Prevention of atrial fibrillation

Leonardi, Marino; Bissett, Joe K.

doi:10.1097/01.hco.0000172703.44898.27

Cited by 20 publications

(20 citation statements)

References 49 publications

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“…Multiple factors may alter the electrical and structural properties of the atrium (atrial remodeling) and predispose the patient to AF. 25 Although we did not examine oxidative stress in this study, it may be involved in the pathogenesis of AF. Therefore, the reduction of the ratio of L-PAF-AH to H-PAF-AH using medications might prevent atrial remodeling.…”

Section: Discussionmentioning

confidence: 99%

Ratio of LDL- to HDL-Associated Platelet-Activating Factor Acetylhydrolase may be a Marker of Inflammation in Patients With Paroxysmal Atrial Fibrillation

Okamura

Miura

Zhang

et al. 2007

Circ J

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Section: Discussionmentioning

confidence: 99%

Ratio of LDL- to HDL-Associated Platelet-Activating Factor Acetylhydrolase may be a Marker of Inflammation in Patients With Paroxysmal Atrial Fibrillation

Okamura

Miura

Zhang

et al. 2007

Circ J

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“…Also, several pharmacologic approaches with antioxidant properties are effective for treating AF [79,81,142]. AF is often accompanied by oxidative changes, which include mitochondrial DNA damage and upregulation of NADPH oxidase, a major producer of ROSs [31,143].…”

Section: Oxidative Stressmentioning

confidence: 99%

Regulatory mechanisms of atrial fibrotic remodeling in atrial fibrillation

Lin

Pan

2008

Cell. Mol. Life Sci.

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Electrical, contractile and structural remodeling have been characterized in atrial fibrillation (AF), and the latter is considered to be the major contributor to AF persistence. Recent data show that interstitial fibrosis can predispose to atrial conduction impairment and AF induction. The interplay between cardiac matrix metalloproteinases (MMPs) and their endogenous inhibitors, tissue inhibitors of MMPs (TIMPs), is thought to be critical in atrial extracellular matrix (ECM) metabolism. At the molecular level, angiotensin II, transforming growth factor-beta1, inflammation and oxidative stress are particularly important for ECM dysregulation and atrial fibrotic remodeling in AF. Therefore, we review recent advances in the understanding of the atrial fibrotic process, the major downstream components in this remodeling process, and the expression and regulation of MMPs and TIMPs. We also describe the activation of bioactive molecules in both clinical studies and animal models to modulate MMPs and TIMPs and their effects on atrial fibrosis in AF.

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“…Also, several pharmacologic approaches with non-channel-blocking drugs that have antioxidant and anti-inflammatory properties show beneficial effects on AF development [17][18][19][20]. Since the publication of the first brief review regarding these issues [10], several novel observations have reinforced such notions.…”

Section: Introductionmentioning

confidence: 98%