The risk of atrial fibrillation associated with hyperuricemia

2021 ◽  
Author(s):  
V. A. Chernyshov
Keyword(s):  
Oxidative Stress ◽  
Atrial Fibrillation ◽  
Elevated Serum ◽  
Renin Angiotensin System ◽  
Oxidase Inhibitor ◽  
Important Place ◽  
Xanthine Oxidase Inhibitor ◽  
Increased Risk ◽  
The Relationship

The article summarizes mechanisms, linking hyperuricemia, the elevated serum levels of uric acid (UA), and atrial fibrillation (AF), the most frequent cardiac arrhythmia. The actuality of the problem is explained by the fact that UA is considered as an independent risk marker of AF closely associated with the onset and subsequent persistence of AF as well as by the AF increased risk in males and females with hyperuricemia. It has been shown how hyperuricemia, combined with other AF risk factors, contributeы to the development of arrhythmia, as well as the role of hyperuricemia, oxidative stress and renin‑angiotensin system (RAS) activation in the AF pathogenesis. The consideration have been given to the hyperuricemia association with a prevalence of AF among the patients with carbohydrate exchange disorders such as metabolic syndrome and type 2 diabetes mellitus as well as to the relationship between hyperuricemia and endothelial vascular dysfunction, oxidative stress, high blood concentration of systemic inflammatory markers and insulin resistance (IR). Some mechanisms of hyperuricemia participation in cardiac remodeling as a risk factor of AF are adduced. In particular, the relationship between hyperuricemia and left atrial (LA) size that could be mediated through systemic inflammation and IR is discussed. A significance of a direct impaired action of UA on LA cardiomyocytes resulted in their structural and ionic remodeling is shown. The role of xanthinoxidase (XO) activation in initiation of oxidative stress and inflammation in cardiomyocytes and endothelial cells is discussed. All these mechanisms are emphasized to be able to shorten a potential of action of atrial cardiomyocytes as well as to reduce a threshold of re‑entry mechanism initiation and to promote an appearance of the first and the following AF episodes. An important place in the review is taken for an intracellular UA and its cellular transporters in the context of their participation in pathogenesis of AF. The possibilities of drug hyperuricemia correction have been described in regards the reduction of AF risk, in particular, the role of reducing of the oxidative stress intensity with the use of xanthine oxidase inhibitor allopurinol, the inhibitor of NADPH oxidase apocynin, the antioxidant N‑acetylcysteine in the reduction of the risk of onset and subsequent recurrences of AF episodes, and transition of arrhythmia in the persistent form. Some perspectives of probenecid (an inhibitor of UA intracellular transporter activity) usage in the reduction of AF risk due to such of its mechanisms as a reduction of intracellular UA accumulation and antiapoptotic action as well as an ability of this agent to inhibit a locally activated oxidative stress and locally activated tissue RAS are discussed. A significance of the further detailed study of pathophysiological mechanisms of AF in hyperuricemia is emphasized for elaboration of the most effective practical recommendations in prevention of this arrhythmia in persons with UA exchange disorders.

scholarly journals New insights into mechanisms of atrial fibrillation

2010 ◽  
pp. 1-12 ◽  
Author(s):  
B Aldhoon ◽  
V Melenovský ◽  
P Peichl ◽  
J Kautzner
Keyword(s):  
Oxidative Stress ◽  
Atrial Fibrillation ◽  
Pulmonary Veins ◽  
Renin Angiotensin System ◽  
Predominant Role ◽  
Stress Injury ◽  
Angiotensin System ◽  
Inflammatory State ◽  
Made In

Although atrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice, precise mechanisms that lead to the onset and persistence of AF have not completely been elucidated. Over the last decade, outstanding progress has been made in understanding the complex pathophysiology of AF. The key role of ectopic foci in pulmonary veins as a trigger of AF has been recognized. Furthermore, structural remodeling was identified as the main mechanism for AF persistence, confirming predominant role of atrial fibrosis. Systemic inflammatory state, oxidative stress injury, autonomic balance and neurohormonal activation were discerned as important modifiers that affect AF susceptibility. This new understanding of AF pathophysiology has led to the emergence of novel therapies. Ablative interventions, renin-angiotensin system blockade, modulation of oxidative stress and targeting tissue fibrosis represent new approaches in tackling AF. This review aims to provide a brief summary of novel insights into AF mechanisms and consequent therapeutic strategies.

scholarly journals Xanthine oxidase inhibitor febuxostat reduces atrial fibrillation susceptibility by inhibition of oxidized CaMKII in Dahl salt-sensitive rats

2021 ◽  
Author(s):  
DongZhu Xu ◽  
Nobuyuki Murakoshi ◽  
Kazuko Tajiri ◽  
Feng Duo ◽  
Yuta Okabe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Atrial Fibrillation ◽  
Gap Junction ◽  
Xanthine Oxidase ◽  
Oxidase Inhibitor ◽  
Xanthine Oxidase Inhibitor ◽  
Junction Protein ◽  
Low Salt ◽  
Gap Junction Protein ◽  
Related Increase

Abstract Oxidative stress could be a possible mechanism and a therapeutic target of atrial fibrillation (AF). However, the effects of the xanthine oxidase (XO) inhibition for AF remain to be fully elucidated. We investigated the effects of a novel XO inhibitor febuxostat on AF compared to allopurinol in hypertension rat model. Five-week-old Dahl salt-sensitive rats were fed to either low-salt (LS) (0.3% NaCl) or high-salt (HS) (8% NaCl) diet. After 4 weeks of diet, HS diet rats were divided into 3 groups: orally administered to vehicle (HS-C), febuxostat (5mg/kg/day) (HS-F), or allopurinol (50mg/kg/day) (HS-A). After 4 weeks of treatment, systolic blood pressure was significantly higher in HS-C than LS, and it was slightly but significantly decreased by treatment with each XO inhibitor. AF duration was significantly prolonged in HS-C compared with LS, and significantly suppressed in both HS-F and HS-A (LS; 5.8±3.5 sec, HS-C; 33.9±23.7 sec, HS-F; 15.0±14.1 sec, HS-A; 20.1±11.9 sec: P<0.05). Ca2+ spark frequency was obviously increased in HS-C rats and reduced in the XO inhibitor-treated rats, especially in HS-F group. Western blotting revealed that the atrial expression levels of methionine 281/282-oxidized Ca2+/Calmodulin-dependent kinase II and serine 2814-phosphorylated ryanodine receptor 2 were significantly increased in HS-C, and those were suppressed in HS-F and HS-A. Decreased expression of gap junction protein connexin 40 in HS-C was partially restored by treatment with each XO inhibitor. In conclusion, XO inhibitor febuxostat, as well as allopurinol, could reduce hypertension-related increase in AF perpetuation by restoring Ca2+ handling and gap junction.

Oxidative Stress Levels, JAK2V617F Mutational Status and Thrombotic Complications in Patients with Essential Thrombocythemia

2019 ◽  
Vol 70 (8) ◽  
pp. 2822-2825 ◽  
Author(s):  
Cornel Moisa ◽  
Mihnea Alexandru Gaman ◽  
Camelia Cristina Diaconu ◽  
Amelia Maria Gaman
Keyword(s):  
Oxidative Stress ◽  
Essential Thrombocythemia ◽  
Myeloproliferative Neoplasm ◽  
Oxygen Species ◽  
Mutational Status ◽  
Increased Risk ◽  
Stress Levels ◽  
Total Antioxidant ◽  
Thrombotic Complications ◽  
The Relationship

Essential thrombocythemia (ET) is a BCR-ABL1-negative myeloproliferative neoplasm associated with thrombotic and haemorrhagic complications. Reactive oxygen species (ROS) overexpression induces a growth advantage to JAK2V617F-positive clones and, in association with a higher number of immature platelets, leukocytosis, and additional cardiovascular risk factors, leads to an increased risk for thrombotic events. We evaluated oxidative stress by measuring ROS levels and the total antioxidant capacity (TAC) in 62 ET patients and investigated the relationship between oxidative stress, JAK2V617F mutational status and the development of thrombotic events. We found higher oxidative stress levels in JAK2V617F-positive vs. JAK2V617F-negative ET cases with no significant differences between homozygous and heterozygous genotypes. Increased ROS levels and thrombotic events were more frequent in ET patients with old age at diagnosis, higher haematocrit levels or leukocytosis.

scholarly journals Acute Dental Periapical Abscess and New-Onset Atrial Fibrillation: A Nationwide, Population-Based Cohort Study

2021 ◽  
Vol 10 (13) ◽  
pp. 2927
Author(s):  
Amaar Obaid Hassan ◽  
Gregory Y. H. Lip ◽  
Arnaud Bisson ◽  
Julien Herbert ◽  
Alexandre Bodin ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Cohort Study ◽  
Multivariable Analysis ◽  
National Database ◽  
Increased Risk ◽  
Periapical Abscess ◽  
The Relationship ◽  
Onset Atrial Fibrillation ◽  
New Onset

There are limited data on the relationship of acute dental infections with hospitalisation and new-onset atrial fibrillation (AF). This study aimed to assess the relationship between acute periapical abscess and incident AF. This was a retrospective cohort study from a French national database of patients hospitalized in 2013 (3.4 million patients) with at least five years of follow up. In total, 3,056,291 adults (55.1% female) required hospital admission in French hospitals in 2013 while not having a history of AF. Of 4693 patients classified as having dental periapical abscess, 435 (9.27%) developed AF, compared to 326,241 (10.69%) without dental periapical abscess that developed AF over a mean follow-up of 4.8 ± 1.7 years. Multivariable analysis indicated that dental periapical abscess acted as an independent predictor for new onset AF (p < 0.01). The CHA2DS2VASc score in patients with acute dental periapical abscess had moderate predictive value for development of AF, with Area Under the Curve (AUC) 0.73 (95% CI, 0.71–0.76). An increased risk of new onset AF was identified for individuals hospitalized with dental periapical abscess. Careful follow up of patients with severe, acute dental periapical infections is needed for incident AF, as well as investigations of possible mechanisms linking these conditions.

Serum uric acid levels and risk of prehypertension: a meta-analysis

2017 ◽  
Vol 55 (3) ◽  
Author(s):  
Menglin Jiang ◽  
Dandan Gong ◽  
Yu Fan
Keyword(s):  
Uric Acid ◽  
Serum Uric Acid ◽  
Meta Analysis ◽  
Elevated Serum ◽  
China National Knowledge Infrastructure ◽  
Cross Sectional ◽  
Knowledge Infrastructure ◽  
Increased Risk ◽  
Cross Sectional Studies ◽  
The Relationship

AbstractElevated serum uric acid (SUA) levels may increase the risk of prehypertension. However, the findings from these studies remain conflicting. The objective of this study was to determine the relationship between SUA levels and risk of prehypertension by conducting a meta-analysis. We conducted a comprehensive literature search of PubMed, Embase, China National Knowledge Infrastructure, VIP, and the Wangfang database without language restrictions through May 2015. Observational studies assessing the relationship between SUA levels and prevalence of prehypertension were included. Pooled adjust odds ratio (OR) and corresponding 95% confidence intervals (CI) of prehypertension were calculated for the highest vs. lowest SUA levels. Prehypertension was defined as systolic blood pressure (BP) ranging from 120 to 139 mmHg or diastolic BP ranging from 80 to 89 mmHg. Eight cross-sectional studies with a total of 21,832 prehypertensive individuals were included. Meta-analysis showed that elevated SUA levels were associated with increased risk of prehypertension (OR: 1.84; 95% CI: 1.42–2.38) comparing the highest vs. lowest level of SUA levels. Subgroup analyses showed that elevated SUA levels significantly increased the risk of prehypertension among men (OR: 1.60; 95% CI: 1.12–2.21) and women (OR: 1.59; 95% CI: 1.17–2.16). Elevated SUA levels are positively associated with the risk of prehypertension in the general population. However, more well-designed longitudinal studies are needed before a definitive conclusion can be drawn due to the cross-sectional studies included are susceptible to bias.

scholarly journals CZY JESTEŚMY GOTOWI NA EKOGLOTTODYDAKTYKĘ W POLSKIM KONTEKŚCIE EDUKACYJNYM?

Neofilolog ◽  
2020 ◽  
pp. 11-26
Author(s):  
Jolanta Sujecka-Zając
Keyword(s):  
Foreign Language ◽  
English Language ◽  
Sense Making ◽  
Main Function ◽  
Important Place ◽  
Nature And Culture ◽  
Language Environment ◽  
Language Context ◽  
The Relationship

The trend for eco-linguistics, which has been dynamically developing in the English-language literature since the 1970s, proposes a change in the perception of the relationship between language, nature, and culture, in a sense making language a link which brings together nature and culture, rather than separating them as is traditional. This approach poses important questions: How do languages ​​work in the ecosystem created by the language environment of all users of a given language context? What relationships can they enter into? How should one perceive the development of multilingualism in such an ecological approach, in which not only does "strong" affect the "weak" but “weak” reciprocates? "Weak" has an important place in the language ecosystem, which risks serious changes due to excessive weakening of one of its components. This paper aims to examine the possible inspirations that eco-linguistics offers Foreign Language Teaching (FLT), highlighting the role of each language and sensitizing the reader to the relationships that arise between languages ​​and their users in a given environment. From this perspective Claire Kramsch (2008) postulates a change in the perception of the main function of the teacher from the "teacher of a code" to the "teacher of meaning", which has specific didactic consequences in how language activities are approached. Is the school classroom a place for activities which have their origin in the trend for eco-FLT?

scholarly journals Hypertension Burden and the Risk of New-Onset Atrial Fibrillation

Hypertension ◽  
2021 ◽  
Vol 77 (3) ◽  
pp. 919-928
Author(s):  
So-Ryoung Lee ◽  
Chan Soon Park ◽  
Eue-Keun Choi ◽  
Hyo-Jeong Ahn ◽  
Kyung-Do Han ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Total Study Population ◽  
Increased Risk ◽  
Burden Scale ◽  
History Of ◽  
Study Population ◽  
Korean National Health Insurance ◽  
Stage 1 ◽  
The Relationship

The association between the cumulative hypertension burden and the development of atrial fibrillation (AF) is unclear. We aimed to investigate the relationship between hypertension burden and the development of incident AF. Using the Korean National Health Insurance Service database, we identified 3 726 172 subjects who underwent 4 consecutive annual health checkups between 2009 and 2013, with no history of AF. During the median follow-up of 5.2 years, AF was newly diagnosed in 22 012 patients (0.59% of the total study population; 1.168 per 1000 person-years). Using the blood pressure (BP) values at each health checkup, we determined the burden of hypertension (systolic BP ≥130 mm Hg or diastolic BP ≥80 mm Hg), stratified as 0 to 4 per the hypertension criteria. The subjects were grouped according to hypertension burden scale 1 to 4: 20% (n=742 806), 19% (n=704 623), 19% (n=713 258), 21% (n=766 204), and 21% (n=799 281). Compared with normal people, subjects with hypertension burdens of 1, 2, 3, and 4 were associated with an 8%, 18%, 26%, and 27% increased risk of incident AF, respectively. On semiquantitative analyses with further stratification of stage 1 (systolic BP of 130–139 mm Hg or diastolic BP of 80–89 mm Hg) and stage 2 (systolic BP ≥140 mm Hg or diastolic BP ≥90 mm Hg) hypertension, the risk of AF increased with the hypertension burden by up to 71%. In this study, both a sustained exposure and the degree of increased BP were associated with an increased risk of incident AF. Tailored BP management should be emphasized to reduce the risk of AF.

Higher Angiotensin II type 1 receptor (AT1R) levels and activity in the post-mortem brains of older persons with Alzheimer's disease

2021 ◽  
Author(s):  
Caglar Cosarderelioglu ◽  
Lolita S Nidadavolu ◽  
Claudene J George ◽  
Ruth Marx ◽  
Laura Powell ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Amyloid Β ◽  
Renin Angiotensin System ◽  
Angiotensin Receptors ◽  
Post Mortem ◽  
Protein Levels ◽  
Normal Individuals ◽  
Markers Of Oxidative Stress

Abstract Aging is a key risk factor in Alzheimer's dementia (AD) development and progression. The primary dementia-protective benefits of Angiotensin II subtype 1 receptor (AT1R) blockers are believed to arise from systemic effects on blood pressure. However, a brain-specific renin-angiotensin system (b-RAS) exists, which can be altered by AT1R blockers. Brain RAS acts mainly through three angiotensin receptors: AT1R, AT2R, and AT4R. Changes in these brain angiotensin receptors may accelerate the progression of AD. Using post-mortem frontal cortex brain samples of age- and sex-matched cognitively normal individuals (n = 30) and AD patients (n = 30), we sought to dissect the b-RAS changes associated with AD and assess how these changes correlate with brain markers of oxidative stress, inflammation, and mitochondrial dysfunction as well as amyloid-β and paired helical filament tau pathologies. Our results show higher protein levels of the pro-inflammatory AT1R and phospho-ERK (pERK) in the brains of AD participants. Brain AT1R levels and pERK correlated with higher oxidative stress, lower cognitive performance, and higher tangle and amyloid-β scores. This study identifies molecular changes in b-RAS and offers insight into the role of b-RAS in AD-related brain pathology.

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