COVID-19 has caused millions of deaths primarily caused by an inappropriate systemic inflammatory response to SARS-CoV-2 and progression to refractory hypoxemia, leading to acute respiratory distress syndrome. Cardiac lesions, including increased biomarkers, pulmonary embolism, and impaired ventricular function on echocardiography have also been associated with increased mortality. Furthermore, SARS-CoV-2 uses the receptor for angiotensin-converting enzyme 2 (ACE-2) to enter cells and modulates the renin-angiotensin-aldosterone system (RAAS), a major factor in the unwanted cardiac remodeling.
In this article, French clinicians report the results of a study aimed at clarifying the interaction between RAAS, systemic inflammation and pulmonary and cardiac involvement in COVID-19 (NCT04320017). The main objectives here were to delineate how these variables are associated with each other and to identify among them independent predictors of 30-day mortality.
The authors showed that:
- right ventricular dysfunction in COVID-19 is independent of RAAS pathway alterations,
- circulating aldosterone concentrations emerge as a potential new predictor of COVID-19 mortality, after adjusting for echocardiographic findings, cardiac biomarkers, systemic inflammation, and extension of lung damage.
Clinicians advocate large-scale prospective studies to consolidate these results.
