The potential role of SARS‐CoV‐2 infection in acute coronary syndrome and type 2 myocardial infarction (T2MI): Intertwining spread

Abstract

Coronavirus disease 2019 (COVID‐19) is a novel pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). It has been shown that SARS‐CoV‐2 infection‐induced inflammatory and oxidative stress and associated endothelial dysfunction may lead to the development of acute coronary syndrome (ACS). Therefore, this review aimed to ascertain the link between severe SARS‐CoV‐2 infection and ACS. ACS is a spectrum of acute myocardial ischemia due to a sudden decrease in coronary blood flow, ranging from unstable angina to myocardial infarction (MI). Primary or type 1 MI (T1MI) is mainly caused by coronary plaque rupture and/or erosion with subsequent occlusive thrombosis. Secondary or type 2 MI (T2MI) is due to cardiac and systemic disorders without acute coronary atherothrombotic disruption. Acute SARS‐CoV‐2 infection is linked with the development of nonobstructive coronary disorders such as coronary vasospasm, dilated cardiomyopathy, myocardial fibrosis, and myocarditis. Furthermore, SARS‐CoV‐2 infection is associated with systemic inflammation that might affect coronary atherosclerotic plaque stability through augmentation of cardiac preload and afterload. Nevertheless, major coronary vessels with atherosclerotic plaques develop minor inflammation during COVID‐19 since coronary arteries are not initially and primarily targeted by SARS‐CoV‐2 due to low expression of angiotensin‐converting enzyme 2 in coronary vessels. In conclusion, SARS‐CoV‐2 infection through hypercytokinemia, direct cardiomyocyte injury, and dysregulation of the renin‐angiotensin system may aggravate underlying ACS or cause new‐onset T2MI. As well, arrhythmias induced by anti‐COVID‐19 medications could worsen underlying ACS.

Mixed storm in SARS‐CoV‐2 infection: A narrative review and new term in the Covid‐19 era

“… 104 Besides, retrospective studies showed that low levels of TC and LDL‐C could predict more severe involvement and increased risk of cardiovascular diseases due to changes. 105 , 106 , 107 A systematic review and meta‐analysis showed that lipid profile is associated with both the severity and mortality in Covid‐19 patients. Therefore, the lipid profile may be used for assessing the severity and prognosis of Covid‐19.…”

“…However, the Covid‐19 patients had lower TC and LDL‐C levels upon admission that would gradually recover as the patients' clinical condition improved 104 . Besides, retrospective studies showed that low levels of TC and LDL‐C could predict more severe involvement and increased risk of cardiovascular diseases due to changes 105–107 . A systematic review and meta‐analysis showed that lipid profile is associated with both the severity and mortality in Covid‐19 patients.…”

SARS-CoV-2 infection and dysregulation of nuclear factor erythroid-2-related factor 2 (Nrf2) pathway

“…In addition, activators of the Nrf2 pathway can reduce exaggerated intra-renal AngII in diabetic patients and the development of diabetic nephropathy (Abdo et al 2015 ). The SARS-CoV-2 viral spike protein binds to ACE2, which aids viral entrance into the host cell (Al-Kuraishy et al 2023c , 2023e , 2022b ; Alsaidan et al 2023 ). In light of the probable elevation the expression of ACE2 by these drugs, there has been growing suspicion that ACE inhibitors and Ang II receptor blockers may raise the risk of the onset and severity of COVID-19 (Al-Kuraishy et al 2022h ).…”

The possible role of nuclear factor erythroid‐2‐related factor 2 activators in the management of Covid‐19

“…[16][17][18][19]186] In addition to reducing the production of infectious virions, the inhibition of ER glucosidases prevents the entry of some viruses via a post-receptor-binding mechanism. [20][21][22][23] Therefore, dysregulation of RAS in Covid-19 could be the possible reason behind the reduction of Nrf2 activity. Thus, angiotensin receptor blockers (AT1R) may be beneficial in preventing OS and inflammatory reactions via upregulation of the Nrf2 pathway.…”

“…[ 22 ] SARS‐CoV‐2 is highly identical to other CoVs like SARS and Middle East Respiratory Syndrome CoV (MERS‐CoV) and shares 80% and 60% genomic similarity. [ 23 ] In addition, SARS‐CoV‐2 is highly similar at the genomic level with bat CoV 96%. [ 24 ] SARS‐CoV‐2 is 20 times higher in use and binding ACE2 than other CoVs with succeeding downregulation of these receptors.…”