What drives variability in postoperative cardiac surgery transfusion rates?

OBJECTIVE: Wide interhospital variation exists in cardiac surgical postoperative transfusion rates. We aimed to compare transfusion rates at 2 hospitals and identify the institutional practice factors, unrelated to patient or operative characteristics, associated with postoperative transfusion rates. METHODS: Records for adult patients undergoing routine cardiac surgery at 2 hospitals (H and L) from February 2020 to August 2022 were analyzed. Patient and operative characteristics, preoperative and intensive care unit hemoglobin values, and postoperative transfusion rates were compared. Transfusion indication was recorded prospectively. Propensity matching was completed to assess comparability of patient populations. RESULTS: After propensity matching patients at H and L on age, procedure type, predicted morbidity or mortality, crossclamp time, preoperative hypertension, preoperative heart failure, and preoperative stroke, 2111 patients remained, with similar characteristics except hypertension. Matched results showed no significant differences in mortality, reoperation, or other major outcomes. Hospital H transfused 36% of patients (mean postoperative hemoglobin [Hb] 10.5) with 1483 units of packed red blood cells whereas hospital L transfused 12% of patients (mean postoperative Hb 9.4) with 198 units of packed red blood cells (P < .001). For all patients with a Hb >7.5, hospital H versus L transfused 27% versus 0.9% (P < .001). Hospital L's sole transfusion indication for pretransfusion hemoglobin trigger >7.5 was bleeding versus hospital H, which had multiple indications. When Hb concentration alone was the indication for transfusion, the threshold at hospital H was <7.5 g/dL versus <6 g/dL at hospital L. CONCLUSIONS: Variation in transfusion rates between hospitals H and L resulted from strict adherence at hospital L to a transfusion trigger of <6 g/dL with narrow indications for transfusions above that Hb concentration.

Racial Disparities in Waiting List Outcomes of Patients Listed for Lung Transplantation.

BACKGROUND: The Lung Allocation Score, implemented in 2005, prioritized lung transplant candidates by medical urgency rather than waiting list time and was expected to improve racial disparities in transplant allocation. We evaluated whether racial disparities in lung transplant persisted after 2005. METHODS: We identified all wait-listed adult lung transplant candidates in the United States from 2005 through 2021 using the Scientific Registry of Transplant Recipients. We evaluated the association between race and receipt of a transplant by using a multivariable competing risk regression model adjusted for demographics, socioeconomic status, Lung Allocation Score, clinical measures, and time. We evaluated interactions between race and age, sex, socioeconomic status, and Lung Allocation Score. RESULTS: We identified 33,158 candidates on the lung transplant waiting list between 2005 and 2021: 27,074 White (82%), 3350 African American (10%), and 2734 Hispanic (8%). White candidates were older, had higher education levels, and had lower Lung Allocation Scores (P < .001). After multivariable adjustment, African American and Hispanic candidates were less likely to receive lung transplants than White candidates (African American: adjusted subhazard ratio, 0.86; 95% CI, 0.82-0.91; Hispanic: adjusted subhazard ratio, 0.82; 95% CI, 0.78-0.87). Lung transplant was significantly less common among Hispanic candidates aged >65 years (P = .003) and non-White candidates from higher-poverty communities (African-American: P = .013; Hispanic: P =.0036). CONCLUSIONS: Despite implementation of the Lung Allocation Score, racial disparities persisted for wait-listed African American and Hispanic lung transplant candidates and differed by age and poverty status. Targeted interventions are needed to ensure equitable access to this life-saving intervention.

Post-Stroke Timing of ECM Hydrogel Implantation Affects Biodegradation and Tissue Restoration.

Extracellular matrix (ECM) hydrogel promotes tissue regeneration in lesion cavities after stroke. However, a bioscaffold's regenerative potential needs to be considered in the context of the evolving pathological environment caused by a stroke. To evaluate this key issue in rats, ECM hydrogel was delivered to the lesion core/cavity at 7-, 14-, 28-, and 90-days post-stroke. Due to a lack of tissue cavitation 7-days post-stroke, implantation of ECM hydrogel did not achieve a sufficient volume and distribution to warrant comparison with the other time points. Biodegradation of ECM hydrogel implanted 14- and 28-days post-stroke were efficiently (80%) degraded by 14-days post-bioscaffold implantation, whereas implantation 90-days post-stroke revealed only a 60% decrease. Macrophage invasion was robust at 14- and 28-days post-stroke but reduced in the 90-days post-stroke condition. The pro-inflammation (M1) and pro-repair (M2) phenotype ratios were equivalent at all time points, suggesting that the pathological environment determines macrophage invasion, whereas ECM hydrogel defines their polarization. Neural cells (neural progenitors, neurons, astrocytes, oligodendrocytes) were found at all time points, but a 90-days post-stroke implantation resulted in reduced densities of mature phenotypes. Brain tissue restoration is therefore dependent on an efficient delivery of a bioscaffold to a tissue cavity, with 28-days post-stroke producing the most efficient biodegradation and tissue regeneration, whereas by 90-days post-stroke, these effects are significantly reduced. Improving our understanding of how the pathological environment influences biodegradation and the tissue restoration process is hence essential to devise engineering strategies that could extend the therapeutic window for bioscaffolds to repair the damaged brain.

Biodegradation of ECM hydrogel promotes endogenous brain tissue restoration in a rat model of stroke.

The brain is considered to have a limited capacity to repair damaged tissue and no regenerative capacity following injury. Tissue lost after a stroke is therefore not spontaneously replaced. Extracellular matrix (ECM)-based hydrogels implanted into the stroke cavity can attract endogenous cells. These hydrogels can be formulated at different protein concentrations that govern their rheological and inductive properties. We evaluated histologically 0, 3, 4 and 8 mg/mL of porcine-derived urinary bladder matrix (UBM)-ECM hydrogel concentrations implanted in a 14-day old stroke cavity. Less concentrated hydrogels (3 and 4 mg/mL) were efficiently degraded with a 95% decrease in volume by 90 days, whereas only 32% of the more concentrated and stiffer hydrogel (8 mg/mL) was resorbed. Macrophage infiltration and density within the bioscaffold progressively increased in the less concentrated hydrogels and decreased in the 8 mg/mL hydrogels. The less concentrated hydrogels showed a robust invasion of endothelial cells with neovascularization. No neovascularization occurred with the stiffer hydrogel. Invasion of neural cells increased with time in all hydrogel concentrations. Differentiation of neural progenitors into mature neurons with axonal projections was evident, as well as a robust invasion of oligodendrocytes. However, relatively few astrocytes were present in the ECM hydrogel, although some were present in the newly forming tissue between degrading scaffold patches. Implantation of an ECM hydrogel partially induced neural tissue restoration, but a more complete understanding is required to evaluate its potential therapeutic application. STATEMENT OF SIGNIFICANCE: Extracellular matrix hydrogel promotes tissue regeneration in many peripheral soft tissues. However, the brain has generally been considered to lack the potential for tissue regeneration. We here demonstrate that tissue regeneration in the brain can be achieved using implantation of ECM hydrogel into a tissue cavity. A structure-function relationship is key to promote tissue regeneration in the brain. Specifically, weaker hydrogels that were retained in the cavity underwent an efficient biodegradation within 14 days post-implantation to promote a tissue restoration within the lesion cavity. In contrast, stiffer ECM hydrogel only underwent minor biodegradation and did not lead to a tissue restoration. Inductive hydrogels weaker than brain tissue provide the appropriate condition to promote an endogenous regenerative response that restores tissue in a cavity. This approach offers new avenues for the future treatment of chronic tissue damage caused by stroke and other acute brain injuries.