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.

Introduction: Right ventricular dysfunction (RVD) is a key component in the process of risk stratification in patients with acute pulmonary embolism (PE). Echocardiography remains the gold standard for RVD assessment, however, measures of RVD may be seen on CTPA imaging, including increased pulmonary artery diameter (PAD). The aim of our study was to evaluate the association between PAD and echocardiographic parameters of RVD in patients with acute PE. Methods: Retrospective analysis of patients diagnosed with acute PE was conducted at large academic center with an established pulmonary embolism response team (PERT). Patients with available clinical, imaging, and echocardiographic data were included. PAD was compared to echocardiographic markers of RVD. Statistical analysis was performed using the Student’s t test, Chi-square test, or one-way analysis of variance (ANOVA); P < 0.05 was considered statistically significant. Results: 270 patients with acute PE were identified. Patients with a PAD >30 mm measured on CTPA had higher rates of RV dilation (73.1% vs 48.7%, P < 0.005), RV systolic dysfunction (65.4% vs 43.7%, P < 0.005), and RVSP >30 mmHg (90.2% vs 68%, P = 0.004), but not TAPSE ≤1.6 cm (39.1% vs 26.1%, P = 0.086). A weak increasing linear relationship between PAD and RVSP was noted (r = 0.379, P = 0.001). Conclusions: Increased PAD in patients with acute PE was significantly associated with echocardiographic markers of RVD. Increased PAD on CTPA in acute PE can serve as a rapid prognostic tool and assist with PE risk stratification at the time of diagnosis, allowing rapid mobilization of a PERT team and appropriate resource utilization.

Sarcoidosis is an inflammatory disease that predominantly affects lungs. Genetic predisposition and environmental exposure play key roles in the pathophysiology of sarcoidosis. Prior studies have identified that debris from the fallen World Trade Center (WTC) towers is a risk factor for subsequent sarcoidosis development. A unique cohort of patients with sarcoidosis include first responders during the 9/11 WTC attack. We compared the disease phenotype of these first responders managed at the Stony Brook University Hospital (SBUH) to that of unexposed patients managed at Temple University Hospital (TUH). Methods: Patients from both centers who met the ATS diagnostic criteria for sarcoidosis were included in the study. The SBUH cohort included 16 first responders under the care of the WTC Health Program and referred to the Center for ILD at SBUH for sarcoidosis. The TUH cohort included 32 propensity-matched (for age, sex, race, and BMI) patients with sarcoidosis managed at TUH. The two cohorts were compared using Chi-squared tests for categorical variables and 2-sample t-tests for continuous variables. Results: Patients in the WTC cohort had significantly more rhinosinusitis and less wheezing. Initial lung function, and extrapulmonary manifestations were worse in the TUH cohort. There was a greater use of anti-inflammatory treatment, as well as more wheezing and lower lung function on follow-up testing in the TUH cohort. No CT findings were significantly different (Table 1). Conclusions: Our analysis reveals that patients in the WTC cohort had more upper airway symptoms with better lung function compared to the TUH cohort, who had lower respiratory tract disease and reduced lung function. This was also reflected in increased need for anti-inflammatory treatment in the TUH population. Our study is limited by its retrospective nature as well as the contribution of comorbid conditions such rhinosinusitis and laryngopharyngeal reflux, which are well documented in WTC victims. Additionally, the WTC cohort were likely healthier individuals at baseline. This study demonstrates the key differences in patients with sarcoidosis based on exposure type, which may affect disease trajectory and treatment options.

Introduction: Pulmonary artery (PA) enlargement has been demonstrated in patients with chronic pulmonary hypertension. Although assumed, there are no before-and-after studies demonstrating the effect of an acute pulmonary embolism (PE) on the size of the PA. Methods: All patients treated for an acute PE at a tertiary academic center over a 2-year period were assessed. 18 patients were identified to have both pre-PE and post-PE CT chest images that were within 1 year of a PE event diagnosed with CT pulmonary angiography (CTPA). Retrospective measurements of the PA diameter and the PA area were performed on the pre-PE, PE and post-PE CT images. All measurements were performed independently by two experienced radiologists. Pearson correlation (PCC) and paired t-test statistical analysis was used to measure inter-reader agreement for the PA diameter and the PA area measurements. The average between the two radiologist measurements and the paired t-test was used to analyze the before and after differences. Results: The mean time period from pre-PE to PE imaging was 148 days (6-362 days), and from PE to post-PE imaging was 133 days (8-334 days). Inter-reader agreement between the two radiologists was good to excellent (pre-PE measurements [PA diameter PCC 0.85, p<0.05, PA Area PCC 0.90, p<0.05], PE measurements [PA diameter PCC 0.89, p<0.05, PA Area PCC 0.73, p<0.05, post-PE measurements [PA diameter PCC 0.68, p<0.05, PA Area PCC 0.77, p<0.05]. There was minimal to no statistical difference between the two radiologist readings (pre-PE measurements [PA diameter M=0.77mm, SD=2.13, t(17)=1.55, p=0.14; PA Area M=-35.5 mm 2 , SD=97.8, t(17)=-1.54, p=0.14)]; PE measurements [PA diameter M=1.11 mm, SD=1.78, t(17)=2.65, p=0.017; PA Area M=-14.2 mm 2 , SD=157.32, t(17)=-0.38, p=0.706] and post-PE measurements [PA diameter M=0.11 mm, SD=2.65, t(17)=0.178, p=0.861; PA Area M=-43.56 mm 2 , SD=102.3, t(17)=-1.81, p=0.089]).Comparing vessel dimensions on pre-PE to PE images, the mean difference in the PA diameter size was +1.16 mm (SD=2.55, t(17)=1.94, p=0.069), and the mean difference in the PA area size was +77.2mm 2 (SD=141.3, t(17)=2.32, p=0.033). When comparing pre-PE to post-PE images the mean difference in the PA diameter size was +1.0 mm (SD=3.08, t(17)=1.37, p=0.187) and the mean difference in the PA area size was +39mm 2 (SD=137.3, t(17)=1.21, p=0.245). Conclusion: In patients with an acute PE, the PA area, but not the PA diameter, was significantly increased in size at the time of PE diagnosis. This increase in size subsided on later imaging.