Changes in sleep-disordered breathing from the acute to the stable phase of pulmonary embolism: The ESAET study.

BACKGROUND: /Objective: Sleep-disordered breathing (SDB) may change from the acute to stable phase of some cardiovascular disorders, but little is known whether these dynamic changes also exist in pulmonary embolism (PE). This study aimed to analyze the changes in the apnea-hypopnea index (AHI) from the acute to stable phase of PE as well as the factors associated. PATIENTS/METHODS: We conducted a prospective, longitudinal and multicenter study of consecutive adults requiring hospitalization for non-hypotensive acute PE, with a protocol including clinical, imaging (transthoracic echocardiography [TTE] and computed tomography), blood tests and a sleep study within 48 h of diagnosis of PE. After 3 months of follow-up, the sleep study was repeated. Right ventricular (RV) dysfunction was defined according to TTE criteria. RESULTS: One hundred and eleven patients (mean age [SD]: 63 [15] years; body mass index: 28.4 [4.7] kg/m2) were included. The initial AHI was 24.4 (21.8) events/h (AHI≥5: 82.8 %; AHI≥30: 33.3 %). Seventy-seven patients (69.4 %) had RV dysfunction. In the overall cohort, the AHI decreased by 8.7 events/h from the acute to stable phase (24.4/h vs. 15.7/h; p=0.013). Patients with RV dysfunction showed a greater decrease in AHI (mean decrease 12.3/h vs. 0.43/h). In the multivariable analysis a drop of an AHI≥5 events/hour was independently associated with the presence of initial RV dysfunction (hazard ratio 3.9; 95%CI 1.3 to 12.1). CONCLUSIONS: In hemodynamically stable patients with acute PE, there is a transient but clinically significant decrease in the AHI from the acute to stable phase, particularly when initially presenting with RV dysfunction.

Bronchiectasis and COVID-19 infection: a two-way street.

ABSTRACT: Bronchiectasis (BE) has been linked to past viral infections such as influenza, measles, or adenovirus. Two years ago, a new pandemic viral infection severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) broke out and it still persists today, and a significant proportion of surviving patients have radiological and clinical sequelae, including BE. Our aim was to thoroughly review the information available in the literature on the bidirectional relationship between SARS-CoV-2 infection and the development of BE, as well as the impact of this infection on patients already suffering from BE. Available information indicates that only a small percentage of patients in the acute phase of coronavirus disease 2019 (COVID-19) pneumonia develop BE, although the latter is recognized as one of the radiological sequelae of COVID-19 pneumonia, especially when it is caused by traction. The severity of the initial pneumonia is the main risk factor for the development of future BE, but during the COVID-19 pandemic, exacerbations in BE patients were reduced by approximately 50%. Finally, the impact of BE on the prognosis of patients with COVID-19 pneumonia is not yet known.

Incidence, risk factors, and thrombotic load of pulmonary embolism in patients hospitalized for COVID-19 infection.

OBJECTIVE: To determine the incidence, characteristics, and risk factors of pulmonary embolism (PE) among patients hospitalized for COVID-19. PATIENTS AND METHODS: We performed a prospective observational study of a randomly selected cohort of consecutive patients hospitalized for COVID-19 infection between March 8, 2020 through April 25, 2020. All eligible patients underwent a computed tomography pulmonary angiography independently of their PE clinical suspicion and were pre-screened for a baseline elevated D-dimer level. RESULTS: 119 patients were randomly selected from the 372 admitted to one tertiary hospital in Valencia (Spain) for COVID-19 infection during the period of study. Seventy-three patients fulfilled both the inclusion criteria and none of the exclusion criteria and were finally included in the study. Despite a high level of pharmacological thromboprophylaxis (89%), the incidence of PE was 35.6% (95% confidence interval [CI], 29.6 to 41.6%), mostly with a peripheral location and low thrombotic load (Qanadli score 18.5%). Multivariate analysis showed that heart rate (Hazard Ratio [HR], 1.04), room-air oxygen saturation (spO2) (HR, 0.87), D-dimer (HR, 1.02), and C-reactive protein (CRP) levels (HR, 1.01) at the time of admission were independent predictors of incident PE during hospitalization. A risk score was constructed with these four variables showing a high predictive value of incident PE (AUC-ROC: 0.86; 95% CI: 0.80 to 0.93). CONCLUSIONS: Our findings confirmed a high incidence of PE in hospitalized COVID-19 patients. Heart rate, spO2, D-dimer, and CRP levels at admission were associated with higher rates of PE during hospitalization.