An elevated cholesterol concentration has been suspected to increase the
susceptibility for SARS-COV-2 infection. Cholesterol plays a central role in the
mechanisms of the SARS-COV-2 infection. In contrast, higher HDL-cholesterol
levels seem to be protective. During COVID-19 disease, LDL-cholesterol and
HDL-cholesterol appear to be decreased. On the other hand, triglycerides (also
in different lipoprotein fractions) were elevated. Lipoprotein(a) may increase
during this disease and is most probably responsible for thromboembolic events.
This lipoprotein can induce a progression of atherosclerotic lesion formation.
The same is suspected for the SARS-COV-2 infection itself. COVID-19 patients are
at increased risk of incident cardiovascular diseases, including cerebrovascular
disorders, dysrhythmias, ischemic and non-ischemic heart disease, pericarditis,
myocarditis, heart failure, and thromboembolic disorders. An ongoing
lipid-lowering therapy, including lipoprotein apheresis, is recommended to be
continued during the COVID-19 disease, though the impact of lipid-lowering drugs
or the extracorporeal therapy on prognosis should be studied in further
investigations.