Association of atrial fibrillation with outcomes in patients hospitalized with inflammatory bowel disease: an analysis of the National Inpatient Sample.

INTRODUCTION: We aimed to determine in-hospital outcomes, length of hospital stay (LOS) and resource utilization in a contemporary cohort of patients with inflammatory bowel disease (IBD) and atrial fibrillation (AFIB). MATERIAL AND METHODS: The National Inpatient Sample database October 2015 to December 2017 was utilized for data analysis using the International Classification of Diseases, Tenth Revision codes to identify the patients with the principal diagnosis of IBD. RESULTS: Of 714,863 IBD patients, 64,599 had a diagnosis of both IBD and AFIB. We found that IBD patients with AFIB had a greater incidence of in-hospital mortality (OR = 1.3; 95% CI: 1.1-1.4), sepsis (OR = 1.2; 95% CI: 1.1-1.3), mechanical ventilation (OR = 1.2; 95% CI: 1.1-1.5), shock requiring vasopressor (OR = 1.4; 95% CI: 1.1-1.9), lower gastrointestinal bleeding (LGIB) (OR = 1.09, 95% CI: 1.04-1.1), and hemorrhage requiring blood transfusion (OR = 1.2, 95% CI: 1.17-1.37). Mean LOS ± SD, mean total charges and total costs were higher in patients with IBD and AFIB. CONCLUSIONS: In this study, IBD with AFIB was associated with increased in-hospital mortality and morbidity, mean LOS and resource utilization.

Corrigendum: Attenuation of Na/K-ATPase Mediated Oxidant Amplification with pNaKtide Ameliorates Experimental Uremic Cardiomyopathy.

This corrects the article DOI: 10.1038/srep34592.

Attenuation of Na/K-ATPase Mediated Oxidant Amplification with pNaKtide Ameliorates Experimental Uremic Cardiomyopathy.

We have previously reported that the sodium potassium adenosine triphosphatase (Na/K-ATPase) can effect the amplification of reactive oxygen species. In this study, we examined whether attenuation of oxidant stress by antagonism of Na/K-ATPase oxidant amplification might ameliorate experimental uremic cardiomyopathy induced by partial nephrectomy (PNx). PNx induced the development of cardiac morphological and biochemical changes consistent with human uremic cardiomyopathy. Both inhibition of Na/K-ATPase oxidant amplification with pNaKtide and induction of heme oxygenase-1 (HO-1) with cobalt protoporphyrin (CoPP) markedly attenuated the development of phenotypical features of uremic cardiomyopathy. In a reversal study, administration of pNaKtide after the induction of uremic cardiomyopathy reversed many of the phenotypical features. Attenuation of Na/K-ATPase oxidant amplification may be a potential strategy for clinical therapy of this disorder.