Introduction: COVID-19 disease was associated with both thrombo-embolic events and in-situ thrombi formation in small vessels. Antiphospholipidic antibodies were found in some studies.Aim: Assessment of protein S activity in patients with COVID-19 as a cause this prothrombotic state, and of the association of protein S activity with worse outcome.Methods: All patients admitted for COVID-19 disease in a university hospital between 15th of May and 15th of July 2020 were prospectively enrolled into this cohort study. Patients treated with antivitamin K anticoagulants and with liver disease were excluded. All patients had protein S activity determined at admission. The main outcome was survival, secondary outcomes were clinical severity and lung damage.Results: 91 patients were included, of which 21 (23.3%) died. Protein S activity was decreased in 65% of the patients. Death was associated with lower activity of protein S (median 42% vs. 58%, p<0.001), and the association remained after adjustment for age, inflammation markers and ALAT. There was a dose-response relationship between protein S activity and clinical severity (Kendall_tau coefficient = -0.320, p < 0.001; Jonckheere-Terpstra for trend: p<0.001) or pulmonary damage on CT scan (Kendall_tau coefficient = -0.290, p<0.001; Jonckheere-Terpstra for trend: p<0.001). High neutrophil count was also independently associated with death (p=0.002).Conclusion: Protein S activity was lower in COVID-19 patients, and its level was associated with survival and disease severity, suggesting that it may have a role in the thrombotic manifestations of the disease.

Background: Since the beginning of the COVID-19 pandemic, empiric antibiotics (ATBs) have been prescribed on a large scale in both in- and outpatients. We aimed to assess the impact of antibiotic treatment on the outcomes of hospitalised patients with moderate and severe coronavirus disease 2019 (COVID-19). Methods: We conducted a prospective multicentre cohort study in six clinical hospitals, between January 2021 and May 2021. Results: We included 553 hospitalised COVID-19 patients, of whom 58% (311/553) were prescribed antibiotics, while bacteriological tests were performed in 57% (178/311) of them. Death was the outcome in 48 patients—39 from the ATBs group and 9 from the non-ATBs group. The patients who received antibiotics during hospitalisation had a higher mortality (RR = 3.37, CI 95%: 1.7–6.8), and this association was stronger in the subgroup of patients without reasons for antimicrobial treatment (RR = 6.1, CI 95%: 1.9–19.1), while in the subgroup with reasons for antimicrobial therapy the association was not statistically significant (OR = 2.33, CI 95%: 0.76–7.17). After adjusting for the confounders, receiving antibiotics remained associated with a higher mortality only in the subgroup of patients without criteria for antibiotic prescription (OR = 10.3, CI 95%: 2–52). Conclusions: In our study, antibiotic treatment did not decrease the risk of death in the patients with mild and severe COVID-19, but was associated with a higher risk of death in the subgroup of patients without reasons for it.

The patients with acute exacerbation of COPD but no apparent cardiac disease have a higher incidence of supraventricular arrhythmias. P-wave SAECG analysis and ALP detection have little value in the arrhythmic risk evaluation of these patients.

Patients with COPD associate a significant autonomic imbalance and a higher incidence of arrhythmias. DC could be a strong predictor for supraventricular and ventricular arrhythmias in patients with COPD with no clinically apparent cardiac disease. AC could be useful alongside with DC regarding the risk for ventricular arrhythmias, but seems to have lesser value as a predictor for supraventricular arrhythmias.

Patients with chronic obstructive pulmonary disease (COPD) have an increased risk for cardiac arrhythmias. Ventricular late potentials (VLP) on signal-averaged electrocardiography (SAECG) are associated with an increased risk for malignant ventricular arrhythmias. Our aim is to investigate the modifications of SAECG parameters and the presence of VLP as possible indicators of proarrhythmic substrate in patients with COPD. We prospectively enrolled 41 consecutive patients in the COPD group and 63 patients without any history of pulmonary disease, matched for age and hypertension history, in the control group. Pulmonary function tests, arterial blood gases, echocardiography, 24-hour Holter monitoring and SAECG were performed. We measured total filtered QRS duration (QRSf), duration of high frequency, low-amplitude signals < 40 V (HFLA40), and root mean square voltage in the last 40 ms (RMS40). VLP were considered if at least two of these parameters were abnormal. Results. We did not register any significant differences in QRSf, HFLA40 or RMS40 between the two groups. In the COPD group there was a non-significant higher percentage of patients with VLP in comparison with the control group. In the COPD patients we registered a significantly higher number of isolated premature ventricular beats and of combined complex ventricular arrhythmias, consisting of polymorphic PVC, couplets, triplets or nonsustained ventricular tachycardias. None of these arrhythmic parameters correlated with SAECG variables or with the presence of VLP. Conclusion. In COPD patients parameters measured on signal-averaged electrocardiography and ventricular late potentials analysis have little value in risk stratification for ventricular arrhythmias.