Cardiac interventions on total knee arthroplasty: a national inpatient sample-based analysis.

BACKGROUND: Comorbid cardiovascular diseases have been associated with poor outcomes in total knee arthroplasty (TKA); however, our understanding of TKA with prior cardiac treatment procedures has largely been undocumented. In this study, we examined TKA patients who had undergone different cardiac interventions that addressed their condition. The purpose was to characterize and compare outcomes for a growing patient population not yet analyzed. MATERIALS AND METHODS: The 2016-2019 Nationwide Inpatient Sample database was queried for 558,256 patients who had TKA (ICD-10CM). Backgrounds significant for pacemaker [PM] (n = 8025), coronary artery bypass [CABG] (n = 12,683), heart valve surgery [HV] (n = 4125), or coronary stent [CS] (n = 19,483) were compared against those without, across demographics, admission information, and various complications. RESULTS: Cardiac interventions were associated with increased age, male gender, length of stay, and cost of care. CABG, and Stent groups had more diabetics, but HV had significantly fewer (p = 0.008). PM and HV had significantly less tobacco use and, in addition to CABG, less obesity. Postoperatively, mortality was elevated in the PM [Odds ratio (OR) 2.89, p = 0.008], CABG (OR 2.53, p = 0.006) and CS group (OR 1.94, p = 0.018), but not HV. Myocardial infarctions were elevated in the CABG (OR 3.874) and CS group (OR 5.11) (p < 0.001). PM, HV, and CS had increased odds of periprosthetic fracture by 2.15-fold (p < 0.001), 2.09-fold (p < 0.001), 1.29-fold (p = 0.011) respectively. HV saw increased periprosthetic mechanical complications (OR 1.48, p = 0.006). CABG increased the odds of deep surgical site infection 14.23-fold and CS 9.22-fold (p < 0.001). Postoperative pneumonia was increased in PM, CABG, and CS groups (OR 2.15,), (OR 2.21,), (OR 1.64,) (p < 0.001). CONCLUSIONS: Patients who have undergone cardiac intervention are generally at risk for adverse stays. Furthermore, risk factors and complications vary between the groups. Our analysis emphasizes the importance of individualized medical care and as a basis for electing and informing patients for TKA.

Risk factors for in-patient myocardial infarction following total hip arthroplasty.

Purpose: The aim of this study was to identify potential risk factors for myocardial infarction immediately following total hip arthroplasty. Methods: The 2016-2019 Nationwide Inpatient Sample database was used to identify patients who underwent primary total hip arthroplasty (THA) and suffered a myocardial infarction (MI). Patient data including demographics, admission, and comorbidities were recorded. Univariate analysis and subsequent multivariate logistic regression were performed to determine which circumstances affected the odds of MI. Results: A total of 367,890 patients were identified for THA with 142 of those also having a myocardial infarction. Those who experienced an MI had increased length of stay, total charges, and generally negative dispositions compared to their non-MI counterparts (p < 0.001). Through regression analysis, factors that increased the odds of MI included older age [odds ratio (OR) 1.59, 95 % confidence interval (CI) 1.49-1.70], a female sex (OR 1.46, 95 % CI 1.37-1.55), previous coronary artery bypass graft (OR 1.20, 95 % CI 1.01-1.43), obesity (OR 1.12, 95 % CI 1.04-1.21), colostomy (OR 2.07, 95 % CI 1.21-3.56), and Parkinson's disease (OR 1.48, 95 % CI 1.13-1.95). Factors that decreased that risk included elective admission (OR 0.21, 95 % CI 0.19-0.22) and a tobacco related disorder (OR 0.69, 95 % CI 0.63-0.76). Conclusions: Patient risk for myocardial infarction following total hip arthroplasty varies in part based on their background and comorbidities. These findings can be used to better recognize those who should receive further precautions and tailor proper treatment strategies for THA.

Parkland Trauma Index of Mortality in Orthopaedic Trauma Patients: An Initial Report.

OBJECTIVES: The extent and timing of surgery in severely injured patients remains an unsolved problem in orthopaedic trauma. Different laboratory values or scores have been used to try to predict mortality and estimate physiological reserve. The Parkland Trauma Index of Mortality (PTIM) has been validated as an electronic medical record-integrated algorithm to help with operative timing in trauma patients. The aim of this study was to report our initial experience with PTIM and how it relates to other scores. METHODS: A retrospective chart review of level 1 and level 2 trauma patients admitted to our institution between December 2020 and November 2022 was conducted. Patients scored with PTIM with orthopaedic injuries were included in this study. Exclusion criteria were patients younger than 18 years. RESULTS: Seven hundred seventy-four patients (246 female patients) with a median age of 40.5 (18-101) were included. Mortality was 3.1%. Patients in the PTIM high-risk category (≥0.5) had a 20% mortality rate. The median PTIM was 0.075 (0-0.89) and the median Injury Severity Score (ISS) was 9.0 (1-59). PTIM (P < 0.001) and ISS (P < 0.001) were significantly lower in surviving patients. PTIM was mentioned in 7.6% of cases, and in 1.7% of cases, providers indicated an action in response to the PTIM. PTIM and ISS were significantly higher in patients with documented PTIM. CONCLUSION: PTIM is better at predicting mortality compared with ISS. Our low rate of PTIM documentation in provider notes highlights the challenges of implementing a new algorithm. LEVEL OF EVIDENCE: Level III, retrospective cohort study.

Comparative Untargeted Metabolomic Profiling of Induced Mitochondrial Fusion in Pancreatic Cancer.

Mitochondria are dynamic organelles that constantly alter their shape through the recruitment of specialized proteins, like mitofusin-2 (Mfn2) and dynamin-related protein 1 (Drp1). Mfn2 induces the fusion of nearby mitochondria, while Drp1 mediates mitochondrial fission. We previously found that the genetic or pharmacological activation of mitochondrial fusion was tumor suppressive against pancreatic ductal adenocarcinoma (PDAC) in several model systems. The mechanisms of how these different inducers of mitochondrial fusion reduce pancreatic cancer growth are still unknown. Here, we characterized and compared the metabolic reprogramming of these three independent methods of inducing mitochondrial fusion in KPC cells: overexpression of Mfn2, genetic editing of Drp1, or treatment with leflunomide. We identified significantly altered metabolites via robust, orthogonal statistical analyses and found that mitochondrial fusion consistently produces alterations in the metabolism of amino acids. Our unbiased methodology revealed that metabolic perturbations were similar across all these methods of inducing mitochondrial fusion, proposing a common pathway for metabolic targeting with other drugs.