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.

Impact of the SARS-CoV-2 Virus Pandemic on Patients with Bronchiectasis: A Multicenter Study.

BACKGROUND: Infection by SARS-CoV-2 has unquestionably had an impact on the health of patients with chronic respiratory airway diseases, such as COPD and asthma, but little information is available about its impact on patients with bronchiectasis. The objective of the present study was to analyze the effect of the SARS-CoV-2 pandemic on the state of health, characteristics, and clinical severity (including the number and severity of exacerbations) of patients with non-cystic fibrosis bronchiectasis. METHODS: This study was multicenter, observational, and ambispective (with data collected before and during the SARS-CoV-2 pandemic), and included 150 patients diagnosed with non-cystic fibrosis bronchiectasis. RESULTS: A significant drop was observed in the number and severity of the exacerbations (57% in all exacerbations and 50% in severe exacerbations) in the E-FACED and BSI multidimensional scores, in the pandemic, compared with the pre-pandemic period. There was also a drop in the percentage of sputum samples positive for pathogenic microorganisms in general (from 58% to 44.7%) and, more specifically, Pseudomonas aeruginosa (from 23.3% to 13.3%) and Haemophilus influenzae (from 21.3% to 14%). CONCLUSIONS: During the SARS-CoV-2 period, a significant reduction was observed in the exacerbations, severity, and isolations of pathogenic microorganisms in patients with bronchiectasis.

Coagulation disorders and thromboembolic disease in COVID-19: review of current evidence in search of a better approach.

The new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been an unprecedented global health problem, causing more than 20 million infections and more than 900,000 deaths (September 2020). The SARS-CoV-2 infection, known as COVID-19, has various clinical presentations, from asymptomatic or mild catarrhal processes to severe pneumonia that rapidly progresses to acute respiratory distress syndrome (ARDS) and multiple organ failure. In the last few months, much scientific literature has been devoted to descriptions of different aspects of the coagulation disorders and arterial and venous thrombotic complications associated with COVID-19, particularly venous thromboembolism (VTE). These studies have revealed that SARS-CoV-2 could lead to a prothrombotic state reflecting the high cumulative incidence of associated thrombotic events, particularly in patients admitted to intensive care units (ICUs). As regards the coagulopathy observed in association with SARS-CoV-2 infection, the mechanisms that activate coagulation have been hypothesized as being linked to immune responses, through the release of pro-inflammatory mediators that interact with platelets, stimulate the expression of tissue factor, induce an upregulation of plasminogen activator inhibitor-1, suppress the fibrinolytic system and lead to endothelial dysfunction, triggering thrombogenesis. D-dimer elevation has been recognized as a useful biomarker of poor prognosis, although the best cut-off point for predicting VTE in COVID-19 patients has still not been clarified. This review will try to update all the available scientific information on this important topic with enormous clinical and therapeutic implications.

[Thrombotic Risk and Covid-19: Review of Current Evidence for a Better Diagnostic and Therapeutic Approach]. / Riesgo trombótico y COVID-19: revisión de la evidencia actual para una mejor aproximación diagnóstica y terapéutica.

The new SARS-CoV-2 coronavirus has created an unprecedented global health problem, resulting in more than 250,000 confirmed deaths. The disease produced by this virus, called Covid-19, presents with variable clinical manifestations, from practically asymptomatic patients with catarrhal processes to severe pneumonias that rapidly evolve to acute respiratory distress syndrome (ARDS) and multiorgan failure. In recent weeks, papers have been published describing coagulation disorders and arterial and venous thrombotic complications in these patients, mainly among those admitted to intensive care units. The infection triggers an immune response, which causes different inflammatory mediators to be released into the blood. These include cytokines, which interact with platelets and different coagulation proteins, and promote thrombogenesis. One of the most widely studied coagulation markers in Covid-19 is D-dimer (DD), raised levels of which have prognostic implications, although the best cut-off point for the diagnosis of venous thromboembolism (VTE) in this population has not been clarified, nor has its usefulness in determining the intensity of thromboprophylaxis required in these patients. Until sufficiently robust information (preferably from well-designed clinical trials) is available, the recommendations of clinical practice guidelines for the prophylaxis, diagnosis and treatment of VTE should be followed in Covid-19 patients.

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.