Covid-19 and cardiovascular diseases: Breaking news

2021 ◽  
Vol 2 (1) ◽  
pp. 31-34
Author(s):  
Maria Christiane Valéria Braga Braile-Sternieri ◽  
◽  
Idiberto José Zotarelli-Filho ◽  
Victor Rodrigues Ribeiro Ferreira ◽  
Eliana Migliorini Mustafa ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Coenzyme Q10 ◽  
Scientific Evidence ◽  
Vascular Inflammation ◽  
Renin Angiotensin System ◽  
Fulminant Myocarditis ◽  
Iron Ions ◽  
Heme Group ◽  
Breaking News ◽  
Coronavirus Infection

COVID-19 disease is associated with a high inflammatory load that can induce vascular inflammation, myocarditis, and cardiac arrhythmias. Mortality from COVID-19 disease in 2019 is strongly associated with cardiovascular disease, diabetes, and hypertension. These disorders share the underlying pathophysiology related to the renin-angiotensin system (SARS). Cardiovascular disease and SARS pharmacological inhibition increase ACE2 levels, which can increase coronavirus virulence in the lung and heart. On the other hand, there is evidence that coronavirus infection can decrease ACE2, leading to toxic over-accumulation of angiotensin II, which induces acute respiratory distress syndrome and fulminant myocarditis. In addition, there is scientific evidence that SARS-CoV-2 can bind chemically to the heme group of hemoglobin and thus cause the release of iron ions (Fe2+ and Fe3+) that can damage tissues, including the lungs and heart. Another important information is that the heme group is produced by mitochondria and, in this case, the oral or intramuscular use of Coenzyme Q10 (ubiquinone) is strongly recommended, as it stimulates the increase in mitochondrial production. Therefore, the use of chelators of iron ions is notorious, as well as the administration of Coenzyme Q10 as a treatment for patients infected with SARS-CoV-2.

scholarly journals Is There an Association Between COVID-19 Mortality and the Renin-Angiotensin System? A Call for Epidemiologic Investigations

2020 ◽  
Vol 71 (15) ◽  
pp. 870-874 ◽  
Author(s):  
Thomas C Hanff ◽  
Michael O Harhay ◽  
Tyler S Brown ◽  
Jordana B Cohen ◽  
Amir M Mohareb
Keyword(s):  
Cardiovascular Disease ◽  
Research Priorities ◽  
Renin Angiotensin System ◽  
Fulminant Myocarditis ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
System A ◽  
Ras Inhibition

Abstract Mortality from coronavirus disease 2019 (COVID-19) is strongly associated with cardiovascular disease, diabetes, and hypertension. These disorders share underlying pathophysiology related to the renin-angiotensin system (RAS) that may be clinically insightful. In particular, activity of the angiotensin-converting enzyme 2 (ACE2) is dysregulated in cardiovascular disease, and this enzyme is used by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to initiate the infection. Cardiovascular disease and pharmacologic RAS inhibition both increase ACE2 levels, which may increase the virulence of SARS-CoV-2 within the lung and heart. Conversely, mechanistic evidence from related coronaviruses suggests that SARS-CoV-2 infection may downregulate ACE2, leading to toxic overaccumulation of angiotensin II that induces acute respiratory distress syndrome and fulminant myocarditis. RAS inhibition could mitigate this effect. With conflicting mechanistic evidence, we propose key clinical research priorities necessary to clarify the role of RAS inhibition in COVID-19 mortality that could be rapidly addressed by the international research community.

scholarly journals PPAR Agonists and Cardiovascular Disease in Diabetes

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-12 ◽  
Author(s):  
Anna C. Calkin ◽  
Merlin C. Thomas
Keyword(s):  
Cardiovascular Disease ◽  
Cardiovascular Events ◽  
Vascular Inflammation ◽  
Renin Angiotensin System ◽  
Activator Protein 1 ◽  
Atherosclerotic Vascular Disease ◽  
Angiotensin System ◽  
Biologic Effects ◽  
Ppar Agonists ◽  
Peroxisome Proliferators Activated Receptors

Peroxisome proliferators activated receptors (PPARs) are ligand-activated nuclear transcription factors that play important roles in lipid and glucose homeostasis. To the extent that PPAR agonists improve diabetic dyslipidaemia and insulin resistance, these agents have been considered to reduce cardiovascular risk. However, data from murine models suggests that PPAR agonists also have independent anti-atherosclerotic actions, including the suppression of vascular inflammation, oxidative stress, and activation of the renin angiotensin system. Many of these potentially anti-atherosclerotic effects are thought to be mediated by transrepression of nuclear factor-kB, STAT, and activator protein-1 dependent pathways. In recent clinical trials, PPAR agonists have been shown to be effective in the primary prevention of cardiovascular events, while their cardiovascular benefit in patients with established cardiovascular disease remains equivocal. However, the use of PPAR agonists, and more recently dual PPAR/ coagonists, has been associated with an excess in cardiovascular events, possibly reflecting unrecognised fluid retention with potent agonists of the PPAR receptor. Newer pan agonists, which retain their anti-atherosclerotic activity without weight gain, may provide one solution to this problem. However, the complex biologic effects of the PPARs may mean that only vascular targeted agents or pure transrepressors will realise the goal of preventing atherosclerotic vascular disease.

scholarly journals ACE2 Is an Adjacent Element of Atherosclerosis and COVID-19 Pathogenesis

2021 ◽  
Vol 22 (9) ◽  
pp. 4691
Author(s):  
Anastasia V. Poznyak ◽  
Evgeny E. Bezsonov ◽  
Ali H. Eid ◽  
Tatyana V. Popkova ◽  
Ludmila V. Nedosugova ◽  
...  
Keyword(s):  
Cardiovascular System ◽  
Renin Angiotensin System ◽  
Myocardial Damage ◽  
Angiotensin Converting Enzyme 2 ◽  
Adjacent Element ◽  
Chinese Province ◽  
Coronavirus Infection ◽  
First Time ◽  
The Relationship ◽  
Interspecies Barrier

COVID-19 is a highly contagious new infection caused by the single-stranded RNA Sars-CoV-2 virus. For the first time, this infection was recorded in December 2019 in the Chinese province of Wuhan. The virus presumably crossed the interspecies barrier and passed to humans from a bat. Initially, the disease was considered exclusively in the context of damage to the respiratory system, but it quickly became clear that the disease also entails serious consequences from various systems, including the cardiovascular system. Among these consequences are myocarditis, myocardial damage, subsequent heart failure, myocardial infarction, and Takotsubo syndrome. On the other hand, clinical data indicate that the presence of chronic diseases in a patient aggravates the course and outcome of coronavirus infection. In this context, the relationship between COVID-19 and atherosclerosis, a condition preceding cardiovascular disease and other disorders of the heart and blood vessels, is particularly interesting. The renin-angiotensin system is essential for the pathogenesis of both coronavirus disease and atherosclerosis. In particular, it has been shown that ACE2, an angiotensin-converting enzyme 2, plays a key role in Sars-CoV-2 infection due to its receptor activity. It is noteworthy that this enzyme is important for the normal functioning of the cardiovascular system. Disruptions in its production and functioning can lead to various disorders, including atherosclerosis.

scholarly journals The unbearable heaviness of reductionism: the paradigm of the antiatherogenic diet

2017 ◽  
Vol 11 (3) ◽  
pp. 322
Author(s):  
Marco Bobbio ◽  
Antonio Bonaldi ◽  
Luigi Lusiani ◽  
Emma Kidd
Keyword(s):  
Cardiovascular Disease ◽  
Cardiovascular Risk ◽  
Scientific Evidence ◽  
Complex Phenomenon ◽  
Life Styles ◽  
Single Substance ◽  
Obesity And Diabetes ◽  
Food Consumed

Reducing a complex phenomenon into a simplified description may help us to understand general issues and to make limited decisions, but can hardly allow us to accurately predict the consequences of an intervention. The case of the antiatherogenic diet is discussed. Simplified approaches, aimed at correcting single components of a diet, privileging the lipid theory over more comprehensive ones, sustained by the illusion that removing one single substance (the lowering-cholesterol mantra) would defeat cardiovascular disease, have led us to faulty results, because the interactions among components and their interconnections are not negligible. The industry’s interest in shifting the diet of millions of people in well-defined and profitable directions (lowfat, but sugar-rich for tastefulness reasons, as an example), in advance of well founded scientific evidence about benefit, has been mostly relevant. Nowadays, it is well recognized that refined and sweetened foods, not fats, are the main cause of obesity and diabetes, and that the cardiovascular risk is more dependent on the quantity of food consumed rather than the type of food. In recent years the attention of the researchers has moved from qualitative dietary studies and unnatural regimes, to quantitative diets and more naturally balanced regimes, within the concept of globally health life styles, against any reductionism.

Abstract 368: Family History of Premature Cardiac Events and Sub Clinical Atherosclerosis in Children and Young Adults: A Systematic Review

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Pragya Sinha ◽  
Jamal S Rana ◽  
Ebenezer T Oni ◽  
Ehimen C Aneni ◽  
Roger S Blumenthal ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Young Adults ◽  
Family History ◽  
Endothelial Dysfunction ◽  
Subclinical Atherosclerosis ◽  
Vascular Inflammation ◽  
Positive Family History ◽  
Cardiac Risk Factor ◽  
Children And Young Adults ◽  
The Impact

BACKGROUND The association between a positive family history (PFH) of premature cardiovascular disease (PCVD) and atherosclerosis has been explored in numerous studies. In adults, various studies have confirmed a significant positive correlation between a PFH and PCVD. Scant literature however, focuses on young individuals. Nevertheless, it is important to understand the impact that a PFH has in young people because the foundations of atherosclerosis and adverse cardiac behaviors develop in youth. In this paper, we aimed to systematically review the evidence linking a PFH of PCVD to indirect markers of subclinical atherosclerosis. METHODS The search was conducted on Medline, Web of Science and Embase. ‘Family history’, ‘children/young adults’ and ‘subclinical atherosclerosis’ were the three main concepts used. Increase in mean carotid IMT (cIMT), endothelial dysfunction and vascular inflammation were used as indirect measures of subclinical atherosclerosis. RESULTS 1191 articles were identified in the initial search. 24 papers with 5400 participants were included in the final review. There were five cohort studies and nineteen case control studies from twelve countries. Mean cIMT was found to be significantly increased in those with a PFH by eleven of the fourteen papers reviewed. Endothelial dysfunction, measured by flow mediated dilatation (FMD), was found to be significantly increased in five of the seven included studies. The evidence on vascular inflammation was somewhat inconsistent with only ten of the nineteen studies demonstrating significance. The results tend to suggest that an elevated mean cIMT, as well as a greater degree of endothelial dysfunction are seen in children and young adults with a PFH of PCVD. Moreover, these differences exist in asymptomatic children as young as 8-9 years (4 studies) in the absence of any other cardiac risk factor. DISCUSSION Individuals with a PFH of PCVD have evidence of subclinical atherosclerosis in their youth demonstrating an accelerated tendency to acquire cardiovascular disease. Some of this risk may be attributable to behavioral risk clustering in families. However, a significant proportion of this elevated risk is related solely to a positive family history and needs attention.

Covid-19: features of the pathogenesis of the disease and targets for immunotherapeutic effects

2020 ◽  
Vol 20 (3) ◽  
pp. 75-88
Author(s):  
N. A. Klimov ◽  
A. S. Simbirtsev
Keyword(s):  
Life Cycle ◽  
Immune System ◽  
Clinical Picture ◽  
Scientific Literature ◽  
Renin Angiotensin System ◽  
Cytokine Storm ◽  
Laboratory Mice ◽  
Angiotensin System ◽  
Coronavirus Infection ◽  
The Complement System

An analysis of current scientific literature on the pathogenesis of the coronavirus infection that caused the 2019 pandemic, COVID-19, was carried out. The structure, genome, introduction into the cell and the life cycle of the SARS-CoV-2 virus that caused the pandemic, the mechanisms of protection of the virus from the hosts immune system, features of the clinical picture of coronavirus infection, the pathogenesis of viral pneumonia, in particular, disruption of the renin-angiotensin system, cytokine storm, participation of the complement system in the pathogenesis of COVID-19 are reviewed. The models of infections caused by SARS-CoV and SARS-CoV-2 in laboratory mice are also considered.

Abstract 12375: Vascular Inflammation Evaluated by 18F-Fluorodeoxyglucose-Positron Emission Tomography/Computed Tomography is Associated With Endothelial Dysfunction

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Akihiro Honda ◽  
Nobuhiro Tahara ◽  
Atsuko Tahara ◽  
Sachiyo Igata ◽  
Yoshikazu Nitta ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Positron Emission Tomography ◽  
Endothelial Dysfunction ◽  
Pet Imaging ◽  
Carotid Arteries ◽  
Vascular Inflammation ◽  
Emission Tomography ◽  
Percent Change ◽  
Positron Emission ◽  
Fat Volume

Background: Endothelial dysfunction is an initial step for atherosclerotic cardiovascular disease. However, involvement of vascular inflammation in endothelial dysfunction is not fully investigated in humans. We assessed the relationship between endothelial function and vascular inflammation evaluated by 18F-fluorodeoxyglucose (FDG)-positron emission tomography (PET) imaging. Methods and Results: We examined endothelial function and vascular inflammation, which were evaluated by flow-mediated dilation (FMD) of the brachial artery functionally and FDG-PET imaging of carotid arteries, respectively, in 128 subjects (83 males and 45 females; mean age 61.8 ± 10.0 years) who underwent a risk-screening test for cardiovascular disease in Kurume University Hospital. Vascular inflammation of the carotid arteries was measured by blood-normalized standardized uptake value, known as a target-to-background ratio (TBR). Mean percent change in vasodilation (percent change over the baseline values; %FMD) and carotid TBR were 5.60 ± 2.24 % and 1.43 ± 0.22, respectively. %FMD was less in men than in women. In univariate analysis, %FMD was inversely correlated with age (p=0.011), systolic blood pressure (p=0.014), carotid artery maximum intima-media thickness (p=0.014), HbA1c (p=0.020), visceral fat volume (p=0.005), or TBR values (p<0.001). Multiple stepwise regression analysis revealed that age (p=0.034), visceral fat volume (p=0.002), and TBR values (p<0.001) were independently associated with decreased %FMD (R2=0.245). Conclusions: We found here that vascular inflammation in the carotid arteries evaluated by FDG-PET was one of the independent association of decreased %FMD, thus suggesting that vascular inflammation might contribute to endothelial dysfunction in humans.

scholarly journals The role of renin-angiotensin system activated phagocytes in the SARS-CoV-2 coronavirus infection

2020 ◽  
Author(s):  
Laszlo Göbölös ◽  
István Rácz ◽  
Maurice Hogan ◽  
Ernő Remsey-Semmelweis ◽  
Bassam Atallah ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Coronavirus Infection
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