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Background Public reporting of transcatheter aortic valve replacement (TAVR) claims–based outcome measures is used to identify high‐ and low‐performing centers. Whether claims‐based TAVR outcomes can reliably be used for center‐level comparisons is unknown. In this study, we sought to evaluate center variability in claims‐based TAVR outcomes used in public reporting. Methods and Results The study sample included 119 554 Medicare beneficiaries undergoing TAVR between January 2014 and October 2018 based on procedure codes in 100% Medicare inpatient claims. Multivariable hierarchical logistic regression was used to estimate center‐specific adjusted rates and reliability (R) of 30‐day mortality, discharge not to home/self‐care, 30‐day stroke, and 30‐day readmission. Reliability was defined as the ratio of between‐hospital variation to the sum of the between‐ and within‐hospital variation. The median (interquartile range [IQR]) center‐level adjusted outcome rates were 3.1% (2.9%–3.4%) for 30‐day mortality, 41.4% (31.3%–53.4%) for discharge not to home, 2.5% (2.3%–2.7%) for 30‐day stroke, and 14.9% (14.4%–15.5%) for 30‐day readmission. Median reliability was highest for the discharge not to home measure (R=0.95; IQR, 0.94–0.97), followed by the 30‐day stroke (R=0.92; IQR, 0.87–0.94), 30‐day mortality (R=0.86; IQR, 0.81–0.91), and 30‐day readmission measures (R=0.42; IQR, 0.35–0.51). Across outcomes, there was an inverse relationship between center volume and measure reliability. Conclusions Claims‐based TAVR outcome measures for mortality, discharge not to home, and stroke were reliable measures for center‐level comparisons, but readmission measures were unreliable. Stakeholders should consider these findings when evaluating claims‐based measures to compare center‐level TAVR performance.

The purpose of this study was to determine the relationships between possible predictive measures of a 50 m front crawl swimming and a 22.86 m flutter kicking speed. Ten women who were National Collegiate Athletic Association Division I collegiate swimmers and 10 women who were recreational swimmers (mean +/- SD = 20.6 +/- 1.6 years; 66.7 +/- 10.3 kg; 166.7 +/- 8.8 cm) volunteered for the study. Anthropometric measures were obtained including height, leg length, lower leg length, and foot length. Ankle flexibility was assessed by measuring ankle plantar flexion and ankle inversion. Lower body power was measured using a vertical jump. Swimming and kicking speed were measured as the time to complete a 50 m front crawl and a 22.86 m flutter kick, respectively. Significant moderate correlations were demonstrated between ankle plantar flexion and flutter kicking speed (r = 0.509); age and 22.86 m kick time (r = 0.608); age and 50 m swim time (r = 0.476); and 50 m swim time and 22.86 m kick time (r = 0.790). No significant correlations were observed between any of the anthropometric measurements or vertical jump power with either kicking or swimming speed. As anecdotally noted by swim coaches over the years, this study provides some actual data showing that ankle flexibility significantly influences flutter kick capability. Surprisingly, vertical jump power and body size were not strong predictors of kicking or swimming speed in this group of subjects. Strength and conditioning coaches, swim coaches, and athletes should evaluate and carefully develop ankle flexibility to positively contribute to kicking capabilities.

Improved cadaver kidney allograft survival rates, shorter duration of acute tubular necrosis, and a reduction in the incidence of rejection have been achieved using "quadruple sequential therapy"--AZA, prednisone, and antilymphocyte globulin (ALG) induction followed by the delayed addition of CsA. OKT3 has been shown to be effective in preventing and treating rejection, including steroid- and ALG-resistant rejection episodes. A single institution prospective randomized trial comparing ALG and OKT3 prophylaxis in first cadaver kidney allograft recipients was performed to assess their relative advantages and disadvantages. First cadaver kidney allograft recipients were prospectively randomized to receive 7 days of either ALG (n = 58) or OKT3 (n = 59) as part of a quadruple therapy protocol that included AZA, prednisone, and oral CsA. Patient characteristics, patient survival and causes of death, graft survival and causes of graft loss, incidence of and time to rejection and response to treatment, incidence of infections and their type, renal function, and antibody formation to ALG and OKT3 were examined. The 1-, 2-, and 3-year actuarial patient survival rates were 96% in the ALG group and 98% in the OKT3 group. The graft survival rates were 81.1%, 78.4%, and 78.4% in the ALG group and 84.1%, 78.7%, and 78.7% in the OKT3 group. In ALG-treated patients, 63% never had rejection, compared with 49% in the OKT3 patients (P = NS). In the ALG group 31% had a single rejection, 6% had 2 rejections, and none had 3 rejections, compared with 37%, 12%, and 2% in the OKT3 group. In the ALG group, 43% were steroid responsive compared with 65% in the OKT3 group (P = 0.08). There were 1.44 infections per patient in the ALG group compared with 0.76 in the OKT3 group (P = 0.0004). In the ALG group, 37% of patients developed CMV disease compared with 10% in the OKT3 group (P = 0.001). In donor-positive/recipient-negative patients, 8/10 (80%) in the ALG group developed CMV infection, of which 6 (75%) had severe or moderate CMV disease, compared with 2/15 (13%) patients in the OKT3 group (P = 0.002), of whom only one (6.7%) developed moderate disease. In donor-positive/recipient-positive patients, 8/23 (35%) in the ALG group developed CMV infection, of whom 5/8 (62.5%) developed severe or moderate disease compared with 1/21 (4.8%) in the OKT3 group (P = 0.02). Antibody formation to ALG and OKT3 occurred in 11% and 8% of patients, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

With the first demonstration of insulin independence following intraportal islet transplantation into a patient with type 1 diabetes, a new era of clinical islet transplantation will begin. This report provides our initial experience of clinical islet transplantation with a total of nine consecutive portal vein islet transplants in seven diabetic recipients. The first three transplants were done in nonrenal failure diabetics (NRFI) using 6319 +/- 2173 islets/kg body weight with islets processed from single pancreas and cultured for 7 days at 24 degrees C. Prednisone, azathioprine, and cyclosporine were initiated prior to transplant. While all three recipients demonstrated C-peptide function posttransplant, all three rejected their grafts at 2 weeks. Five days of OKT3 treatment failed to recover more than 10% of their rejecting islet grafts. The studies were then shifted to established kidney transplant recipients (EKI) maintaining their basal immunosuppression while adding 7 days of Minnesota antilymphoblast globulin (MALG) to the recipient using islets from single donor pancreas that had been cultured for 7 days at 24 degrees C. There were an average of 6161 +/- 911 islets transplanted intraportally into three EKI recipients. All three had C-peptide response from the transplant, but none achieved insulin independence. While the first patient rejected his graft at 2 weeks, two recipients demonstrated long-term islet function up to 10 months posttransplant. Sustacal challenge testing demonstrated C-peptide responsiveness, but in a delayed pattern suggesting insufficient islet mass had been transplanted. The next three kidney transplant recipients received islets from more than one donor pancreas averaging 13,916 +/- 556 islets/kg body weight. The first of these was the first to achieve insulin independence from 10 to day 25 posttransplant when she appeared to have a rejection episode. The second and third recipients were retransplanted with islets from multiple donors having achieved partial islet function from single pancreas donor. The first patient on triple immunosuppression is demonstrating long-term partial function at 184 days but is not insulin independent. The third patient on prednisone and azathioprine received one half his islets after 7-day culture and the other half after 7-day culture combined with cryopreservation. He is continuing to demonstrate insulin independence for 154 days post-transplant with a glycated hemoglobin value of 5.6%. Sustacal challenge data demonstrate a total stimulated C-peptide response of 155 rhomol/ml at 4 months post-transplant compared with 148 +/- 12 rhomol/ml for normal controls (NC) and 425 rhomol/ml for nondiabetic, established kidney transplant recipients on triple immunosuppression.(ABSTRACT TRUNCATED AT 400 WORDS)

Given the hypothesis that interaction of succinylcholine with nicotinic receptors releases endogenous catecholamines, plasma levels of epinephrine and norepinephrine were determined in anesthetized and manually ventilated patients immediately before and 2 min after intravenous administration of succinylcholine. Anesthesia was induced with intravenous thiopental (3-4 mg/kg) followed by the administration of nitrous oxide and oxygen (1:1) and 0.5-1.0% halothane. Stimulation of the patients was avoided. Succinylcholine (1 mg/kg) or metocurine (0.3 mg/kg) was injected intravenously and ventilation was controlled without intubation. Plasma norepinephrine levels increased from 301 pg/ml to 491 pg/ml (SEM = +/- 19 pg/ml, P less than 0.01, N = 5) 2 min after the injection of succinylcholine; the increase in plasma epinephrine was not statistically significant. The time course of catecholamine elevation was studied in three additional patients. The increase of norepinephrine occurred immediately after the injection of succinylcholine, peaked (647 +/- 67 pg/ml) around the third minute, and disappeared by the 10th min. The increase in epinephrine was less marked. Plasma levels of catecholamines did not change after the injection of metocurine (N = 2). The possibility that succinylcholine stimulates nicotinic receptors on the postganglionic sympathetic terminals is discussed. We propose that the elevation of plasma norepinephrine might contribute to the development of early adverse cardiovascular reactions to succinylcholine.