Wang, Ji-Guang
Source	Medline; PMC
abstract	Systemic arterial hypertension (referred to as hypertension herein) is a major risk factor of mortality worldwide, and its importance is further emphasized in the context of the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection referred to as COVID-19. Patients with severe COVID-19 infections commonly are older and have a history of hypertension. Almost 75% of patients who have died in the pandemic in Italy had hypertension. This raised multiple questions regarding a more severe course of COVID-19 in relation to hypertension itself as well as its treatment with renin–angiotensin system (RAS) blockers, e.g. angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs). We provide a critical review on the relationship of hypertension, RAS, and risk of lung injury. We demonstrate lack of sound evidence that hypertension per se is an independent risk factor for COVID-19. Interestingly, ACEIs and ARBs may be associated with lower incidence and/or improved outcome in patients with lower respiratory tract infections. We also review in detail the molecular mechanisms linking the RAS to lung damage and the potential clinical impact of treatment with RAS blockers in patients with COVID-19 and a high cardiovascular and renal risk. This is related to the role of angiotensin-converting enzyme 2 (ACE2) for SARS-CoV-2 entry into cells, and expression of ACE2 in the lung, cardiovascular system, kidney, and other tissues. In summary, a critical review of available evidence does not support a deleterious effect of RAS blockers in COVID-19 infections. Therefore, there is currently no reason to discontinue RAS blockers in stable patients facing the COVID-19 pandemic.
has issue date	2020-04-15(xsd:dateTime)
bibo:doi	10.1093/cvr/cvaa097
bibo:pmid	32293003
has license	no-cc
sha1sum (hex)	494913c577d051e54e07c4c5afe82793ef98ef97
schema:url	https://doi.org/10.1093/cvr/cvaa097
resource representing a document's title	Hypertension, the renin–angiotensin system, and the risk of lower respiratory tract infections and lung injury: implications for COVID-19: European Society of Hypertension COVID-19 Task Force Review of Evidence
has PubMed Central identifier	PMC7184480
has PubMed identifier	32293003
schema:publication	Cardiovasc Res
resource representing a document's body	covid:494913c577d051e54e07c4c5afe82793ef98ef97#body_text
is schema:about of	named entity 'RENIN-ANGIOTENSIN SYSTEM' named entity 'SEVERE COURSE' named entity 'RISK FACTOR' named entity 'ALMOST' named entity 'EVIDENCE' named entity 'DELETERIOUS' named entity 'POTENTIAL' named entity 'SUPPORT' named entity 'INFECTIONS' named entity 'SYSTEMIC ARTERIAL HYPERTENSION' named entity 'HAVE' named entity 'cell entry' named entity 'haemodynamic' named entity 'ace2' named entity 'angiotensin II receptor type 1' named entity 'case fatality rate' named entity 'SARS-CoV-2' named entity 'severe acute respiratory syndrome coronavirus 2' named entity 'lower respiratory tract infections' named entity 'kidney' named entity 'hypertension' named entity 'hypertension' named entity 'COVID' named entity 'ARBs' named entity 'lung' named entity 'RAS' named entity 'RAS' named entity 'RAS' named entity 'hypertension' named entity 'angiotensin-converting enzyme 2' named entity 'COVID' named entity 'lower respiratory tract infections' named entity 'lung' named entity 'pharmacological' named entity 'ARBs' named entity 'hypertension' named entity 'TMPRSS2' named entity 'granulocyte colony-stimulating factor' named entity 'ACEIs' named entity 'Hypertension' named entity 'SARS-CoV-2' named entity 'China' named entity 'urine' named entity 'Italy' named entity 'SARS-CoV-2' named entity 'lymphocytes' named entity 'single-cell transcriptomic' named entity 'hypertension' named entity 'LRTI' named entity 'receptor' named entity 'ACE2' named entity 'pathogenicity' named entity 'carboxypeptidase' named entity 'pneumonia' named entity 'heart failure' named entity 'RAS' named entity 'AKI' named entity 'up-regulated' named entity 'hypertension' named entity 'ACEIs' named entity 'metalloprotease' named entity 'brush border' named entity 'olmesartan' named entity 'adverse outcome' named entity 'vasodilation' named entity 'ACE2'

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