Predictors of gastrostomy tube placement in patients with head and neck cancer undergoing resection and flap-based reconstruction: systematic review and meta-analysis.

BACKGROUND: Nutritional status may be impaired in patients with head and neck cancer undergoing surgical treatment, often necessitating gastrostomy tube (G-tube) placement. Identifying which patients will require a G-tube remains a challenge. This study identifies predictors of G-tube requirement in patients undergoing tumor resection and reconstruction with pedicled or free flaps. METHODS: Systematic review of the PubMed, Cochrane, and Scopus databases was performed of English language articles, discussing risk factors of perioperative G-tube placement among patients >18 years. Data on patient, tumor, and treatment factors, as well as need for G-tube, were collected. Univariable meta-analysis was conducted to identify predictors for G-tube placement. RESULTS: Eleven studies (1,112 patients) met inclusion criteria. Overall pooled prevalence of postoperative G-tube placement was 25%. Patients with advanced cancer stage IV/recurrence were more likely to require a G-tube (OR 2.81 [CI 1.03-7.69]; p<0.05), as were those who had undergone preoperative radiation (OR 3.55 [CI 2.03-6.20], p<0.05). Reconstruction with a radial forearm free flap was associated with a lower need for G-tube versus rectus abdominis (OR 0.25 [CI 0.08-0.83], p=0.02) and latissimus dorsi flap (OR 0.21 [CI 0.04-1.09], p=0.06). There was no difference in G-tube placement between those receiving pedicled flaps versus free flaps (OR 1.54 [CI 0.38-6.20], p=0.54). CONCLUSIONS: Among patients with head and neck cancer undergoing resection with immediate pedicled or free flap reconstruction, advanced tumor stage and history of prior radiation therapy are associated with increased likelihood of G-tube placement. More randomized controlled trials are needed to develop a decision-making algorithm.

Disparities in peripheral artery disease care: A review and call for action.

Peripheral artery disease (PAD), the pathophysiologic narrowing of arterial blood vessels of the lower leg due to atherosclerosis, is a highly prevalent disease that affects more than 6 million individuals 40 years and older in the United States, with sharp increases in prevalence with age. Morbidity and mortality rates in patients with PAD range from 30% to 70% during the 5- to 15-year period after diagnosis and PAD is associated with poor health outcomes and reduced functionality and quality of life. Despite advances in medical, endovascular, and open surgical techniques, there is striking variation in care among population subgroups defined by sex, race and ethnicity, and socioeconomic status, with concomitant differences in preoperative medication optimization, amputation risk, and overall health outcomes. We reviewed studies from 1995 to 2021 to provide a comprehensive analysis of the current impact of disparities on the treatment and management of PAD and offer action items that require strategic partnership with primary care providers, researchers, patients, and their communities. With new technologies and collaborative approaches, optimal management across all population subgroups is possible.

Leveraging Machine Learning and Artificial Intelligence to Improve Peripheral Artery Disease Detection, Treatment, and Outcomes.

Peripheral artery disease is an atherosclerotic disorder which, when present, portends poor patient outcomes. Low diagnosis rates perpetuate poor management, leading to limb loss and excess rates of cardiovascular morbidity and death. Machine learning algorithms and artificially intelligent systems have shown great promise in application to many areas in health care, such as accurately detecting disease, predicting patient outcomes, and automating image interpretation. Although the application of these technologies to peripheral artery disease are in their infancy, their promises are tremendous. In this review, we provide an introduction to important concepts in the fields of machine learning and artificial intelligence, detail the current state of how these technologies have been applied to peripheral artery disease, and discuss potential areas for future care enhancement with advanced analytics.

Stress testing before abdominal aortic aneurysm repair does not lead to a reduction in perioperative cardiac events.

OBJECTIVE: Stress testing is often used before abdominal aortic aneurysm (AAA) repair. Whether stress testing leads to a reduction in cardiac events after AAA repair has remained unclear. Our objective was to study the national stress test usage rates and compare the perioperative outcomes between centers with high and low usage of stress testing. METHODS: We used the Vascular Quality Initiative to study patients who had undergone elective endovascular AAA repair (EVAR) or open AAA repair (OAR). We measured the usage rates of stress testing across centers and compared the Vascular Study Group of New England cardiac risk index (VSG-CRI) among patients who had and had not undergone preoperative stress testing. We determined the rate of major adverse cardiac events (MACE), a composite of perioperative myocardial infarction, stroke, heart failure exacerbation, and death across the centers. We compared the MACE and 1-year mortality between the centers in the highest quintile of stress test usage and the lowest quintile. RESULTS: We studied 43,396 EVAR patients and 8935 OAR patients across 324 centers. The median proportion of stress test usage across centers before EVAR was 35.9% and varied from 10.2% (5th percentile) to 73.7% (95th percentile), with similar variability for OAR (median, 57.9%; 5th percentile, 13.0%; 95th percentile, 86.0%). The mean VSG-CRI for the EVAR group with preoperative stress testing was 5.6 ± 2.1 compared with 5.4 ± 2.1 (P < .001) for the EVAR group without preoperative stress testing. The findings were similar for OAR, with a VSG-CRI of 5.1 ± 2.0 vs 4.8 ± 2.1 (P < .001) for those with and without preoperative stress testing, respectively. The rate of MACE was 1.8% after EVAR and 11.6% after OAR. The 1-year mortality was 4.6% for EVAR and 6.6% for OAR. The centers in the highest quintile of stress testing had a higher adjusted likelihood of MACE after both EVAR (odds ratio [OR], 1.78; 95% confidence interval [CI], 1.37-2.30) and OAR (OR, 1.99; 95% CI, 1.53-2.59) but similar 1-year mortality (EVAR: OR, 1.18; 95% CI, 1.02-1.37; OAR: OR, 0.87; 95% CI, 0.65-1.17) compared with the centers in the lowest quintile. The VSG-CRI was not different between the high stress test centers (EVAR, 5.5 ± 2.1; OAR: 5.0 ± 2.0), and low stress test centers (EVAR, 5.5 ± 2.1; P = .403; OAR, 4.9 ± 2.0; P = .563). CONCLUSIONS: Stress test usage before AAA repair varied widely across Vascular Quality Initiative centers despite similar patient risk profiles. No reduction was observed in MACE or 1-year mortality among centers with high stress test usage. The value of routine stress testing before AAA repair should be reconsidered, and stress testing should be used more selectively, given these findings and the associated costs of widespread testing.

Microbe-Derived Butyrate and Its Receptor, Free Fatty Acid Receptor 3, But Not Free Fatty Acid Receptor 2, Mitigate Neointimal Hyperplasia Susceptibility After Arterial Injury.

Background Arterial restenosis after vascular surgery is a common cause of midterm restenosis and treatment failure. Herein, we aim to investigate the role of microbe-derived butyrate, FFAR2 (free fatty acid receptor 2), and FFAR3 (free fatty acid receptor 3) in mitigating neointimal hyperplasia development in remodeling murine arteries after injury. Methods and Results C57BL/6 mice treated with oral vancomycin before unilateral femoral wire injury to deplete gut microbiota had significantly diminished serum and stool butyrate and more neointimal hyperplasia development after arterial injury, which was reversed by concomitant butyrate supplementation. Deficiency of FFAR3 but not FFAR2, both receptors for butyrate, exacerbated neointimal hyperplasia development after injury. FFAR3 deficiency was also associated with delayed recovery of the endothelial layer in vivo. FFAR3 gene expression was observed in multiple peripheral arteries, and expression was increased after arterial injury. Treatment of endothelial but not vascular smooth muscle cells with the pharmacologic FFAR3 agonist 1-methylcyclopropane carboxylate stimulated cellular migration and proliferation in scratch assays. Conclusions Our results support a protective role for butyrate and FFAR3 in the development of neointimal hyperplasia after arterial injury and delineate activation of the butyrate-FFAR3 pathway as a valuable strategy for the prevention and treatment of neointimal hyperplasia.