A component-based analysis of metabolic syndrome's impact on 30-day outcomes after hip fracture: reduced mortality in obese patients.

Introduction: Hip fractures are a common injury associated with significant morbidity and mortality. In the United States, there has been a rapid increase in the prevalence of metabolic syndrome (MetS), a condition comprised several common comorbidities, including obesity, diabetes mellitus, and hypertension, that may worsen perioperative outcomes. This article assesses the impact of MetS and its components on outcomes after hip fracture surgery. Methods: Patients who underwent nonelective operative treatment for traumatic hip fractures were identified in the 2015-2020 American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) database. Baseline characteristics between groups were compared, and significant differences were included as covariates. Multivariate regression was performed to assess the impact of characteristics of interest on postoperative outcomes. Patients with MetS, or a single one of its constitutive components-hypertension, diabetes, and obesity-were compared with metabolically healthy cohorts. Results: In total 95,338 patients were included. Patients with MetS had increased complications (OR 1.509; P < 0.001), but reduced mortality (OR 0.71; P < 0.001). Obesity alone was also associated with increased complications (OR 1.14; P < 0.001) and reduced mortality (OR 0.736; P < 0.001). Both hypertension and diabetes alone increased complications (P < 0.001) but had no impact on mortality. Patients with MetS did, however, have greater odds of adverse discharge (OR 1.516; P < 0.001), extended hospital stays (OR 1.18; P < 0.001), and reoperation (OR 1.297; P = 0.003), but no significant difference in readmission rate. Conclusion: Patients with MetS had increased complications but decreased mortality. Our component-based analysis showed had obesity had a similar effect: increased complications but lower mortality. These results may help surgeons preoperatively counsel patients with hip fracture about their postoperative risks.

The Impact of Metabolic Syndrome and Obesity on Perioperative Total Joint Arthroplasty Outcomes: The Obesity Paradox and Risk Assessment in Total Joint Arthroplasty.

Background: The relationship between elevated body mass index (BMI) and adverse outcomes in joint arthroplasty is well established in the literature. This paper aims to challenge the conventional thought of excluding patients from a total knee or hip replacement based on BMI alone. Instead, we propose using the metabolic syndrome (MetS) and its defining components to better identify patients at high risk for intraoperative and postoperative complications. Methods: Patients who underwent primary, elective total knee and total hip arthroplasty were identified in the 2015-2020 American College of Surgeons National Surgical Quality Improvement Program database. Several defining components of MetS, such as hypertension, diabetes, and obesity, were compared to a metabolically healthy cohort. Postoperative outcomes assessed included mortality, length of hospital stay, 30-day surgical and medical complications, and discharge. Results: The outcomes of 529,737 patients from the American College of Surgeons National Surgical Quality Improvement Program who underwent total knee and total hip arthroplasty were assessed. MetS is associated with increased complications and increased mortality. Both hypertension and diabetes are associated with increased complications but have no impact on mortality. Interestingly, while obesity was associated with increased complications, there was a significant decrease in mortality. Conclusions: Our results show that the impact of MetS is more than the sum of its constitutive parts. Additionally, obese patients experience a protective effect, with lower mortality than their nonobese counterparts. This study supports moving away from strict BMI cutoffs alone for someone to be eligible for an arthroplasty surgery and offers more granular data for risk stratification and patient selection.

Mesenchymal stromal cells donate mitochondria to articular chondrocytes exposed to mitochondrial, environmental, and mechanical stress.

Articular cartilage has limited healing capacity and no drugs are available that can prevent or slow the development of osteoarthritis (OA) after joint injury. Mesenchymal stromal cell (MSC)-based regenerative therapies for OA are increasingly common, but questions regarding their mechanisms of action remain. Our group recently reported that although cartilage is avascular and relatively metabolically quiescent, injury induces chondrocyte mitochondrial dysfunction, driving cartilage degradation and OA. MSCs are known to rescue injured cells and improve healing by donating healthy mitochondria in highly metabolic tissues, but mitochondrial transfer has not been investigated in cartilage. Here, we demonstrate that MSCs transfer mitochondria to stressed chondrocytes in cell culture and in injured cartilage tissue. Conditions known to induce chondrocyte mitochondrial dysfunction, including stimulation with rotenone/antimycin and hyperoxia, increased transfer. MSC-chondrocyte mitochondrial transfer was blocked by non-specific and specific (connexin-43) gap-junction inhibition. When exposed to mechanically injured cartilage, MSCs localized to areas of matrix damage and extended cellular processes deep into microcracks, delivering mitochondria to chondrocytes. This work provides insights into the chemical, environmental, and mechanical conditions that can elicit MSC-chondrocyte mitochondrial transfer in vitro and in situ, and our findings suggest a new potential role for MSC-based therapeutics after cartilage injury.