RAS inhibition for the prevention of Acute Respiratory Distress Syndrome (ARDS) in patients admitted with a COVID-19 infection
- Funded by Netherlands Organisation for Health Research and Development (ZonMW)
- Total publications:0 publications
Grant number: 1.043E+13
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Key facts
Disease
COVID-19Start & end year
20202022Known Financial Commitments (USD)
$553,877.84Funder
Netherlands Organisation for Health Research and Development (ZonMW)Principal Investigator
Dr. DHF GommansResearch Location
NetherlandsLead Research Institution
Netherlands Heart InstituteResearch Priority Alignment
N/A
Research Category
Clinical characterisation and management
Research Subcategory
Disease pathogenesis
Special Interest Tags
N/A
Study Type
Unspecified
Clinical Trial Details
N/A
Broad Policy Alignment
Pending
Age Group
Unspecified
Vulnerable Population
Unspecified
Occupations of Interest
Unspecified
Abstract
Project description The COVID-19 pandemic causes high morbidity and mortality because COVID-19 infection can cause acute lung damage and be complicated by severe acute respiratory distress syndrome (ARDS). The renin-angiotensin system (RAS), a well-known cardiovascular cascade, has also been shown to play a role in the development of ARDS. It is believed that the COVID-19 virus consumes the enzyme ACE2. This is an enzyme that normally breaks down angiotensin-II (ANG-II). Reduction of ACE2 can cause an accumulation of ANG-II, which can lead to acute lung damage with IC admissions and possibly death. Research It is hypothesized that RAS inhibition by ACE inhibitors and angiotensin receptor blockers, such as, for example, lisinopril and valsartan, respectively, may reverse the development of acute lung damage and ARDS in hospitalized COVID-19 patients, thereby preventing IC admissions and death.