Washington [US], December 11 (ANI): Advanced statistical analyses of demographic and clinical data from 576 COVID-19 patients, admitted to the Ente Ospedaliero Cantonale in Switzerland between March 1 and May 1 this year average age 72 years, suggest that renin-angiotensin-aldosterone system inhibitors (RAASi) increased survival in Covid-19 patients at elevated risk of in-hospital death due to factors such as age, kidney disease, and cardiovascular disease and support further investigation of RAASi for COVID-19 treatment.
As the COVID-19 pandemic is spreading around the world, increasing evidence highlights the role of cardiometabolic risk factors in determining the susceptibility to the disease.
The fragmented data collected during the initial emergency limited the possibility of investigating the effect of highly correlated covariates and of modeling the interplay between risk factors and medication.
The present study is based on comprehensive monitoring of 576 COVID-19 patients. Different statistical approaches were applied to gain a comprehensive insight in terms of both the identification of risk factors and the analysis of dependency structure among clinical and demographic characteristics.
The study “A data-driven approach to identify risk profiles and protective drugs in COVID-19,” was published in Proceedings of the National Academy of Sciences of the United States of America, a peer-reviewed multidisciplinary scientific journal.
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus enters host cells by binding to the angiotensin-converting enzyme 2 (ACE2), but whether or not renin-angiotensin-aldosterone system inhibitors (RAASi) would be beneficial to Covid-19 cases remains controversial.
The survival tree approach was applied to define a multilayer risk stratification and better profile patient survival with respect to drug regimens, showing a significant protective effect of RAASi with a reduced risk of in-hospital death. Bayesian networks were estimated, to uncover complex interrelationships and confounding effects.
The results confirmed the role of RAASi in reducing the risk of death in Covid-19 patients. De novo treatment with RAASi in patients hospitalized with COVID-19 should be prospectively investigated in a randomized controlled trial to ascertain the extent of risk reduction for in-hospital death in COVID-19.
The need of discovering rapidly new findings on COVID-19 medications has been rushing publication, whereas the type of data collected in emergency needed a further degree of caution in data management and analysis with respect to the usual observational designed studies.
Hence, in the recent literature, standard statistical approaches often failed to provide reliable and reproducible results and to control for the highly correlated structure among covariates, while accounting for potential confounders in risk prediction.
Covid-19 is characterized by highly variable clinical manifestations and severity, ranging from asymptomatic to multiorgan failure. Older age and cardiovascular comorbidities are among the most important risk factors influencing the virus-host interaction and the clinical outcome of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.
Understanding the relationship between cardiovascular disease (CVD), therapy, and COVID-19 outcomes is important to guide clinical and public health interventions. Several treatment approaches, also in light of previous comorbidities, have been adopted to reduce Covid-19 mortality in hospitalized patients.
Among other medications, renin-angiotensin-aldosterone system inhibitors (RAASi) have been a major object of interest. There are two major arms of RAAS; one arm, the Angiotensin II (Ang II) type 1 receptor (AT1R) pathway, is proinflammatory and can cause acute lung injury. The other arm, the angiotensin-converting enzyme 2 (ACE2)-Ang-(1-7)-Mas receptor (MasR) pathway is anti-inflammatory because ACE2 metabolizes Ang II, thus reducing its levels and converting it to the anti-inflammatory peptide, Ang-(1-7).
ACE2 is the receptor for coronaviruses, including SARS-CoV-2. When SARS-CoV-2 binds to ACE2, the enzyme is no longer functional, and therefore the proinflammatory Ang II-AT1R is no longer blocked by the ACE2-Ang-(1-7)-MasR pathway; this imbalance can cause acute lung injury. RAASi have been hypothesized to influence the clinical course of COVID-19 because of the role of ACE2 as a functional receptor for the virus entrance into the cells.
Initially, some authors raised concerns regarding the potential harm of RAASi in COVID-19, but these were not confirmed, and, more recently, a potential protective role was postulated, but until now not unequivocally proven.