Faculty Bibliography

BACKGROUND: Congestive heart failure (CHF) is one of the leading causes of hospital readmissions within 30 days of discharge. Due to the substantial costs associated with these readmissions, several interventions to reduce CHF readmissions have been developed and implemented. METHODS: To reduce CHF readmissions at our community teaching hospital, the Smooth Transitions Equal Less Readmission (STELR) program was developed. Utilizing the Plan-Do-Check-Act cycle for quality improvement, resident physicians tracked patients enrolled in the STELR program. The resident contribution to the program was substantial in that they were able to quantify the improvement in both physician practices and patient readmissions. This provided insight into program areas requiring further modification, which the hospital would not have obtained without resident participation. RESULTS: The readmission rate for patients diagnosed with heart failure decreased from 32% prior to program implementation, to 24% hospital wide (including patients who were not tracked in the STELR program), and 21% among patients tracked by the residents. CONCLUSION: This effective CHF readmission reduction program requires less financial resources compared to government funded programs. The resident involvement in the STELR program helped to assess and improve the program and also allowed the residents to gain an awareness of the resources available to their patients to facilitate their transition home. The program exposed the residents to systems-based practice, a fundamental element of their residency training and, more generally, community care.

OBJECTIVE: We have previously demonstrated that endothelial xanthine oxidase (XO) levels are dependent on the NADPH oxidase. We postulated that H2O2 may modulate the irreversible conversion of xanthine dehydrogenase (XDH) to XO and sought to examine mechanisms involved. METHODS AND RESULTS: H2O2 (100 micromol/L) decreased bovine aortic endothelial cell (BAEC) XDH protein expression, and metabolic labeling studies indicated that H2O2 stimulated conversion of XDH to XO. The decline in XDH was mimicked by the reactive oxygen species (ROS) generating compounds SIN-1 and Menadione, as well as by stimulating BAECs with angiotensin II (200 nmol/L). BAPTA-AM prevented the decline in XDH by H2O2, indicating that it was calcium-dependent. In keeping with calcium acting downstream of H2O2, the calcium ionophore A23187 (1 micromol/L) caused XDH-to-XO conversion, and this was not prevented by the antioxidants. In addition, XDH-to-XO conversion was blocked by 2-APB and NO donors and induced by thapsigargin and M-3M3FBS, implicating phospholipase C and endoplasmic reticulum calcium stores in this process. CONCLUSIONS: Endothelial XO and XDH expression are strongly dependent on H2O2 and calcium. Stimulation of XDH conversion to XO may represent a feed-forward mechanism whereby H2O2 can stimulate further production of ROS.