The impact of rapid atrial pacing on ADMA and endothelial NOS

Goette, Andreas; Hammwöhner, Matthias; Bukowska, Alicja; Scalera, Fortunato; Martens‐Lobenhoffer, Jens; Dobrev, Dobromir; Ravens, Ursula; Weinert, Sönke; Medunjanin, Senad; Lendeckel, Uwe; Bode‐Böger, Stefanie M.

doi:10.1016/j.ijcard.2010.09.004

Cited by 69 publications

(51 citation statements)

References 37 publications

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“…305 Endocardial thrombogenic alterations in diseased atria, which appear to be related to oxidative stress, appear to contribute to clot formation, particularly in the left atrial appendage. [306][307][308][309][310] Thus, the impact and the relation between EHRAS Classses and the extend of endocardial thrombogenic alterations have to be assessed in future studies. Interestingly, duration of AF does not correlate with the extent of abserved endocardial changes.…”

Section: Prothrombotic Indices: Coagulation Plateletsmentioning

confidence: 99%

EHRA/HRS/APHRS/SOLAECE expert consensus on atrial cardiomyopathies: definition, characterization, and clinical implication

et al. 2016

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Section: Prothrombotic Indices: Coagulation Plateletsmentioning

confidence: 99%

EHRA/HRS/APHRS/SOLAECE expert consensus on atrial cardiomyopathies: definition, characterization, and clinical implication

et al. 2016

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“…In addition, the plasma level of the endogenous NOS inhibitor, ADMA, has been shown to be elevated in animals and individuals with persistent AF and to decrease after cardioversion (53). In failing canine hearts, atrial iNOS uncoupling due to BH4 depletion increased myocardial oxidative stress and was associated with shortening of the atrial effective refractory period and development of a substrate for inducible AF (116).…”

Section: What Is the Role Of Myocardial Endogenous Oxidase Systems Inmentioning

confidence: 99%

Targeting Inflammation and Oxidative Stress in Atrial Fibrillation: Role of 3-Hydroxy-3-Methylglutaryl-Coenzyme A Reductase Inhibition with Statins

Pinho-Gomes

Reilly

Brandes

et al. 2014

Antioxidants & Redox Signaling

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Significance: Atrial fibrillation (AF) is a burgeoning health-care problem, and the currently available therapeutic armamentarium is barely efficient. Experimental and clinical evidence implicates inflammation and myocardial oxidative stress in the pathogenesis of AF. Recent Advances: Local and systemic inflammation has been found to both precede and follow the new onset of AF, and NOX2-dependent generation of reactive oxygen species in human right atrial samples has been independently associated with the occurrence of AF in the postoperative period in patients undergoing cardiac surgery. Anti-inflammatory and antioxidant agents can prevent atrial electrical remodeling in animal models of atrial tachypacing and the new onset of AF after cardiac surgery, suggesting a causal relationship between inflammation/oxidative stress and the atrial substrate that supports AF. Critical Issues: Statin therapy, by redressing the myocardial nitroso-redox balance and reducing inflammation, has emerged as a potentially effective strategy for the prevention of AF. Evidence indicates that statins prevent AF-induced electrical remodeling in animal models of atrial tachypacing and may reduce the new onset of AF after cardiac surgery. However, whether statins have antiarrhythmic properties in humans has yet to be conclusively demonstrated, as data from randomized controlled trials specifically addressing the relevance of statin therapy for the primary and secondary prevention of AF remain scanty. Future Directions: A better understanding of the mechanisms underpinning the putative antiarrhythmic effects of statins may afford tailoring AF treatment to specific clinical settings and patient's subgroups. Large-scale randomized clinical trials are needed to support the indication of statin therapy solely on the basis of AF prevention. Antioxid. Redox Signal. 20, 1268Signal. 20, -1285

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“…Similarly, uncoupling of endothelial NO synthase has been observed in response to tachycardia [7], pressure overload [8], or exposure to HOCl [9] -all situations conducive to the development of AF. Furthermore, rapid atrial pacing, which may precipitate AF, results in elevations in plasma asymmetric dimethylarginine (ADMA, an endogenous inhibitor of NO synthase) concentrations [10]. There is also substantial evidence that thrombospondin-1 (TSP-1), a protein released predominantly from platelet α-granules, may diminish NO signaling both at the level of NO synthase and of soluble guanylate cyclase (sGC) activation [11,12], and promote platelet aggregation in vitro [13].…”

mentioning

confidence: 99%