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ISSN: 1734-1922
Archives of Medical Science
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vol. 16

Lipid-lowering therapy and renin-angiotensin-aldosterone system inhibitors in the era of the COVID-19 pandemic

Niki Katsiki
Maciej Banach
2, 3
Dimitri P. Mikhailidis

First Department of Internal Medicine, Diabetes Centre, Division of Endocrinology and Metabolism, AHEPA University Hospital, Thessaloniki, Greece
Cardiovascular Research Centre, University of Zielona Gora, Zielona Gora, Poland
Polish Mother’s Memorial Hospital Research Institute (PMMHRI), Lodz, Poland
Department of Clinical Biochemistry, Royal Free Hospital campus, University College London Medical School, University College London (UCL), London, UK
Arch Med Sci 2020; 16 (3): 485–489
Online publish date: 2020/04/14
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The novel coronavirus (severe acute respiratory syndrome coronavirus 2 – SARS-Cov-2) disease 2019 (COVID-19) pandemic has been associated with severe respiratory disease incidence and increased mortality [1]. Angiotensin converting enzyme (ACE) 2 is a homologue of ACE, but also a receptor for the coronaviruses [2]. ACE2 is highly expressed in the lungs, heart, gastrointestinal (GI) tract and kidney, thus affecting the cardiovascular system (CV) and the immune system [3]. The overexpression of ACE2 was reported to enhance viral entry and replication intracellularly [4]. COVID-19, also called SARS-CoV-2, may also use ACE2 as a receptor to initiate infection, leading to severe complications from the heart (acute coronary syndrome (ACS) and fulminant myocarditis), lungs (pneumonia and acute respiratory distress syndrome (ARDS)) and GI tract (diarrhoea syndrome) [5].
ACE2 gene expression is affected by several factors, including gender (ACE2 gene is X-linked), ACE2 gene polymorphisms, comorbidities (increased in the presence of CVD, hypertension, diabetes), and drug therapy [6]. With regard to drugs, angiotensin II receptor blockers (ARBs) and mineralocorticoid receptor antagonists (MRA) have been reported to raise ACE2 activity in human and animal studies [7]. There are only a few animal studies available showing that statins may also increase ACE2 activity [8, 9]. In the era of the COVID-19 pandemic, such a drug effect may be considered as potentially worrying [10]. In this context, it was recently even suggested that ARBs could be replaced with ACE inhibitors and that statin treatment may be discontinued during the pandemic, particularly in primary prevention settings [11].
However, before implementing such strategies, we should consider several issues. Firstly, as the COVID-19 infection progresses, ACE2 is downregulated, thus potentially generating an inflammatory response leading to impaired cardiac contractility and acute lung injury [5, 7, 12]. Therefore, reduced ACE2 expression is linked to worse outcomes. On the other hand, ACE2 overexpression has been associated with several beneficial effects, i.e. prevention of adverse cardiac remodelling and fibrosis, improvement of vascular endothelial dysfunction, reduction of blood pressure, and protection from ARDS [7, 12]. Both statins and ARBs were reported to exert these benefits.
Secondly, a combination of statins/ARBs were used during the 2014 Ebola virus disease epidemic in Sierra...

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