Telehealth Physical Therapy for Sports Medicine Rehabilitation: What Is Its Role in the Postpandemic Era?

Background: The adoption of telehealth visits for physical therapy (PT) has accelerated because of the COVID-19 pandemic. Patient reception of virtual PT at the outbreak of the pandemic was positive, but it is unclear how telehealth visits compare to in-person visits in the postpandemic era. Purpose: To evaluate utilization trends and patient satisfaction with virtual PT compared with in-person PT during and after the COVID-19 pandemic. Study Design: Cross-sectional study; Level of evidence, 3. Methods: We identified 59,461 in-person and 2016 telehealth visits at a single physical rehabilitation center between March 2020 and December 2021. Patient socioeconomic and demographic variables, including insurance status, were compared between telehealth users and in-person visitors. A total of 1012 patient satisfaction surveys were available and analyzed using the top-box method. Univariable statistics (t test or Mann-Whitney U and chi-square tests) were used for group comparisons. Results: Overall, telehealth users when compared with in-person visitors were older (median age, 47 vs 42 years, respectively; P < .001), and a higher proportion was female (60.6% vs 54.8%; P < .001), was White (69.7% vs 66.6%; P = .023), spoke English as their primary language (99.2% vs 98.1%; P = .001), and had Medicare insurance (20.3% vs 16.1%; P < .001). Telehealth patients more often lived out-of-county (50.7% vs 45.8%; P < .001) and in small towns rather than in urban areas (1.0% vs 0.3%; P < .001). When we compared telehealth use before and after official reopening of the PT center in September 2020, telehealth users in the postpandemic era had an out-of-county rate of 58.7%, and 68.7% were female. Patient satisfaction survey results demonstrated that telehealth patients compared with in-person patients were less likely to recommend visits to others (75.0% vs 89.1%, respectively; P = .008) and had lower overall assessment of their visits (71.7% vs 88.6%; P = .001). Accordingly, there was a significant reduction in telehealth visits from 2020 to 2021 (from 6.9% to 0.9% of visits; P < .001). Conclusion: We noted a decline in telehealth PT use during the postpandemic era, consistent with reduced patient satisfaction when compared with in-person visits. Telehealth is a useful option for populations with limited time or access to care and may serve a role in a hybrid care model. Further studies on long-term outcomes after telehealth PT are warranted to evaluate its efficacy.

SARS-CoV-2 Spike Protein Destabilizes Microvascular Homeostasis.

SARS-CoV-2 infection can cause compromised respiratory function and thrombotic events. SARS-CoV-2 binds to and mediates downregulation of angiotensin converting enzyme 2 (ACE2) on cells that it infects. Theoretically, diminished enzymatic activity of ACE2 may result in increased concentrations of pro-inflammatory molecules, angiotensin II, and Bradykinin, contributing to SARS-CoV-2 pathology. Using immunofluorescence microscopy of lung tissues from uninfected, and SARS-CoV-2 infected individuals, we find evidence that ACE2 is highly expressed in human pulmonary alveolar epithelial cells and significantly reduced along the alveolar lining of SARS-CoV-2 infected lungs. Ex vivo analyses of primary human cells, indicated that ACE2 is readily detected in pulmonary alveolar epithelial and aortic endothelial cells. Exposure of these cells to spike protein of SARS-CoV-2 was sufficient to reduce ACE2 expression. Moreover, exposure of endothelial cells to spike protein-induced dysfunction, caspase activation, and apoptosis. Exposure of endothelial cells to bradykinin caused calcium signaling and endothelial dysfunction (increased expression of von Willibrand Factor and decreased expression of Krüppel-like Factor 2) but did not adversely affect viability in primary human aortic endothelial cells. Computer-assisted analyses of molecules with potential to bind bradykinin receptor B2 (BKRB2), suggested a potential role for aspirin as a BK antagonist. When tested in our in vitro model, we found evidence that aspirin can blunt cell signaling and endothelial dysfunction caused by bradykinin in these cells. Interference with interactions of spike protein or bradykinin with endothelial cells may serve as an important strategy to stabilize microvascular homeostasis in COVID-19 disease. IMPORTANCE SARS-CoV-2 causes complex effects on microvascular homeostasis that potentially contribute to organ dysfunction and coagulopathies. SARS-CoV-2 binds to, and causes downregulation of angiotensin converting enzyme 2 (ACE2) on cells that it infects. It is thought that reduced ACE2 enzymatic activity can contribute to inflammation and pathology in the lung. Our studies add to this understanding by providing evidence that spike protein alone can mediate adverse effects on vascular cells. Understanding these mechanisms of pathogenesis may provide rationale for interventions that could limit microvascular events associated with SARS-CoV-2 infection.

CD8+ CD73+ T cells in the tumor microenvironment of head and neck cancer patients are linked to diminished T cell infiltration and activation in tumor tissue.

Recent studies have implicated a role for adenosine-dependent immunosuppression in head and neck tumor microenvironments. We describe expression of CD73, an enzyme critical to the generation of adenosine from extracellular AMP, in T cells and other cell types within human head and neck tumors. Flow cytometric analyses of tumor-infiltrating cells indicate that CD3+ cells are the predominant source of CD73 among immune infiltrating cells and that CD73 expression, especially among CD8+ T cells, is inversely related to indices of T cell infiltration and T cell activation in the microenvironment of head and neck tumors. We provide evidence that CD73 expression on peripheral T cells and levels of soluble CD73 in circulation are correlated with CD73 expression on CD8+ T cells in tumors. Moreover, fluorescent microscopy studies reveal that CD8+ CD73+ cells are observed in close proximity to tumor cells as well as in surrounding tissue. In vitro studies with peripheral blood T cells indicate that anti-CD3-stimulation causes loss of CD73 expression, especially among cells that undergo proliferation and that exogenous AMP can impair T cell proliferation, while sustaining CD73 expression. These data suggest that CD8+ CD73+ T cells may be especially important mediators of immunosuppression in human head and neck cancer.