Introduction
Patients with cardiovascular and renal diseases are frequently treated
with drugs interfering with the Renin-Angiotensin-Aldosterone (RAAS)
System. The clinical benefit of angiotensin-converting enzyme (ACE)
inhibitors and angiotensin II receptor blockers (ARBs) are well
established and hence became part of treatment guidelines for these
patients worldwide. Angiotensin-converting enzyme 2 (ACE2) is an
isoenzyme of angiotensin-converting enzyme 1 (ACE). Both are essential
parts of the RAAS, see figure 1. ACE2 is involved in cardiac function,
the development of hypertension and diabetes mellitus. Also, ACE2 has
been identified as a functional receptor for coronaviruses, including
SARS-CoV and SARS-CoV-2. SARS-CoV-2 infection is triggered by the
binding of the spike protein of the virus to ACE2. It was suggested that
patients with cardiac and renal diseases, hypertension, and diabetes,
who are treated with drugs potentially increasing ACE2 expression in the
lungs such as ACE inhibitors or angiotensin II receptor blockers are at
higher risk for severe COVID-19 infection (Fang, Karakiulakis & Roth,
2020; Zheng, Ma, Zhang & Xie, 2020). In the current review, we are
summarizing the molecular evidence for this hypothesis (see figure 1 and
supplementary material: Molecular Background), next we present results
of a meta-analysis of studies analyzing the effects of RAAS blocking
drugs (ACE inhibitors, ARBs) on the risk and mortality of pneumonia in
non-COVID-19 patients and also meta-analysed the 17 so far published
studies on this topic in COVID-19 patients.