Inpatient palliative care referral and 9-month hospital readmission in patients with congestive heart failure: a linked nationwide analysis.

OBJECTIVE: End-stage heart failure (HF) is characterized by high symptom burden and frequent hospitalization. Palliative care (PC) is recommended for advanced HF, and there is some evidence in other diseases that this may reduce readmission rates. We attempted examine the association of an inpatient PC visit on hospital readmission for patients admitted with HF. METHODS: Retrospective linked nationwide analysis from 2013 with 9-month follow-up for all hospital readmissions for patients admitted with HF exacerbations using the Nationwide Readmission Database (NRD). The NRD gathers all hospital admissions for patients from 22 states and tracks patients throughout the year, allowing for examination of readmission statistics. A propensity score model for PC visit was made, and patients were matched in a 1 : 1 fashion. RESULTS: There were 102 746 patients who survived an admission for HF in the first 3 months of 2013. Of these, 2287 (2.2%) patients had a PC visit as inpatients. After matching based on propensity for a PC visit during the index hospitalization, 2282 patients who received a PC visit were matched to 2282 patients who did not. Those receiving a PC visit were less likely to be readmitted for HF (9.3% vs. 22.4%, P < 0.01) or for any cause (29.0% vs. 63.2%, P < 0.01) during the 9-month follow-up period. The average hospital charges during the follow-up period for the non-PC cohort were $77 643 per patient. The average charges for PC patients were $23 200 (P < 0.01). CONCLUSIONS: Patients with HF who received an inpatient PC visit had significantly lower rates of all-cause and HF-specific readmission in the subsequent 9 months. Total 9-month hospital charges were also significantly lower for patients who received an inpatient PC visit.

A novel AHI-1-BCR-ABL-DNM2 complex regulates leukemic properties of primitive CML cells through enhanced cellular endocytosis and ROS-mediated autophagy.

Tyrosine kinase inhibitor (TKI) therapies induce clinical remission with remarkable effects on chronic myeloid leukemia (CML). However, very few TKIs completely eradicate the leukemic clone and persistence of leukemic stem cells (LSCs) remains challenging, warranting new, distinct targets for improved treatments. We demonstrated that the scaffold protein AHI-1 is highly deregulated in LSCs and interacts with multiple proteins, including Dynamin-2 (DNM2), to mediate TKI-resistance of LSCs. We have now demonstrated that the SH3 domain of AHI-1 and the proline rich domain of DNM2 are mainly responsible for this interaction. DNM2 expression was significantly increased in CML stem/progenitor cells; knockdown of DNM2 greatly impaired their survival and sensitized them to TKI treatments. Importantly, a new AHI-1-BCR-ABL-DNM2 protein complex was uncovered, which regulates leukemic properties of these cells through a unique mechanism of cellular endocytosis and ROS-mediated autophagy. Thus, targeting this complex may facilitate eradication of LSCs for curative therapies.