Transient atrial fibrillation after open abdominal aortic revascularization surgery is associated with increased length of stay, mortality, and readmission rates.

BACKGROUND: It is well established that transient postoperative atrial fibrillation (TPAF) is associated with adverse postoperative outcomes after major cardiac and noncardiac operations. The purpose of this study was to elucidate the incidence, impact, and risk factors associated with the development of TPAF in patients undergoing revascularization surgery for occlusive diseases of the abdominal aorta and its branches (AAB). METHODS: By use of the Healthcare Cost and Utilization Project State Inpatient Database from Florida and California, patients who underwent open revascularization of AAB between 2006 and 2011 were identified. Patients diagnosed with aortic dissection or abdominal aortic aneurysm were excluded to limit the study cohort to include only patients with occlusive etiology. Also excluded were those with a pre-existing diagnosis of atrial fibrillation and those who underwent thoracic aortic repair and peripheral artery revascularization procedures. Multivariable logistic and linear regression analyses with treatment effects were conducted to analyze the association between TPAF and length of stay (LOS); the mortality rates at index admission, 1 month, and 1 year; and the readmission rates at 1 month and 1 year (adjusted for comorbidities and surgical and demographic factors). A backwards stepwise logistic regression model was built to identify predictors of TPAF. RESULTS: A total of 4462 patients were identified; 3253 underwent aortoiliac/femoral bypasses (72.9%), 1514 endarterectomies of AAB (33.9%), and 288 bypasses of AAB (6.5%). The incidence of TPAF was 2.4% (109 patients). Multivariate regression analysis with treatment effects showed that TPAF was associated with significantly increased LOS, mortality, and readmission rates. Factors identified as predictors of TPAF by backwards stepwise logistic regression modeling include electrolyte disorders, increasing age, and Charlson Comorbidity Index (C statistic = .69; accuracy = 58%). CONCLUSIONS: TPAF after revascularization of AAB is associated with increased LOS, inpatient mortality, 1-year mortality, and hospital readmissions. Strategies to identify patients at risk for development of TPAF and implementation of appropriate prophylactic measures may improve surgical outcomes and reduce cost of care.

Transient postoperative atrial fibrillation after abdominal aortic aneurysm repair increases mortality risk.

OBJECTIVE: The purpose of this study was to determine whether new-onset transient postoperative atrial fibrillation (TPAF) affects mortality rates after abdominal aortic aneurysm (AAA) repair and to identify predictors for the development of TPAF. METHODS: Patients who underwent open aortic repair or endovascular aortic repair for a principal diagnosis AAA were retrospectively identified using the Healthcare Cost and Utilization Project-State Inpatient Database (Florida) for 2007 to 2011 and monitored longitudinally for 1 year. Inpatient and 1-year mortality rates were compared between those with and without TPAF. TPAF was defined as new-onset atrial fibrillation that developed in the postoperative period and subsequently resolved in patients without a history of atrial fibrillation. Cox proportional hazards models, adjusted for age, gender, comorbidities, rupture status, and repair method, were used to assess 1-year survival. Predictive models were built with preoperative patient factors using Chi-squared Automatic Interaction Detector decision trees and externally validated on patients from California. RESULTS: A 3.7% incidence of TPAF was identified among 15,148 patients who underwent AAA repair. The overall mortality rate was 4.3%. The inpatient mortality rate was 12.3% in patients with TPAF vs 4.0% in those without TPAF. In the ruptured setting, the difference in mortality was similar between groups (33.7% vs 39.9%, P = .3). After controlling for age, gender, comorbid disease severity, urgency (ruptured vs nonruptured), and repair method, TPAF was associated with increased 1-year postoperative mortality (hazard ratio, 1.48; P < .001) and postdischarge mortality (hazard ratio, 1.56; P = .028). Chi-squared Automatic Interaction Detector-based models (C statistic = 0.70) were integrated into a Web-based application to predict an individual's probability of developing TPAF at the point of care. CONCLUSIONS: The development of TPAF is associated with an increased risk of mortality in patients undergoing repair of nonruptured AAA. Predictive modeling can be used to identify those patients at highest risk for developing TPAF and guide interventions to improve outcomes.

Contributions of dysregulated energy metabolism to type 2 diabetes development in NZO/H1Lt mice with polygenic obesity.

New Zealand Obese (NZO) male mice develop a polygenic juvenile-onset obesity and maturity-onset hyperinsulinemia and hyperglycemia (diabesity). Here we report on metabolic and molecular changes associated with the antidiabesity action of CL316,243 (CL), a beta(3)-adrenergic receptor agonist. Dietary CL treatment initiated at weaning reduced the peripubertal rise in body weight and adiposity while promoting growth without suppressing hyperphagia. The changes in adiposity, in turn, suppressed development of hyperinsulinemia, hyperleptinemia, hyperlipidemia, and hyperglycemia. These CL-induced alterations were reflected by decreased adipose tissue mass, increased expression of transcripts for uncoupling protein-1 (UCP-1), peroxisome proliferator-activated receptor alpha (PPARalpha), peroxisome proliferater-activated receptor coactivator-1 (PGC-1), and robust development of brown adipocyte function in white fat. Increased drug-mediated energy dissipation elicited a 1.5 degrees C increase in whole body temperature under conditions of increased food intake but with no change in physical activity. Indirect calorimetry of mice treated with CL showed both increased energy expenditure and a restoration of a prominent diurnal pattern in the respiratory exchange ratio suggesting improved nutrient sensing. Our data suggest that CL promotes increased energy dissipation in white and brown fat depots by augmenting thermogenesis and by metabolic re-partitioning of energy in a diabesity-protective fashion. This is the first report demonstrating the effects of dietary beta(3)-agonist in preventing the onset of diabesity in a polygenic rodent model of type 2 diabetes.