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10.1093/cvr/cvaa097 http://scihub22266oqcxt.onion/10.1093/cvr/cvaa097 32293003!7184480!32293003     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32293003&cmd=llinks): Failed to open stream: HTTP request failed! 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Hypertension, the renin-angiotensin system, and the risk of lower respiratory tract infections and lung injury: implications for COVID-19 |pdf=|usr=}}{{32293003}} gab.com Text Hypertension, the renin-angiotensin system, and the risk of lower respiratory tract infections and lung injury: implications for COVID-19 JO: Cardiovasc Res http://www.kidney.de/pget.php?&tw=1&pmid=32293003 #FOAvip 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. Twit Text FOAVip Hypertension, the renin-angiotensin system, and the risk of lower respiratory tract infections and lung injury: implications for COVID-19 ????Cardiovasc Res http://www.kidney.de/pget.php?&tw=1&pmid=32293003 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32293003 #FOAvip English Wikipedia <ref>{{Cite pmid|32293003}}</ref> Hypertension, the renin-angiotensin system, and the risk of lower respiratory tract infections and lung injury: implications for COVID-19 #MMPMID32293003 Kreutz R; Algharably EAE; Azizi M; Dobrowolski P; Guzik T; Januszewicz A; Persu A; Prejbisz A; Riemer TG; Wang JG; Burnier M Cardiovasc Res 2020[Aug]; 116 (10): 1688-1699 PMID32293003show ga 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. |Angiotensin II Type 1 Receptor Blockers/pharmacology[MESH] |Angiotensin-Converting Enzyme Inhibitors/*pharmacology[MESH] |Betacoronavirus/*pathogenicity[MESH] |COVID-19[MESH] |Coronavirus Infections/diagnosis/*drug therapy[MESH] |Humans[MESH] |Lung Injury/*complications/drug therapy/virology[MESH] |Pandemics[MESH] |Pneumonia, Viral/diagnosis/*drug therapy[MESH] |Renin-Angiotensin System/drug effects[MESH] |Respiratory Tract Infections/*drug therapy/virology[MESH] |Risk Factors[MESH]Hypertension, the renin-angiotensin system, and the risk of lower resp(epmc).pdf DeepDyve Pubget Overpricing