ABSTRACT
ABSTRACT Introduction: The objective of this study is to investigate the possible impact of coronary artery disease (CAD) on clinical outcomes of catheter ablation in patients with atrial fibrillation (AF). Methods: Patients with AF who underwent coronary computed tomography and catheter ablation were enrolled. The presence of stenotic severity and plaque, characteristics of coronary arteries, clinical data, and adverse outcomes of catheter ablation were analysed. Results: A total of 243 patients were enrolled, 100 (41%) patients with CAD. The CHA2DS2-VASc (congestive heart failure, hypertension, age ≥ 75 years, diabetes mellitus, stroke or transient ischemic attack, vascular disease, age 65-74 years, and sex category) score of AF patients with CAD was significantly (P<0.001) higher than of those without CAD. Presence of stenotic artery and plaques increased significantly with increase of CHA2DS2-VASc score (P<0.05). There was no significant (P=0.342) difference in AF recurrence between patients with and without CAD (30% versus 24%). Age, AF type, duration of AF, heart failure, CHA2DS2-VASc score, left ventricular ejection fraction, and left atrial diameter were significantly (P<0.05) correlated with AF recurrence in univariant analysis. Multivariable analysis revealed that duration of AF (hazard ratio [HR] 1.769), heart failure (HR 1.821), and left atrial diameter (HR 1.487, P=0.022) remained significant independent predictors of AF recurrence. Patients with AF and concomitant CAD were significantly (P=0.030) associated with a worse outcome. Conclusion: CAD concomitant with AF may be associated with a worse clinical outcome even though CAD does not significantly affect the risk of AF recurrence after ablation therapy.
ABSTRACT
This study has investigated the effect of a potent bioflavonoid, troxerutin,on diabetes-induced changes in pro-inflammatory mediators and expression ofmicroRNA-146a and nuclear factor-kappa-B (NF-κB) signaling pathway in aortic tissueof type-I diabetic rats. Male Wistar rats were randomly divided into four groups(n = 6/each): healthy, healthy-troxerutin, diabetic, and diabetic-troxerutin. Diabeteswas induced by streptozotocin injection (60 mg/kg; intraperitoneally) and lasted 10weeks. Troxerutin (150 mg/kg/day) was administered orally for last month of experiment.Inflammatory cytokines IL-1, IL-6, and TNF-, as well as intercellular adhesionmolecule-1 (ICAM-1), vascular cell adhesion molecule (VCAM), cyclooxygenase-II(COX-II), and inducible-nitric oxide synthase (iNOS) were measured on aortic samplesby enzyme-linked immunosorbent assay. Gene expressions for transcription factorNF-κB, interleukin-1 receptor-associated kinase-1 (IRAK-1), TNF receptor-associatedfactor-6 (TRAF-6), and microRNA-146a were determined using real-time polymerasechain reaction. Ten-week diabetes significantly increased mRNA levels of IRAK-1,TRAF-6, NF-κB, and protein levels of cytokines IL-1, IL-6, TNF-, adhesion moleculesICAM-1, VCAM, and iNOS, COX-II, and decreased expression of microRNA-146a ascompared with healthy rats (p < 0.05 to p < 0.01). However, one month treatmentof diabetic rats with troxerutin restored glucose and insulin levels, significantly decreasedexpression of inflammatory genes and pro-inflammatory mediators andincreased microRNA level in comparison to diabetic group (p < 0.05 to p < 0.01). Inhealthy rats, troxerutin had significant reducing effect only on NF-κB, TNF- and COXIIlevels (p < 0.05). Beside slight improvement of hyperglycemia, troxerutin preventedthe activation of NF-κB-dependent inflammatory signaling in
ABSTRACT
This study has investigated the effect of a potent bioflavonoid, troxerutin,on diabetes-induced changes in pro-inflammatory mediators and expression ofmicroRNA-146a and nuclear factor-kappa-B (NF-κB) signaling pathway in aortic tissueof type-I diabetic rats. Male Wistar rats were randomly divided into four groups(n = 6/each): healthy, healthy-troxerutin, diabetic, and diabetic-troxerutin. Diabeteswas induced by streptozotocin injection (60 mg/kg; intraperitoneally) and lasted 10weeks. Troxerutin (150 mg/kg/day) was administered orally for last month of experiment.Inflammatory cytokines IL-1, IL-6, and TNF-, as well as intercellular adhesionmolecule-1 (ICAM-1), vascular cell adhesion molecule (VCAM), cyclooxygenase-II(COX-II), and inducible-nitric oxide synthase (iNOS) were measured on aortic samplesby enzyme-linked immunosorbent assay. Gene expressions for transcription factorNF-κB, interleukin-1 receptor-associated kinase-1 (IRAK-1), TNF receptor-associatedfactor-6 (TRAF-6), and microRNA-146a were determined using real-time polymerasechain reaction. Ten-week diabetes significantly increased mRNA levels of IRAK-1,TRAF-6, NF-κB, and protein levels of cytokines IL-1, IL-6, TNF-, adhesion moleculesICAM-1, VCAM, and iNOS, COX-II, and decreased expression of microRNA-146a ascompared with healthy rats (p < 0.05 to p < 0.01). However, one month treatmentof diabetic rats with troxerutin restored glucose and insulin levels, significantly decreasedexpression of inflammatory genes and pro-inflammatory mediators andincreased microRNA level in comparison to diabetic group (p < 0.05 to p < 0.01). Inhealthy rats, troxerutin had significant reducing effect only on NF-κB, TNF- and COXIIlevels (p < 0.05). Beside slight improvement of hyperglycemia, troxerutin preventedthe activation of NF-κB-dependent inflammatory signaling in