Abstract
Coronavirus Disease 2019 (COVID-19) is caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which primarily targets the human respiratory system and may lead to severe pneumonia and ultimately death. Mortality rate is particurlarly high among people beyond the sixth decade of life with cardiovascular and metabolic diseases. The discovery that the SARS-CoV-2 uses the renin-angiotensin system (RAS) component ACE2 as a receptor to invade host epithelial cells and cause organs damage resulted in a debate regarding the role of ACE inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) therapies during COVID-19 pandemic. Some authors proposed the discontinuation of ACEIs and ARBs for cardiovascular, kidney, and metabolic diseases, while expert opinions have discouraged that due to limited empirical evidence of their negative effect on COVID-19 outcomes, and that withdrawing treatment may contribute to clinical decompensation in high-risk patients. Moreover, as cardiovascular and metabolic diseases are associated with neurodegenerative and psychiatric disorders, especially among older adults, a critical appraisal of the potential positive effects of ACEIs and ARBs is highly needed. Herein, we aim to discuss the conundrum of ACEIs and ARBs use in high-risk patients for COVID-19, and their potential protective role on the development and/or progression of geriatric neuropsychiatric disorders.
Highlights
Coronavirus Disease 2019 (COVID-19, named by WHO on Feb 11, 2020) outbreak was officially reported in December 2019 in Wuhan, Hubei Province, China, and rapidly reached a pandemic status [1,2,3]
The COVID-19 is caused by a novel positive-sense single-stranded RNA virus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [2, 4]
The first case of viral meningoencephalitis caused by the 2019-nCoV was reported in a 24-years-old man admitted to a hospital with seizures accompanied by impaired arousal, with the virus genome being identified in the cerebrospinal fluid (CSF) [12]
Summary
Coronavirus Disease 2019 (COVID-19, named by WHO on Feb 11, 2020) outbreak was officially reported in December 2019 in Wuhan, Hubei Province, China, and rapidly reached a pandemic status [1,2,3]. The COVID-19 is caused by a novel positive-sense single-stranded RNA virus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [2, 4]. Similar to other coronavirus like the SARS-CoV-1, the novel SARS-CoV-2 primarily targets the human respiratory system and may cause severe pneumonia and death. 36.4% (78/214) of patients diagnosed with COVID-19 experienced neurological symptoms like dizziness, headache, impaired arousal, ataxia, and seizure. The first case of viral meningoencephalitis caused by the 2019-nCoV was reported in a 24-years-old man admitted to a hospital with seizures accompanied by impaired arousal, with the virus genome being identified in the cerebrospinal fluid (CSF) [12]. Further evidence provided by systematic reviews and meta-analysis has supported the occurrence of neurological manifestations in patients with COVID-19 [13, 14]
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