Clinical variables associated with late-onset thrombotic and cardiovascular events, after SARS-CoV-2 infection, in a cohort of patients from the first epidemic wave: an 18-month analysis on the "Surviving-COVID" cohort from Bergamo, Italy.

Importance: Population studies have recorded an increased, unexplained risk of post-acute cardiovascular and thrombotic events, up to 1 year after acute severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Objectives: To search for clinical variables and biomarkers associated with late post-acute thrombotic and cardiovascular events after SARS-CoV-2 infection. Design: Retrospective cohort study. Setting: Third-level referral hospital in Bergamo (Italy). Participants: Analysis of an existing database of adult patients, who received care for SARS-CoV-2 infection at our institution between 20 February and 30 September 2020, followed up on a single date ("entry date") at 3-6 months. Exposure: Initial infection by SARS-CoV-2. Main outcomes and measures: Primary outcome: occurrence, in the 18 months after entry date, of a composite endpoint, defined by the International Classification of Diseases-9th edition (ICD-9) codes for at least one of: cerebral/cardiac ischemia, venous/arterial thrombosis (any site), pulmonary embolism, cardiac arrhythmia, heart failure. Measures (as recorded on entry date): history of initial infection, symptoms, current medications, pulmonary function test, blood tests results, and semi-quantitative radiographic lung damage (BRIXIA score). Individual clinical data were matched to hospitalizations, voluntary vaccination against SARS-CoV-2 (according to regulations and product availability), and documented reinfections in the following 18 months, as recorded in the provincial Health Authority database. A multivariable Cox proportional hazard model (including vaccine doses as a time-dependent variable) was fitted, adjusting for potential confounders. We report associations as hazard ratios (HR) and 95% confidence intervals (CI). Results: Among 1,515 patients (948 men, 62.6%, median age 59; interquartile range: 50-69), we identified 84 endpoint events, occurring to 75 patients (5%): 30 arterial thromboses, 11 venous thromboses, 28 arrhythmic and 24 heart failure events. From a multivariable Cox model, we found the following significant associations with the outcome: previous occurrence of any outcome event, in the 18 months before infection (HR: 2.38; 95% CI: 1.23-4.62); BRIXIA score ≥ 3 (HR: 2.43; 95% CI: 1.30-4.55); neutrophils-to-lymphocytes ratio ≥ 3.3 (HR: 2.60; 95% CI: 1.43-4.72), and estimated glomerular filtration rate < 45 ml/min/1.73 m2 (HR: 3.84; 95% CI: 1.49-9.91). Conclusions and relevance: We identified four clinical variables, associated with the occurrence of post-acute thrombotic and cardiovascular events, after SARS-CoV-2 infection. Further research is needed, to confirm these results.

[Variations of hematic viscosity due to water-electrolyte disorders induced by muscular stress]. / Le variazioni della viscosita' ematica in rapporto a perturbazioni idroelettrolitiche indotte da stress muscolare.

In view of the increasingly widespread tendency of common people to undertake sports activities without adequate athletic preparation, and in consideration of certain cardiovascular alterations detected in subjects cultivating athletic activities of some magnitude for a number of years, the authors set out to explore the effects of severe muscular activity on circulation. More precicely, they measured blood and plasma viscosity at rest and after 50 minutes of intense athletic activity, competitive or otherwise, at the same time looking for possible changes of volemia, blood lipid composition, and hemodynamic parameters. Trained subjects, even if no longer very young, showed viscosity values in the lower range of normal, with no increase following muscular exertion; and likewise no changes of circulating blood volumes. Untrained subjects, conversely, showed more significant increase of both said values, albeit not beyond the limits of norm. The definitely if not dramatically different behavior of the two groups of subjects (trained versus untrained) brings out the value of this simple test. The authors discuss the factors and mechanisms that may be responsible for the observed changes: namely the loss of water and associated changes of electrolyte and protein concentrations, the alterations of blood pH, the changes of paO2, and the increased velocity of blood flow.

[The behavior of blood viscosity in polyglobulism]. / Il comportamento della viscosita' plasmatica nelle poliglobulie.

In polyglobulic subjects we have found a variable reduction of plasmatic viscosity, with an increase of total viscosity. If the increase of Ht is the first cause of the increase of total viscosity, it is less simple to find the cause of plasmatic viscosity decrease; to this end we have analysed direct and indirect factors (coagulation factors, proteinous and lipidic components). We haven't found any significant qualitative alterations. It is proposed the importance of the interventions of basic proteins of polication type. To this end it has been studied the connection between plasmatic viscosity and ESR, being both influenced by the same factors, but in a contrary way and with variable results. Then the role of plasmatic viscosity in these subjects, in substitution of ESR, is significant.