COVID-19 disease causes severe lung damage with thousands of deaths. It is already known that the SARS-CoV-2 virus attacks lung cells that display a specific protein on their surface, the so-called receptor ACE2. So far, the main focus of research has been on the effects of COVID-19 on lung conditions. However, patients with cardiovascular disease are affected by a much more severe course of the disease. They have a much higher mortality rate from COVID-19 disease.
There is currently much controversy as to which cells carry ACE2 and whether so-called angiotensin-converting enzyme inhibitors (ACE inhibitors) or angiotensin-receptor blockers (ARBs) lead to an increased presence of the SARS CoV-2 receptor ACE2 in lung and heart cells. Both are drugs that are frequently used to treat cardiovascular diseases. This could contribute to severe COVID-19 progression in patients.
An interdisciplinary cardiac research team at the University Hospital Frankfurt led by Prof. Stefanie Dimmeler, Director of the Institute for Cardiovascular Regeneration, Prof. Andreas Zeiher, Director of Cardiology, and Prof. Thomas Walther, Director of Cardiac Surgery, has now shown in a publication in the European Heart Journal the differences of the ACE2 presentation on tissue samples from patients with cardiovascular diseases.
The researchers discovered that ACE2 was significantly elevated in heart muscle cells and vascular cells of the heart of patients with heart disease compared to healthy controls. Interestingly, the studies also demonstrated for the first time that heart cells of patients treated with ACE inhibitors showed a significantly higher ACE2 presentation.
These data suggest that it is not only essential to monitor SARS-CoV-2-infected patients for cardiovascular complications, but especially to investigate further the influence of ACE2 inhibitors and ARB blockers on the course of COVID-19.
Original paper:
Cell type-specific expression of the putative SARS-CoV-2 receptor ACE2 in human hearts. Luka Nicin et al. European Heart Journal, ehaa311
Source: Press release University Hospital Frankfurt