RAS inhibition to prevent 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
20202023Funder
Netherlands Organisation for Health Research and Development (ZonMW)Principal Investigator
I GommansResearch Location
N/ALead Research Institution
Netherlands Heart InstituteResearch Priority Alignment
N/A
Research Category
Clinical characterisation and management
Research Subcategory
Supportive care, processes of care and management
Special Interest Tags
N/A
Study Type
Clinical
Clinical Trial Details
Not applicable
Broad Policy Alignment
Pending
Age Group
Unspecified
Vulnerable Population
Unspecified
Occupations of Interest
Unspecified
Abstract
The COVID-19 pandemic causes high morbidity and mortality because COVID-19 infection can cause acute lung damage and be complicated with severe acute respiratory distress syndrome (ARDS). The renin-angiotensin system (RAS), a well-known cardiovascular cascade, also appears to play a role in the development of ARDS. The COVID-19 virus is believed to consume 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, resulting in ICU admissions and possible death. Research The hypothesis is that RAS inhibition using ACE inhibitors and angiotensin receptor blockers, such as lisinopril and valsartan respectively, can prevent the development of acute lung damage and ARDS in hospitalized COVID-19 patients, thereby preventing ICU admissions and deaths.