COVID-19 and the cardiovascular system: an update

Salabei, Joshua K.; Asnake, Zekarias T.; Ismail, Zeeshan; Charles, Kipson; Stanger, Gregory-Thomas; Abdullahi, Abdullahi H.; Abraham, Andrew T.; Okonoboh, Peters

doi:10.1016/j.amjms.2022.01.022

Cited by 26 publications

(21 citation statements)

References 94 publications

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“…Myocardial injury is an important pathogenic feature of COVID-19, where cardiovascular histopathology findings are reported in up to 48% of patients; moreover, cardiovascular magnetic resonance abnormalities are detected in 26% to 60% of recovered hospitalized patients [ 687 , 688 , 689 , 690 ]. The frequent presence of elevated high-sensitive troponin I (hs-TnI) in COVID-19 patients is significantly associated with higher rates of cardiac complications [ 691 ].…”

Section: Melatonin Regulates Sars-cov-2-mediated Crosstalk Between Th...mentioning

confidence: 99%

Melatonin: Regulation of Viral Phase Separation and Epitranscriptomics in Post-Acute Sequelae of COVID-19

Loh¹,

Reíter

2022

IJMS

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The relentless, protracted evolution of the SARS-CoV-2 virus imposes tremendous pressure on herd immunity and demands versatile adaptations by the human host genome to counter transcriptomic and epitranscriptomic alterations associated with a wide range of short- and long-term manifestations during acute infection and post-acute recovery, respectively. To promote viral replication during active infection and viral persistence, the SARS-CoV-2 envelope protein regulates host cell microenvironment including pH and ion concentrations to maintain a high oxidative environment that supports template switching, causing extensive mitochondrial damage and activation of pro-inflammatory cytokine signaling cascades. Oxidative stress and mitochondrial distress induce dynamic changes to both the host and viral RNA m6A methylome, and can trigger the derepression of long interspersed nuclear element 1 (LINE1), resulting in global hypomethylation, epigenetic changes, and genomic instability. The timely application of melatonin during early infection enhances host innate antiviral immune responses by preventing the formation of “viral factories” by nucleocapsid liquid-liquid phase separation that effectively blockades viral genome transcription and packaging, the disassembly of stress granules, and the sequestration of DEAD-box RNA helicases, including DDX3X, vital to immune signaling. Melatonin prevents membrane depolarization and protects cristae morphology to suppress glycolysis via antioxidant-dependent and -independent mechanisms. By restraining the derepression of LINE1 via multifaceted strategies, and maintaining the balance in m6A RNA modifications, melatonin could be the quintessential ancient molecule that significantly influences the outcome of the constant struggle between virus and host to gain transcriptomic and epitranscriptomic dominance over the host genome during acute infection and PASC.

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Section: Melatonin Regulates Sars-cov-2-mediated Crosstalk Between Th...mentioning

confidence: 99%

Melatonin: Regulation of Viral Phase Separation and Epitranscriptomics in Post-Acute Sequelae of COVID-19

Loh¹,

Reíter

2022

IJMS

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“…SARS-CoV2 affects the CV system through several mechanisms: (1) direct virus effect on cardiomyocytes and endothelial cells due to the great expression of angiotensin-converting enzyme 2 receptors, used by the virus to enter human cells, in cardiovascular system tissues; (2) hypercoagulability because of the interaction between the virus and endothelial cells and also due to the inflammatory status; (3) cytokine release, which could evolve into a “cytokine storm” during exaggerated immune responses; and (4) hypoxia as a consequence of pneumonia or acute respiratory distress syndrome [ 14 ]. As a result, CV manifestations could be heterogeneous, including myocardial infarction, arrhythmias, heart failure, thromboembolism, myocarditis, and myocardial injury [ 2 , 15 ].…”

Section: Discussionmentioning

confidence: 99%

Short and Long-Term Cardiovascular Sequelae after SARS-CoV-2 Infection: A Narrative Review Focusing on Athletes

Monosilio

Prosperi

Squeo³

et al. 2023

Viruses

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Cardiovascular (CV) involvement after severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection was found to be frequent among the general population, especially in the pre-vaccination era, and particularly for hospitalized patients or those who experienced a more severe course of the disease. The spectrum of CV disease varies; however, acute myocarditis is particularly fearsome for the athletic population due to the possible associated risk of malignant arrhythmias during training. Alarming percentages of CV injuries, even in young and healthy athletes with a benign course of the disease, arose from a few initial studies limited to case series. Subsequent single-center studies and larger observational registries reported a lower prevalence of SARS-CoV2 CV involvement in athletes. Studies showing the occurrence of CV adverse events during follow-up periods are now available. The objective of our narrative review is to provide an updated summary of the literature on CV involvement after coronavirus disease 2019, both in the early post-infection period and over a longer period of time, with a focus on athletic populations.

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“…It is likely that there are additional toxic substances and medical conditions which might potentiate the adverse (cardiovascular) effects of cyanotoxins but the data on this topic are scarce. One interesting aspect is whether the COVID-19 disease known to have cardiovascular effects (Salabei et al 2022 ; Xie et al 2022 ) may have any interactions with cyanobacterial toxicity.…”

Section: Conclusion and Gaps In Knowledgementioning

confidence: 99%

A review and assessment of cyanobacterial toxins as cardiovascular health hazards

et al. 2022

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Eutrophicated waters frequently support bloom-forming cyanobacteria, many of which produce potent cyanobacterial toxins (cyanotoxins). Cyanotoxins can cause adverse health effects in a wide range of organisms where the toxins may target the liver, other internal organs, mucous surfaces and the skin and nervous system. This review surveyed more than 100 studies concerning the cardiovascular toxicity of cyanotoxins and related topics. Over 60 studies have described various negative effects on the cardiovascular system by seven major types of cyanotoxins, i.e. the microcystin (MC), nodularin (NOD), cylindrospermopsin (CYN), anatoxin (ATX), guanitoxin (GNTX), saxitoxin (STX) and lyngbyatoxin (LTX) groups. Much of the research was done on rodents and fish using high, acutely toxin concentrations and unnatural exposure routes (such as intraperitoneal injection), and it is thus concluded that the emphasis in future studies should be on oral, chronic exposure of mammalian species at environmentally relevant concentrations. It is also suggested that future in vivo studies are conducted in parallel with studies on cells and tissues. In the light of the presented evidence, it is likely that cyanotoxins do not constitute a major risk to cardiovascular health under ordinary conditions met in everyday life. The risk of illnesses in other organs, in particular the liver, is higher under the same exposure conditions. However, adverse cardiovascular effects can be expected due to indirect effects arising from damage in other organs. In addition to risks related to extraordinary concentrations of the cyanotoxins and atypical exposure routes, chronic exposure together with co-existing diseases could make some of the cyanotoxins more dangerous to cardiovascular health.

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COVID-19 and the cardiovascular system: an update

Cited by 26 publications

References 94 publications

Melatonin: Regulation of Viral Phase Separation and Epitranscriptomics in Post-Acute Sequelae of COVID-19

Melatonin: Regulation of Viral Phase Separation and Epitranscriptomics in Post-Acute Sequelae of COVID-19

Short and Long-Term Cardiovascular Sequelae after SARS-CoV-2 Infection: A Narrative Review Focusing on Athletes

A review and assessment of cyanobacterial toxins as cardiovascular health hazards

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