Establishment of a model of atrial fibrillation associated with chronic kidney disease in rats and the role of oxidative stress

Fukunaga, Naoya; Takahashi, Naohiko; Hagiwara, Satoshi; Kume, Osamu; Fukui, Atsushi; Teshima, Yasushi; Shinohara, Tetsuji; Nawata, Tomoko; Hara, Masahide; Noguchi, Takayuki; Saikawa, Tetsunori

doi:10.1016/j.hrthm.2012.08.019

Cited by 46 publications

(48 citation statements)

References 26 publications

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“…In experiments in vivo, the P-wave duration was prolonged in 5/6Nx-treated rats and this was suppressed by DHLHZn (Figure 8). 14 The cardiovascular pathologic features of our CKD model, including cardiac hypertrophy with left ventricular hyperkinetic motion, were consistent with those of previous studies. 45, 46 The LA of 5/6Nx-treated rats showed heterogeneous interstitial fibrosis.…”

Section: Chronic Kidney Disease (Ckd) and Novel Antioxidant Agentsupporting

confidence: 90%

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Novel Strategy to Prevent Atrial Fibrosis and Fibrillation

Takahashi

Kume

Wakisaka

et al. 2012

Circ J

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Section: Chronic Kidney Disease (Ckd) and Novel Antioxidant Agentsupporting

confidence: 90%

“…We have induced atrial fibrosis by pressure overload, 12 continuous infusion of angiotensin II (AII), 13 and 5/6 nephrectomy (5/6Nx). 14 In these 3 AF models, we have evaluated the anti-AF effects of pioglitazone, 12 induction of heat shock protein (HSP), 13 and an antioxidant agent, 14 respectively.…”

mentioning

confidence: 99%

Novel Strategy to Prevent Atrial Fibrosis and Fibrillation

Takahashi

Kume

Wakisaka

et al. 2012

Circ J

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“…Reninangiotensin-aldosterone system (RAAS) has been implicated in the activation of proliferative pathways promoting cellular growth and fibroblast activation that participate to ventricular and atrial structural abnormalities [22,23]. In keeping with this, recent in vivo experimental data demonstrates that oxidative stress is involved in the pathogenesis of atrial fibrosis and enhanced vulnerability for AF appearance [24]. Finally, also the sympathetic activation RAAS-related has been proposed to atrial dysrhythmogenesis and AF development [25].…”

Section: Discussionmentioning

confidence: 91%

CHADS2 and CHA2DS2-VASc scores are independently associated with incident atrial fibrillation: the Catanzaro Atrial Fibrillation Project

et al. 2015

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No data exist concerning a possible association between CHADS2 or CHA2DS2-VASc scores and atrial fibrillation (AF). In this prospective observational study, we tested the hypothesis whether thromboembolic risk scores predict AF. We investigated 3549 subjects, 1829 men and 1720 women, aged 60.7 ± 10.6 years, without baseline AF. Patients with thyroid disorders were excluded. CHADS2 and CHA2DS2-VASc scores were evaluated as categorical variables. To test the effect of some clinical confounders on incident AF, we constructed different models including clinical and laboratory parameters. During follow-up (53.3 ± 18.1 months), 546 subjects developed AF (4.5 events/100 patient-years). Progressors to AF are older, have a higher body mass index (BMI), blood pressure, LDL-cholesterol, and glucose. Hypertension, metabolic syndrome, diabetes and carotid wall thickening were more common among AF cases than among control subjects. In the final Cox-regression model, variables that remained significantly associated with incident AF were BMI (HR = 1.022, 95% CI = 1.008-1.037), LDL-cholesterol (HR = 1.032, 95% CI = 1.008-1.056), CHA2DS2-VASc score (HR = 1.914, 95% CI = 1.439-2.546), and CHADS2 score (HR = 2.077, 95% CI = 1.712-2.521). In conclusion, CHADS2 and CHA2DS2-VASc scores are independent predictors of AF.

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“…Indices of oxidative stress are increased with severity of kidney disease and correlates significantly with level of renal function [26]. For example, in the left atrium, expressions of nicotinamide adenine dinucleotide phosphate oxidase and malondialdehyde were increased by CKD [27].…”

Section: Discussionmentioning

confidence: 99%