Arginine derivatives in atrial fibrillation progression phenotypes

Büttner, Petra; Bahls, Martin; Böger, Rainer H.; Hindricks, Gerhard; Thiele, Holger; Schwedhelm, Edzard; Kornej, Jelena

doi:10.1007/s00109-020-01932-9

Cited by 6 publications

(4 citation statements)

References 45 publications

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“…Atrial fibrillation causes a detrimental increase in morbidity and mortality and elevates the risk of cardiogenic stroke. Previously, we found that patients with persistent atrial fibrillation at the time of blood sampling had the lowest homoarginine concentrations compared to paroxysmal atrial fibrillation [22]. In contrast, homoarginine levels did not correlate with the occurrence or persistence of atrial fibrillation in a population-based study [32].…”

Section: Discussionmentioning

confidence: 74%

“…In addition to atherosclerotic phenotypes, cardio-embolic etiologies, especially those due to atrial fibrillation, are a main and independent cause of ischemic stroke. Previous studies demonstrated that homoarginine is also inversely associated with corrected QT interval duration and seems to predict prevalent atrial fibrillation [21] as well as advanced atrial fibrillation progression phenotypes [22]. In 3331 participants of the Framingham Offspring Study, lower plasma homoarginine concentrations were associated with higher all-cause mortality during a median follow-up of 18 years [23].…”

Section: Introductionmentioning

confidence: 98%

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Homoarginine Associates with Carotid Intima-Media Thickness and Atrial Fibrillation and Predicts Adverse Events after Stroke

Schwieren,

Jensen,

Schulz

et al. 2023

Life

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Homoarginine is associated with cardio- and cerebrovascular morbidity and mortality. However, the underlying pathomechanisms remain elusive. Here, we evaluated the association of homoarginine with adverse events (i.e., death, stroke, and myocardial infarction) and carotid intima-media thickness (cIMT) in stroke patients. In the prospective bioMARKers in STROKE (MARK-STROKE) cohort, patients with acute ischemic stroke or transient ischemic attack (TIA) were enrolled. Plasma homoarginine concentrations were analyzed and associated with clinical phenotypes in cross-sectional (374 patients) and prospective (273 patients) analyses. Adjustments for possible confounders were evaluated. A two-fold increase in homoarginine was inversely associated with the National Institutes of Health Stroke Scale (NIHSS) score at admission, cIMT, and prevalent atrial fibrillation (mean factor −0.68 [95% confidence interval (CI): −1.30, −0.07], −0.14 [95% CI: −0.22, −0.05]; and odds ratio 0.57 [95% CI: 0.33, 0.96], respectively). During the follow-up (median 284 [25th, 75th percentile: 198, 431] days), individuals with homoarginine levels in the highest tertile had fewer incident events compared with patients in the lowest homoarginine tertile independent of traditional risk factors (hazard ratio 0.22 [95% CI: 0.08, 0.63]). A lower prevalence of atrial fibrillation and a reduced cIMT pinpointed potential underlying pathomechanisms.

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Section: Discussionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 98%

Homoarginine Associates with Carotid Intima-Media Thickness and Atrial Fibrillation and Predicts Adverse Events after Stroke

Schwieren,

Jensen,

Schulz

et al. 2023

Life

Self Cite

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“…Asymmetric dimethylarginine (ADMA) is a well-known biomarker of endothelial dysfunction that indirectly reflects vascular NO production and exhibits certain predictive information for mortality and morbidity of cardiovascular diseases, including AF [214,215]. In the population-based Gutenberg Health Study (n = 5000), ADMA levels were correlated with left ventricular hypertrophy and AF prevalence [216].…”

Section: Asymmetric Dimethylargininementioning

confidence: 99%

Biomarkers of Atrial Fibrillation Recurrence in Patients with Paroxysmal or Persistent Atrial Fibrillation Following External Direct Current Electrical Cardioversion

et al. 2023

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Atrial fibrillation (AF) is associated with atrial remodeling, cardiac dysfunction, and poor clinical outcomes. External direct current electrical cardioversion is a well-developed urgent treatment strategy for patients presenting with recent-onset AF. However, there is a lack of accurate predictive serum biomarkers to identify the risks of AF relapse after electrical cardioversion. We reviewed the currently available data and interpreted the findings of several studies revealing biomarkers for crucial elements in the pathogenesis of AF and affecting cardiac remodeling, fibrosis, inflammation, endothelial dysfunction, oxidative stress, adipose tissue dysfunction, myopathy, and mitochondrial dysfunction. Although there is ample strong evidence that elevated levels of numerous biomarkers (such as natriuretic peptides, C-reactive protein, galectin-3, soluble suppressor tumorigenicity-2, fibroblast growth factor-23, turn-over collagen biomarkers, growth differential factor-15) are associated with AF occurrence, the data obtained in clinical studies seem to be controversial in terms of their predictive ability for post-cardioversion outcomes. Novel circulating biomarkers are needed to elucidate the modality of this approach compared with conventional predictive tools. Conclusions: Biomarker-based strategies for predicting events after AF treatment require extensive investigation in the future, especially in the presence of different gender and variable comorbidity profiles. Perhaps, a multiple biomarker approach exerts more utilization for patients with different forms of AF than single biomarker use.

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“…Little data are available regarding the impact of AF on cardioprotective mediators and pathways. Patients with AF have been noted to show dynamic alterations in critical determinants of NO production and metabolism, specifically arginine, homoarginine asymmetric dimethylarginine, and symmetric dimethylarginine, the levels of which were strictly dependent on acute heart rhythm at blood sampling, the degree of AF progression, and the success rate of sinus rhythm restoration ( Büttner et al, 2020 ). Thus, NO-dependent pathways of cardioprotection will therefore be difficult to predict in patients with AF.…”

Section: Effects Of Nonmodifiable Risk Factors and Comorbidities On I...mentioning

confidence: 99%

Interaction of Cardiovascular Nonmodifiable Risk Factors, Comorbidities and Comedications With Ischemia/Reperfusion Injury and Cardioprotection by Pharmacological Treatments and Ischemic Conditioning

et al. 2022

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Preconditioning, postconditioning, and remote conditioning of the myocardium enhance the ability of the heart to withstand a prolonged ischemia/reperfusion insult and the potential to provide novel therapeutic paradigms for cardioprotection. While many signaling pathways leading to endogenous cardioprotection have been elucidated in experimental studies over the past 30 years, no cardioprotective drug is on the market yet for that indication. One likely major reason for this failure to translate cardioprotection into patient benefit is the lack of rigorous and systematic preclinical evaluation of promising cardioprotective therapies prior to their clinical evaluation, since ischemic heart disease in humans is a complex disorder caused by or associated with cardiovascular risk factors and comorbidities. These risk factors and comorbidities induce fundamental alterations in cellular signaling cascades that affect the development of ischemia/reperfusion injury and responses to cardioprotective interventions. Moreover, some of the medications used to treat these comorbidities may impact on cardioprotection by again modifying cellular signaling pathways. The aim of this article is to review the recent evidence that cardiovascular risk factors as well as comorbidities and their medications may modify the response to cardioprotective interventions. We emphasize the critical need for taking into account the presence of cardiovascular risk factors as well as comorbidities and their concomitant medications when designing preclinical studies for the identification and validation of cardioprotective drug targets and clinical studies. This will hopefully maximize the success rate of developing rational approaches to effective cardioprotective therapies for the majority of patients with multiple comorbidities. Significance Statement Ischemic heart disease is a major cause of mortality; however, there are still no cardioprotective drugs on the market. Most studies on cardioprotection have been undertaken in animal models of ischemia/reperfusion in the absence of comorbidities; however, ischemic heart disease develops with other systemic disorders (e.g., hypertension, hyperlipidemia, diabetes, atherosclerosis). Here we focus on the preclinical and clinical evidence showing how these comorbidities and their routine medications affect ischemia/reperfusion injury and interfere with cardioprotective strategies.

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Arginine derivatives in atrial fibrillation progression phenotypes

Cited by 6 publications

References 45 publications

Homoarginine Associates with Carotid Intima-Media Thickness and Atrial Fibrillation and Predicts Adverse Events after Stroke

Homoarginine Associates with Carotid Intima-Media Thickness and Atrial Fibrillation and Predicts Adverse Events after Stroke

Biomarkers of Atrial Fibrillation Recurrence in Patients with Paroxysmal or Persistent Atrial Fibrillation Following External Direct Current Electrical Cardioversion

Interaction of Cardiovascular Nonmodifiable Risk Factors, Comorbidities and Comedications With Ischemia/Reperfusion Injury and Cardioprotection by Pharmacological Treatments and Ischemic Conditioning

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