Extended offset stems are infrequently required in anterior approach total hip arthroplasty and low usage does not compromise stability.

INTRODUCTION: Extended offset (EO) stems are commonly used in posterior approach (PA) total hip arthroplasty (THA), but usage rates and complications are not well studied with anterior approach (AA) THA. This study evaluated usage rates, radiographic outcomes and complications following AA THA between patients receiving EO stems and a matched cohort receiving standard offset (SO) stems. MATERIALS AND METHODS: This retrospective review evaluated 1515 consecutive AA THA performed between 2014 and 2021. The recent 100 EO were included in radiographic and complication analysis and were matched to 100 SO stems based on stem size, procedure (unilateral/bilateral), sex, body mass index (BMI), and age. Data collection included patient demographics; pre- and postoperative radiographic measurements of leg length difference (LLD) and global hip offset difference (GHOD); and complications within 1 year. Independent t-tests and Chi-squared analyses compared EO and SO groups. RESULTS: EO was utilized in 8% of all AA THA. Despite matching procedures, the distribution of racial groups was different between EO and SO groups, respectively: Caucasian (75% vs. 43%), Asian (12% vs. 35%), Native Hawaiian/Pacific Islander (NHPI) (9% vs. 13%), and other (4% vs. 9%) (p < 0.001). No fractures, dislocations, or revisions occurred within 1 year after surgery in either group. One deep infection was noted in the SO group. The proportions of patients following surgery who had a GHOD < 6 mm (76% vs. 82%; p = 0.193) and LLD < 6 mm (81% vs. 86%; p = 0.223) were not significantly different between EO and SO groups, respectively. CONCLUSIONS: Prioritizing hip symmetry over stability results in a high proportion of patients achieving hip symmetry without high usage of EO stems in AA THA. Furthermore, low use of EO stems did not result in increased dislocations. Due to racial anatomical differences, Caucasian patients required EO stems to achieve hip symmetry more frequently than Asian and NHPI patients.

Racial Disparities in General Surgery Outcomes.

INTRODUCTION: While disparities in Black and Hispanic and Latino patients undergoing general surgeries are well described, most analyses leave out Asian, American Indian or Alaskan Native (AIAN), and native Hawaiian or Pacific Islander patients. This study identified general surgery outcomes for each racial group in the National Surgical Quality Improvement Program. METHODS: National Surgical Quality Improvement Program was queried to identify all procedures conducted by a general surgeon from 2017 to 2020 (n = 2,664,197). Multivariable regression models were used to investigate the impact of race and ethnicity on 30-day mortality, readmission, reoperation, major and minor medical complications, and non-home discharge destinations. Adjusted odds ratios (AOR) and 95% confidence intervals were calculated. RESULTS: Compared to non-Hispanic White patients, Black patients had higher odds of readmission and reoperation, and Hispanic and Latino patients had higher odds of major and minor complications. AIAN patients had higher odds of mortality (AOR: 1.003 (1.002-1.005), P < 0.001), major complication (AOR: 1.013 (1.006-1.020), P < 0.001), reoperation (AOR: 1.009, (1.005-1.013), P < 0.001), and non-home discharge destination (AOR: 1.006 (1.001-1.012), P = 0.025), while native Hawaiian or Pacific Islander patients had lower odds of readmission (AOR: 0.991 (0.983-0.999), P = 0.035) and non-home discharge destination (AOR: 0.983 (0.975-0.990), P < 0.001) compared to non-Hispanic White patients. Asian patients had lower odds of each adverse outcome. CONCLUSIONS: Black, Hispanic and Latino, and AIAN patients are at higher odds for poor postoperative results than non-Hispanic White patients. AIANs had some of the highest odds of mortality, major complications, reoperation, and non-home discharge. Social health determinants and policy adjustments must be targeted to ensure optimal operative results for all patients.

Sarcomere length affects Ca2+ sensitivity of contraction in ischemic but not non-ischemic myocardium.

In healthy hearts, myofilaments become more sensitive to Ca2+ as the myocardium is stretched. This effect is known as length-dependent activation and is an important cellular-level component of the Frank-Starling mechanism. Few studies have measured length-dependent activation in the myocardium from failing human hearts. We investigated whether ischemic and non-ischemic heart failure results in different length-dependent activation responses at physiological temperature (37°C). Myocardial strips from the left ventricular free wall were chemically permeabilized and Ca2+-activated at sarcomere lengths (SLs) of 1.9 and 2.3 µm. Data were acquired from 12 hearts that were explanted from patients receiving cardiac transplants; 6 had ischemic heart failure and 6 had non-ischemic heart failure. Another 6 hearts were obtained from organ donors. Maximal Ca2+-activated force increased at longer SL for all groups. Ca2+ sensitivity increased with SL in samples from donors (P < 0.001) and patients with ischemic heart failure (P = 0.003) but did not change with SL in samples from patients with non-ischemic heart failure. Compared with donors, troponin I phosphorylation decreased in ischemic samples and even more so in non-ischemic samples; cardiac myosin binding protein-C (cMyBP-C) phosphorylation also decreased with heart failure. These findings support the idea that troponin I and cMyBP-C phosphorylation promote length-dependent activation and show that length-dependent activation of contraction is blunted, yet extant, in the myocardium from patients with ischemic heart failure and further reduced in the myocardium from patients with non-ischemic heart failure. Patients who have a non-ischemic disease may exhibit a diminished contractile response to increased ventricular filling.

Mavacamten decreases maximal force and Ca2+ sensitivity in the N47K-myosin regulatory light chain mouse model of hypertrophic cardiomyopathy.

Morbidity and mortality associated with heart disease is a growing threat to the global population, and novel therapies are needed. Mavacamten (formerly called MYK-461) is a small molecule that binds to cardiac myosin and inhibits myosin ATPase. Mavacamten is currently in clinical trials for the treatment of obstructive hypertrophic cardiomyopathy (HCM), and it may provide benefits for treating other forms of heart disease. We investigated the effect of mavacamten on cardiac muscle contraction in two transgenic mouse lines expressing the human isoform of cardiac myosin regulatory light chain (RLC) in their hearts. Control mice expressed wild-type RLC (WT-RLC), and HCM mice expressed the N47K RLC mutation. In the absence of mavacamten, skinned papillary muscle strips from WT-RLC mice produced greater isometric force than strips from N47K mice. Adding 0.3 µM mavacamten decreased maximal isometric force and reduced Ca2+ sensitivity of contraction for both genotypes, but this reduction in pCa50 was nearly twice as large for WT-RLC versus N47K. We also used stochastic length-perturbation analysis to characterize cross-bridge kinetics. The cross-bridge detachment rate was measured as a function of [MgATP] to determine the effect of mavacamten on myosin nucleotide handling rates. Mavacamten increased the MgADP release and MgATP binding rates for both genotypes, thereby contributing to faster cross-bridge detachment, which could speed up myocardial relaxation during diastole. Our data suggest that mavacamten reduces isometric tension and Ca2+ sensitivity of contraction via decreased strong cross-bridge binding. Mavacamten may become a useful therapy for patients with heart disease, including some forms of HCM.NEW & NOTEWORTHY Mavacamten is a pharmaceutical that binds to myosin, and it is under investigation as a therapy for some forms of heart disease. We show that mavacamten reduces isometric tension and Ca2+ sensitivity of contraction in skinned myocardial strips from a mouse model of hypertrophic cardiomyopathy that expresses the N47K mutation in cardiac myosin regulatory light chain. Mavacamten reduces contractility by decreasing strong cross-bridge binding, partially due to faster cross-bridge nucleotide handling rates that speed up myosin detachment.