Background and Purpose—: Formation of denser fiber networks has been reported in atrial fibrillation and ischemic stroke. In this longitudinal cohort study, we evaluated whether fibrin clot density may predict thromboembolic and bleeding risk in patients with atrial fibrillation on vitamin K antagonists.Methods—: In 236 patients with atrial fibrillation receiving vitamin K antagonists treatment, we measured ex vivo plasma clot permeability (K_s), a measure of the pore size in fibrin networks.Results—: During a median follow-up of 4.3 (interquartile range, 3.7–4.8) years, annual rates of ischemic stroke or transient ischemic attack and major bleeds were 2.96% and 3.45%, respectively. In multivariate Cox regression analysis, patients with lower K_s(<6.8 cm²×10⁻⁹, median) had increased risk of ischemic stroke or transient ischemic attack (hazard ratio [HR], 6.55; 95% confidence interval [CI], 2.17–19.82) and major bleeds (HR, 10.65; 95% CI, 3.52–32.22). Patients with elevated K_s(≥6.8 cm²×10⁻⁹) had an increased rate of minor bleeding compared with the remainder (11.63% per year versus 3.55% per year;P<0.0001). The independent predictors of stroke or transient ischemic attack were low K_s(<6.8 cm²×10⁻⁹; HR, 7.24; 95% CI, 2.53–20.76), age (HR, 1.05; 95% CI, 1.01–1.10), and treatment with angiotensin-converting enzyme inhibitors (HR, 2.27; 95% CI, 1.08–4.77). Major bleeds were predicted by low K_s(<6.8 cm²×10⁻⁹; HR, 8.48; 95% CI, 2.99–24.1) and HAS-BLED score ≥3 (HR, 2.22; 95% CI, 1.12–4.38).Conclusions—: This study is the first to show that unfavorable fibrin properties reflected by formation of denser fibrin networks determine, in part, the efficacy and safety of anticoagulation with vitamin K antagonists in patients with atrial fibrillation.

Background: There is still a need for studies on the quality of life (QoL) at work among COVID-19 survivors. Therefore, we aimed to evaluate the association between the brain fog symptoms and the QoL at work in non-hospitalized patients with previous SARS-CoV-2 infection. Methods: Three hundred non-hospitalized patients (79.33% women; median age, 36 years; interquartile range, 30–48 years) were included in the final analysis. An anonymous neuropsychological questionnaire containing eight different questions on the presence of brain fog symptoms in four time intervals, i.e., pre-COVID-19 and 0–4, 4–12, and >12 weeks after infection, was retrospectively introduced to patients and staff of the University Hospital in Krakow. Additionally, a four-point Likert scale was used to evaluate QoL at work in four time periods. Included were participants aged ≥ 18 years in whom the diagnosis of COVID-19 was confirmed by the RT-PCR from nasopharyngeal swab and the first symptoms occurred no earlier than 3 months before the completion of the questionnaire. Results: Before SARS-CoV-2 infection, 28.00% (n = 84) of patients reported poor QoL at work. Within 4, 4–12, and >12 weeks after infection, a decrease in QoL was observed in 75.67% (n = 227), 65.00% (n = 195), and 53.66% (n = 161) of patients, respectively (p < 0.001). With increasing deterioration of the QoL at work, the number of brain fog symptoms increased, and patients with severe QoL impairment exhibited a median of five symptoms for 12 weeks post-COVID-19. In the multivariable logistic regression model, predictors of the deterioration of the QoL at work depended on the time from COVID-19 onset; in the acute phase of the disease (<4 weeks), it was predicted by impairment in remembering information from the past (OR 1.88, 95%CI: 1.18–3.00, p = 0.008) and multitasking (OR 1.96, 95%CI: 1.48–2.58, p < 0.001). Furthermore, an impairment in the QoL at work 4–12 weeks and >12 weeks after COVID-19 was independently associated with age (OR 0.46, 95%CI: 0.25–0.85, p = 0.014 and OR 1.03, 95%CI: 1.01–1.05, p = 0.025, respectively), problems with multitasking (OR 2.05, 95%CI: 1.40–3.01, p < 0.001 and OR 1.75, 95%CI: 1.15–2.66, p = 0.009, respectively), answering questions in an understandable/unambiguous manner (OR 1.99, 95%CI: 1.27–3.14, p = 0.003 and OR 2.00, 95%CI: 1.47–2.36, p = 0.001, respectively), and, only for the >12 week interval, problems with remembering information from the past (OR 2.21, 95%CI: 1.24–3.92, p = 0.007). Conclusions: Certain brain fog symptoms, such as impaired memory or multitasking, are predictors of a poorer QoL at work not only during the acute phase of COVID-19 but also within more than 12 weeks after the onset of infection.

An increased risk of atherosclerotic and thrombotic complications characterizes connective tissue diseases. Endothelial dysfunction is the basis for the initiation and progression of atherosclerosis and thrombosis. We present systemic lupus erythematosus (SLE) as a model rheumatic disease with endothelial dysfunction and discuss its mechanisms, factors that influence the early onset and rapid progression of atherosclerosis, and the increased risk of thromboembolic events. We focus on established methods to improve endothelium function, including statins, antiplatelet, and antithrombotic therapy. Hypercoagulable and hypofibrinolitic states and a hyperinflammatory response characterize severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Several pathogenic mechanisms are typical for an acute phase of Covid-19 post-Covid syndrome and connective tissue diseases: endothelial dysfunction, elevated antiphospholipid antibody titer, activation of the complement system, and formation of extracellular neutrophil traps (NET). The current review discusses the mechanisms underlying SLE and the COVID-19 in the context of endothelial function, atherosclerosis, and thrombosis (Graphical abstract). Key Points• The pathophysiology of systemic lupus erythematosus (SLE) and Covid-19 shows some similarities, such as endothelial cell activation and dysfunction, the activation of complementary systems, the presence of antiphospholipid antibodies, and the formation of extracellular neutrophil traps.• Autoimmunity in both diseases creates the basis for hyperinflammatory, hypercoagulable, and hypofibrinolitic states and their thromboembolic complications.• This paper presents our perspective on the mechanisms behind the cardiovascular manifestations of SLE and COVID-19, with a particular emphasis on endothelial dysfunction. Graphical abstract Covid-19 and systemic lupus erythematosus—potential similarities in pathophysiology. Figures of the panel illustrate the clinical manifestations of endothelial dysfunction, atherosclerosis, and thromboembolism, including coronary artery disease ([A] coronary angiography with left anterior descending artery stenosis and [B] scintigraphy with reduced perfusion in the myocardial apical segments), stroke ([C] carotid angiography, left carotid artery occlusion) and pulmonary embolism ([D]computed tomography with thrombus in the right pulmonary artery).

Objectives. To evaluate the spectrum of neurological symptoms in patients with COVID-19 during the first 14 days of hospitalisation and its association with in-hospital mortality. Material and methods. We included 200 patients with RT-PCR-confirmed COVID-19 admitted to University Hospital in Krakow, Poland. In 164 patients, a detailed questionnaire concerning neurological symptoms and signs was performed prospectively within 14 days of hospitalisation. In the remaining 36 patients, such questionnaires were completed retrospectively based on daily observations in the Department of Neurology. Results. During hospitalisation, 169 patients (84.5%) experienced neurological symptoms; the most common were: fatigue (62.5%), decreased mood (45.5%), myalgia (43.5%), and muscle weakness (42.5%). Patients who died during hospitalisation compared to the remainder were older (79 [70.5–88.5] vs. 63.5 [51–77] years, p = 0.001), and more often had decreased level of consciousness (50.0% vs. 9.3%, p < 0.001), delirium (33.3% vs. 4.4%, p < 0.001), arterial hypotension (50.0% vs. 19.6%, p = 0.005) or stroke during (18.8% vs. 3.3%, p = 0.026) or before hospitalisation (50.0% vs. 7.1, p < 0.001), whereas those who survived more often suffered from headache (42.1% vs. 0%, p = 0.012) or decreased mood (51.7% vs. 0%, p = 0.003). Conclusions. Most hospitalised patients with COVID-19 experience neurological symptoms. Decreased level of consciousness, delirium, arterial hypotension, and stroke during or before hospitalisation increase the risk of in-hospital mortality. Objectives. To evaluate the spectrum of neurological symptoms in patients with COVID-19 during the first 14 days of hospitalisation and its association with in-hospital mortality. Material and methods. We included 200 patients with RT-PCR-confirmed COVID-19 admitted to University Hospital in Krakow, Poland. In 164 patients, a detailed questionnaire concerning neurological symptoms and signs was performed prospectively within 14 days of hospitalisation. In the remaining 36 patients, such questionnaires were completed retrospectively based on daily observations in the Department of Neurology. Results. During hospitalisation, 169 patients (84.5%) experienced neurological symptoms; the most common were: fatigue (62.5%), decreased mood (45.5%), myalgia (43.5%), and muscle weakness (42.5%). Patients who died during hospitalisation compared to the remainder were older (79 [70.5–88.5] vs. 63.5 [51–77] years, p = 0.001), and more often had decreased level of consciousness (50.0% vs. 9.3%, p < 0.001), delirium (33.3% vs. 4.4%, p < 0.001), arterial hypotension (50.0% vs. 19.6%, p = 0.005) or stroke during (18.8% vs. 3.3%, p = 0.026) or before hospitalisation (50.0% vs. 7.1, p < 0.001), whereas those who survived more often suffered from headache (42.1% vs. 0%, p = 0.012) or decreased mood (51.7% vs. 0%, p = 0.003). Conclusions. Most hospitalised patients with COVID-19 experience neurological symptoms. Decreased level of consciousness, delirium, arterial hypotension, and stroke during or before hospitalisation increase the risk of in-hospital mortality.