Background Infection with the novel severe acute respiratory syndrome coronavirus 2 has been associated with a hypercoagulable state. Emerging data from China and Europe have consistently shown an increased incidence of venous thromboembolism (VTE). We aimed to identify the VTE incidence and early predictors of VTE at our high-volume tertiary care center. Methods We performed a retrospective cohort study of 147 patients who had been admitted to Temple University Hospital with coronavirus disease 2019 (COVID-19) from April 1, 2020 to April 27, 2020. We first identified the VTE (pulmonary embolism [PE] and deep vein thrombosis [DVT]) incidence in our cohort. The VTE and no-VTE groups were compared by univariable analysis for demographics, comorbidities, laboratory data, and treatment outcomes. Subsequently, multivariable logistic regression analysis was performed to identify the early predictors of VTE. Results The 147 patients (20.9% of all admissions) admitted to a designated COVID-19 unit at Temple University Hospital with a high clinical suspicion of acute VTE had undergone testing for VTE using computed tomography pulmonary angiography and/or extremity venous duplex ultrasonography. The overall incidence of VTE was 17% (25 of 147). Of the 25 patients, 16 had had acute PE, 14 had had acute DVT, and 5 had had both PE and DVT. The need for invasive mechanical ventilation (adjusted odds ratio, 3.19; 95% confidence interval, 1.07-9.55) and the admission D-dimer level ≥1500 ng/mL (adjusted odds ratio, 3.55; 95% confidence interval, 1.29-9.78) were independent markers associated with VTE. The all-cause mortality in the VTE group was greater than that in the non-VTE group (48% vs 22%; P = .007). Conclusion Our study represents one of the earliest reported from the United States on the incidence rate of VTE in patients with COVID-19. Patients with a high clinical suspicion and the identified risk factors (invasive mechanical ventilation, admission D-dimer level ≥1500 ng/mL) should be considered for early VTE testing. We did not screen all patients admitted for VTE; therefore, the true incidence of VTE could have been underestimated. Our findings require confirmation in future prospective studies.

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Introduction Positional OSA (non-supine apnea-hypopnea index [AHI] < 5 events/hr) is present in 30% of patients with OSA. We demonstrated that in patients with OSA- COPD overlap syndrome the AHI inversely correlated with the degree of gas trapping, suggesting a stabilizing effect on the upper airway. We hypothesized that sleep position would be less important, resulting in a lower prevalence of positional OSA. Methods Patients underwent a polysomnogram that demonstrated OSA (AHI > 5 events/hr). To confirm COPD, patients had spirometry performed and a chest computed tomography for measurements of percent gas trapping. Results Sixteen patients [6 (38%) males, 55±7 years/old, FEV1 1.2±0.5 L, FEV1 % Predicted 45±19%, FVC 2.3±0.8 L, FVC % Predicted 69±20%, FEV1/FVC 51±12%, BMI 33±9 kg/m2)] were diagnosed with OSA (AHI 15±12 events/hour). Four patients (25%) had positional OSA (AHI 13±6 events/hr, non-supine AHI 1±1 event/hr) compared to 12 patients who were non-positional [AHI 16±13 events/hr (p=0.95)]. There was no difference in age [52±8 and 56±7 yrs (p=0.3)] or severity of obstruction in those with and without positional OSA [FEV1 1.4±4 L and 1.1±0.5 L, (p=0.3), FEV1 % predicted 50±17% and 44±20%, (p=0.7), FVC 2.9±0.8 L and 2.1±0.8 L (p=0.1), FVC % predicted 78±21% and 66±20%, (p=0.3), and FEV1/FVC 50±11% and 51±12%, (p=0.8), respectively]. However, patients with positional OSA were less heavy than those with non-positional OSA [BMI 23±3 and 37±8 kg/m2, respectively (p=0.005)]. Finally, there was no difference in the CT-Derived % Gas Trapping in those with and without positional OSA [48±37% and 36±25%, (p=0.6), respectively]. Conclusion The prevalence of positional OSA in patients with OSA-COPD overlap is similar to OSA patients without COPD. Despite the presence of obstructive disease and gas trapping that may affect upper airway stability, other factors including body position and BMI remain important determinants for developing OSA in patients with COPD. Support R01-HL089856, R01-HL089897

Introduction Approximately 30% of patient with obstructive sleep apnea (OSA) have positional OSA [non-supine apnea-hypopnea index (AHI) < 5 events/hr]. However, the prevalence is based on variable definitions for hypopneas related to the degree of oxygen desaturation. In addition, use of a home sleep apnea test (HSAT) to identify positional OSA is limited. We hypothesized that in patients evaluated with an HSAT, using a definition for hypopneas based on 4% compared to 3% oxygen desaturation will significantly decrease the percentage diagnosed with positional OSA. Methods Fourteen patients with positional OSA based on a non-supine respiratory event index (REI) < 5 events/hr were included. The initial diagnosis was determined based on a hypopnea definition of ≥ 3% oxygen desaturation. The studies were reanalyzed using a hypopnea definition of ≥ 4% oxygen desaturation. Results Fourteen patients [9 (64%) males, 46±14 yrs, BMI 31±6 kg/m2, ESS 7±5, REI 9±3 events/hr, mean SaO2 94±2%, lowest SaO2 81±6%, %TST SaO2 < 90% 4±6%] were identified with positional OSA (supine REI 16±7 events/hr, non-supine REI 3±1 events/hr) using a hypopneas definition of ≥ 3% oxygen desaturation. When reanalyzed using a hypopnea ≥ 4% oxygen desaturation there was a significant decrease in the REI to 7±2 events/hr (p<0.001). Three patients (21%) no longer were considered to have OSA. These patients were younger (32±14 vs. 50±11yrs, p=0.03) and had less severe OSA (REI 6±1 vs. 9±3 events/hr (p=0.04), but there was no difference in BMI (32±11 vs. 31±5 kg/m2, p=0.9) or mean and lowest SaO2 (96±0.4 vs. 94±2%, p=0.13, and 82±8 vs. 81±6%, p=0.9, respectively). Conclusion In patients with mild positional OSA, using a hypopnea definition of at least 4% vs. 3% oxygen desaturation on a HSAT will have a significant effect on the overall REI and often exclude patients who would otherwise be treated for OSA. Support None.