Familial Hypercholesterolemia and COVID-19: Connections and Risks
Patients with familial hypercholesterolemia (FH) likely have a higher risk of COVID-19 complications both in the acute phase of the infection and for a relatively long period after its occurrence.
Pathophysiological Connections
The level of cholesterol in the form of low-density lipoproteins (LDL-c) is elevated prenatally in patients with FH, which in the long term leads to very early development of systemic endothelial dysfunction. Patients with FH (both homozygous and heterozygous variants) already have dysfunctional endothelium at a relatively young age, which is susceptible to further damage from the direct effect of viral infection or the inflammatory response typical of severe COVID-19. Additionally, higher serum lipoprotein (a) levels are often noted in FH patients, further exacerbating endothelial damage.
Statin Treatment in the Acute Phase of COVID-19
Statins are indicated for the treatment of FH from the age of 8. Current data suggest that individuals who use statins long-term to prevent atherosclerotic cardiovascular diseases should continue this treatment during the acute phase of COVID-19. It should even be considered whether statin treatment should be intensified during the acute phase of the infection to effectively reduce LDL-c levels and thus lower the risk of developing cardiovascular complications of COVID-19. This recommendation primarily pertains to FH patients treated with statins, but it can likely be applied to the use of other lipid-lowering treatments or other diagnoses.
Available data further suggest that the most important mechanism behind the beneficial effect of statins in COVID-19 infection is the reduction of microthrombi formation. Additionally, COVID-19 may trigger persistent acceleration of atherosclerosis from a long-term perspective. Statins, therefore, have the potential to improve prognosis in the acute phase by reducing arterial-level endothelial dysfunction (in epicardial coronary circulation, carotids, and intracranial arteries) and during convalescence by improving microvascular-level endothelial dysfunction (in intramyocardial microvessels). They should thus be administered continuously during the acute, convalescent, and chronic phases of COVID-19.
Conclusion
Currently, we do not have data to precisely determine the increased risk of atherothrombotic complications of COVID-19 in FH patients. However, it is necessary to inform these patients that they likely have an increased risk of COVID-19 complications. They should be aware that lipid-lowering treatment must be taken during the acute phase of the infection. In conjunction with other COVID-19 treatments, emphasis should be placed on effectively reducing high LDL-c levels in FH patients.
(epa)
Source: Vuorio A., Raal F., Kaste M., Kovanen P. T. Familial hypercholesterolaemia and COVID-19: a two-hit scenario for endothelial dysfunction amenable to treatment. Atherosclerosis 2021 Jan 24; 320: 53−60, doi: 10.1016/j.atherosclerosis.2021.01.021.
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