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Background: Quality measurement has become a priority for national healthcare reform, and valid measures are necessary to discriminate hospital performance and support value‐based healthcare delivery. The Commission on Cancer (CoC) is the largest cancer‐specific accreditor of hospital quality in the United States and has implemented Quality of Care Measures to evaluate cancer care delivery. However, none has been formally tested as a valid metric for assessing hospital performance based on actual patient outcomes. Methods: Eligibility and compliance with the Quality of Care Measures are reported within the National Cancer Database, which also captures data for robust patient‐level risk adjustment. Hospital‐level compliance was calculated for the core measures, and the association with patient survival was tested using Cox regression. Results: Seven hundred sixty‐eight thousand nine hundred sixty‐nine unique cancer cases were included from 1323 facilities. Increasing hospital‐level compliance was associated with improved survival for only two measures, including a 35% reduced risk of mortality for the gastric cancer measure G15RLN (HR 0.65, 95% CI 0.58–0.72) and a 19% reduced risk of mortality for the colon cancer measure 12RLN (HR 0.81, 95% CI 0.77–0.85). For the lung cancer measure LNoSurg, increasing compliance was paradoxically associated with an increased risk of mortality (HR 1.14, 95% CI 1.08–1.20). For the remaining measures, hospital‐level compliance demonstrated no consistent association with patient survival. Conclusion: Hospital‐level compliance with the CoC's Quality of Care Measures is not uniformly aligned with patient survival. In their current form, these measures do not reliably discriminate hospital performance and are limited as a tool for value‐based healthcare delivery. [ABSTRACT FROM AUTHOR]

Recipients of liver allografts from diabetic donors have decreased graft survival. However, limited data exist on the effects of donor HbA1c. We hypothesized that allografts from nondiabetic donors with elevated HbA1c would be associated with decreased survival. Liver transplant recipients from the UNOS database from nondiabetic donors were stratified into two groups: euglycemic (HbA1c<6.5) and hyperglycemic (HbA1c≥6.5). Propensity score matching (10:1) was used to adjust for donor and recipient characteristics. Kaplan-Meier analysis was used to assess survival. Donors of hyperglycemic allografts were older (49 vs 36, P<.001), were more likely to be non-white, had a higher BMI (29.8 vs 26.2, P<.001), were more likely to engage in heavy cigarette use (1.5% vs 1.3%, P=.004), had higher serum creatinine levels (1.3 vs 1.0, P=.002), and were more likely to be an expanded-criteria donor (35.8% vs 14.4%, P<.001). After propensity matching to account for these differences, allograft survival was significantly decreased in the recipients of hyperglycemic allografts ( P=.049), and patient survival showed a trend toward reduction ( P=.082). These findings suggest that HbA1c may be a simple and inexpensive test with potential utility for better organ risk stratification. [ABSTRACT FROM AUTHOR]

Background Orthotopic heart transplantation ( OHT) is the gold-standard therapy for end-stage heart failure. An increasing deficit between suitable allograft availability and clinical demand for OHT exists. The role of donor diabetes mellitus ( DM) on post-transplant recipient outcomes in OHT is controversial. The purpose of this study was to examine donor hemoglobin A1c (HbA1c) levels to identify the impact of donor glycemic control on recipient survival. Methods Adult OHT recipients with donor HbA1c data were identified in the UNOS database from 2010 to 2015. Recipients were stratified on the basis of donor glycemic status: Hyperglycemic-donor and euglycemic-donor cohorts were defined as HbA1c levels ≥6.5% and <6.5%, respectively. Outcomes were compared between unadjusted and propensity-matched hyperglycemic versus euglycemic donors. Primary end point was three-year survival. Results Of 5342 OHT recipients, 208 (3.89%) received an allograft from a hyperglycemic donor and 5134 (96.1%) received an allograft from a euglycemic donor. There was no significant difference in survival in the hyperglycemic group before ( P=.87) or after ( P=.78) propensity matching. Conclusions No difference in four-year survival was noted in recipients who received allografts from hyperglycemic donors. These results suggest that recent cumulative donor glycemic status alone may not be an important predictor of recipient outcomes. [ABSTRACT FROM AUTHOR]

Background Kidney transplantation has been advocated as a therapeutic option in lung recipients who develop end-stage renal disease ( ESRD). This analysis outlines patterns of allograft survival following kidney transplantation in previous lung recipients ( KAL). Methods Data from the UNOS lung and kidney transplantation registries (1987-2013) were cross-linked to identify lung recipients who were subsequently listed for and/or underwent kidney transplantation. Time-dependent Cox models compared the survival rates in KAL patients with those waitlisted for renal transplantation who never received kidneys. Survival analyses compared outcomes between KAL patients and risk-matched recipients of primary, kidney-only transplantation with no history of lung transplantation ( KTx). Results A total of 270 lung recipients subsequently underwent kidney transplantation ( KAL). Regression models demonstrated a lower risk of post-listing mortality for KAL patients compared with 346 lung recipients on the kidney waitlist who never received kidneys ( P<.05). Comparisons between matched KAL and KTx patients demonstrated significantly increased risk of death and graft loss ( P<.05), but not death-censored graft loss, for KAL patients ( P = .86). Conclusions KAL patients enjoy a significant survival benefit compared with waitlisted lung recipients who do not receive kidneys. However, KAL patients do poorly compared with KTx patients. Decisions about KAL transplantation must be made on a case-by-case basis considering patient and donor factors. [ABSTRACT FROM AUTHOR]

The newborn heart adapts to postnatal life by shifting from a fetal glycolytic metabolism to a mitochondrial oxidative metabolism. Abcc9, an ATP-binding cassette family member, increases expression concomitant with this metabolic shift. Abcc9 encodes a membrane-associated receptor that partners with a potassium channel to become the major potassium-sensitive ATP channel in the heart. Abcc9 also encodes a smaller protein enriched in the mitochondria. We now deleted exon 5 of Abcc9 to ablate expression of both plasma membrane and mitochondria-associated Abcc9-encoded proteins, and found that the myocardium failed to acquire normal mature metabolism, resulting in neonatal cardiomyopathy. Unlike wild-type neonatal cardiomyocytes, mitochondria from Ex5 cardiomyocytes were unresponsive to the KATP agonist diazoxide, consistent with loss of KATP activity. When exposed to hydrogen peroxide to induce cell stress, Ex5 neonatal cardiomyocytes displayed a rapid collapse of mitochondria membrane potential, distinct from wild-type cardiomyocytes. Ex5 cardiomyocytes had reduced fatty acid oxidation, reduced oxygen consumption and reserve. Morphologically, Ex5 cardiac mitochondria exhibited an immature pattern with reduced cross-sectional area and intermitochondrial contacts. In the absence of Abcc9, the newborn heart fails to transition normally from fetal to mature myocardial metabolism. [ABSTRACT FROM AUTHOR]