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1.
Am J Med ; 2024 May 23.
Artigo em Inglês | MEDLINE | ID: mdl-38795941

RESUMO

BACKGROUND: Long-COVID is a syndrome persisting 12+ weeks after COVID-19 infection, impacting life and work ability. Autonomic nervous system imbalance has been hypothesised as the cause. This study aims to investigate cardiovascular autonomic function in health care workers (HCWs) with Long-COVID and the effectiveness of slow paced breathing SPB on autonomic modulation. METHODS: From 1st December 2022 to 31th March 2023, 6655 HCWs of the University Hospitals of Trieste (Northeast Italy) were asked to participate the study by company-email. Inclusion/exclusion criteria were assessed. Global health status and psychosomatic disorders were evaluated through validated questionnaires. Heart rate variability was assessed by finger-photoplethysmography during spontaneous breathing (SB) and SPB, which stimulate vagal response. Long-COVID-HCWs (G1) were contrasted with never infected (G2) and fully recovered COVID-19 workers (G3). RESULTS: 126 HCWs were evaluated. The. 58 Long-COVID were assessed at a median time since COVID-19 of 419.5 days (IQR 269-730) and had significantly more psychosomatic symptoms and lower detectability of spontaneous systolic pressure oscillation at 0.1 Hz (Mayer wave - baroreflex arc) during SB compared to 53 never-infected and 14 fully-recovered HCWs (19%, 42% and 40%, respectively, p=0.027). During SPB, the increase in this parameter was close to controls (91.2%, 100% and 100%, respectively, p=0.09). No other differences in HRV parameters were found among groups. CONCLUSIONS: Resting vascular modulation was reduced in Long-COVID, while during SPB baroreflex sensitivity effectively improved. Long-term studies are needed to evaluate whether multiple sessions of breathing exercises can restore basal vascular reactivity and reduce cardiovascular risk in these patients.

2.
Preprint em Inglês | medRxiv | ID: ppmedrxiv-21255657

RESUMO

BackgroundThere is a risk of novel mutations of SARS-CoV-2 that may render COVID-19 resistant to most of the therapies, including antiviral drugs. The evidence around the application of therapeutic plasma exchange (TPE) for the management of critically ill COVID-19 patients is still provisional and further investigations are needed to confirm its eventual beneficial effects. MethodsWe therefore carried out a single-centered retrospective observational non-placebo-controlled trial enrolling 73 inpatients from Baqiyatallah Hospital in Tehran (Iran) with diagnosis of COVID-19 pneumonia confirmed by real-time polymerase chain reaction (RT-PCR) on nasopharyngeal swabs and high-resolution computerized tomography chest scan. These patients were broken down into two groups: Group 1 (30 patients) receiving standard of care (corticosteroids, ceftriaxone, azithromycin, pantoprazole, hydroxychloroquine, lopinavir/ritonavir); and Group 2 (43 patients) receiving the above regimen plus TPE (replacing 2 liter of patients plasma by a solution, 50% of normal plasma and 50% of albumin at 5%) administered according to various time schedules. The follow-up time was 30 days and all-cause mortality was the endpoint. ResultsDeaths were 6 (14%) in Group 2 and 14 (47%) in Group 1. However, different harmful risk factors prevailed among patients not receiving TPE rather than being equally split between the intervention and control group. We used an algorithm of Structural Equation Modeling (of STATA) to summarize a large pool of potential confounders into a single score (called with the descriptive name "severity"). Disease severity was significantly (Wilkinson rank sum test p-value=0.0000) lower among COVID-19 patients undergoing TPE (median: -2.82; range: -5.18; 7.96) as compared to those non receiving TPE (median: -1.35; range: -3.89; 8.84), confirming that treatment assignment involved a selection bias of patients according to the severity of COVID-19 at hospital admission. The adjustment for confounding was carried out using severity as covariate in Cox regression models. The univariate Hazard Ratio (HR) of 0.68 (95%CI: 0.26; 1.80; p=0.441) for TPE turned to 1.19 (95%CI: 0.43; 3.29; p=0.741) after adjusting for severity. ConclusionsThe lower mortality observed among patients receiving TPE was due to a lower severity of COVID-19 rather than TPE effects. TRIAL REGISTRATIONIRCT registration number: IRCT20080901001165N58 (Iranian Registry of Clinical Trials) Registration date: 2020-05-27, 1399/03/07 (retrospectively registered)

3.
Preprint em Inglês | bioRxiv | ID: ppbiorxiv-387571

RESUMO

SARS-CoV-2 replicates efficiently in the upper airway during prodromal stage with resulting viral shedding into the environment from patients with active disease as well as from asymptomatic individuals. So far, virus spread has been exclusively contained by non-pharmacological interventions (social distancing, face masks, hand washing and several measures limiting business activities or movement of individuals)1,2. There is a need to find pharmacological interventions to mitigate the viral spread, supporting yet limiting the existing health protection measures while an effective and safe vaccine will hopefully become available. Hypothiocyanite and lactoferrin as part of the innate human immune system were shown to have a large spectrum of cidal activity against bacteria, fungi and viruses2,3. To test their virucidal activity against SARS-CoV-2 we conducted an in-vitro study. Here we show a dose-dependent virucidal activity of hypothiocyanite at micromolar concentrations, slightly improved by the presence of lactoferrin. The two substances are devoid of any cytotoxicity and may be administered combined by aerosol to exploit their antiviral activity at the port of entry (mouth, nasal cavity, conjunctiva) or exit (mouth, through emission of respiratory droplets) of SARS-CoV-2 in the human body. Furthermore, aerosol with hypothiocyanite and lactoferrin combined could also have a therapeutic effect in the lower respiratory tract, at the level of gas exchange units of the lung, preventing the devastating infection of alveolar type II cells where ACE2 is highly expressed. An in-vivo validation of in-vitro results is urgently required.

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