Does COVID-19 vaccination protect against pulmonary embolism?

The prevalence of venous thromboembolism (VTE) in COVID-19 patients is highly variable, depending on methodological and clinical factors, among which vaccination (1). The hypothesis of a possible protective role of vaccination in preventing pulmonary embolism (PE) in hospitalized COVID-19 patients has not been explored. The aim of the study was to evaluate PE prevalence in vaccinated versus unvaccinated hospitalized COVID-19 patients. We conducted a retrospective case-control study from 2021/11/01 to 2022/01/15; we reviewed all the chest computed topographies (chest-CT) performed because of a clinical suspicion for PE at our Institution. Sixty-two patients were included in the study: 27/62 (43.5%) were vaccinated and 35/62 (56.4%) were not. Vaccinated patients were older and with more comorbidities than unvaccinated people. Overall, PE was diagnosed in 19/62 patients (30.1% prevalence). CT Severity Score (CT-SS) differs between the two groups; not vaccinated patients had a more severe CT imaging than the vaccinated (< 0.00005). PE prevalence in ICU was 43.2% (16/37 patients), while in the Internal Medicine ward, it was 12% (3/25 cases). PE was significantly higher among unvaccinated people: 16/35 (45.7%) vs 3/27 (11.1%), OR p = 0.04. We observed a strong association between vaccination and protection from PE in hospitalized COVID-19 patients: morbidity was significantly lower in vaccinated versus not vaccinated patients. The issue of the protective role of vaccination in COVID-19-associated VTE should be addressed in adequately designed and powered future prospective studies.

Postresuscitation treatment with argon improves early neurological recovery in a porcine model of cardiac arrest.

INTRODUCTION: Effects of postresuscitation treatment with argon on neurologic recovery were investigated in a porcine model of cardiac arrest (CA) with an underlying acute myocardial infarction. METHODS: The left anterior descending coronary artery was occluded in 12 pigs, and CA was induced. After 8 min of untreated CA, cardiopulmonary resuscitation was performed for 5 min before defibrillation. Following resuscitation, animals were subjected to 4-h ventilation with 70% argon/30% oxygen or 70% nitrogen/30% oxygen. Myocardial function was echocardiographically assessed, and serum neuron-specific enolase was measured. Animals were observed up to 72 h for assessment of survival and neurologic recovery. RESULTS: All the animals were resuscitated and survived for 72 h, except for a control pig. Ventilation with argon did not have any detrimental effects on hemodynamics and respiratory gas exchange. All the six argon-treated animals had a fast and complete 72-h neurologic recovery, in contrast to only two of the six controls (P < 0.05). Seventy-two-hour neurologic alertness score and neurologic deficit score were, respectively, 100 and 0 in the argon group and 79 and 29 in the control one (P < 0.01 and P < 0.05). Significantly lower increases in serum neuron-specific enolase (12% vs. 234%) and minimal histological brain injury (neuronal degeneration: 0 vs. 1) were also observed in argon-treated animals, in comparison to controls. CONCLUSIONS: In this model, postresuscitation treatment with argon allowed for a faster and complete neurologic recovery, without detrimental effects on hemodynamics and respiratory gas exchanges.

Hypothermia improves ventricular myocyte contractility under conditions of normal perfusion and after an interval of ischemia.

AIM: Recent investigations have reported improved myocardial function during hypothermia following resuscitation from cardiac arrest. The effects of hypothermia on myocyte contractility were investigated under conditions of normal perfusion and after a 10min interval of ischemia. METHODS: Ventricular myocytes were obtained from 10 male Sprague-Dawley rats weighing 400+/-50g. The myocytes were randomized to be perfused at: 37 degrees C, 34 degrees C, 32 degrees C, or 30 degrees C. A subsequent set of myocytes was subjected to 10min of ischemia at 37 degrees C, prior to being randomized to reperfusion at: 37 degrees C, 34 degrees C, 32 degrees C or 30 degrees C. Myocyte contractility was expressed as length-shortening percentage. Intracellular Ca(2+) transients were assessed in a separate group of myocytes preloaded with Fura-2/AM. Sensitivity to Ca(2+) was tested by increasing perfusate Ca(2+) content, i.e. 0.5mM, 1mM and 2mM. RESULTS: During normal perfusion and following reperfusion after 10min of ischemia, myocyte contractility increased at 34 degrees C compared to 37 degrees C (P<0.01). When the perfusion temperature was decreased to 32 degrees C and 30 degrees C, contractility further increased (P<0.001). Intracellular Ca(2+) transients were greater during perfusion at 34 degrees C compared to those at 37 degrees C (P<0.001) and further increased at 30 degrees C (P<0.001). Increases in extracellular Ca(2+) concentration from 0.5mM to 2mM resulted in greater myocyte contractility during perfusion at 30 degrees C compared to that observed at 37 degrees C (P<0.001). Effects of hypothermia on intracellular Ca(2+) transients and sensitivity to Ca(2+) persisted after ischemia. CONCLUSIONS: Hypothermia improved myocyte contractility, intracellular Ca(2+) transients and sensitivity to Ca(2+) under conditions of normal perfusion and following reperfusion after 10min of ischemia.

Gas distribution in a two-compartment model during volume or pressure ventilation: role of elastic elements.

The results of the studies on pulmonary gas distribution during constant-flow controlled-volume inflation (VCV) and inspiratory constant pressure inflation (PCV) in experimental studies are conflicting. In a mathematical model, with the characteristics of two lung compartments including tissue viscoelastic properties, pulmonary gas distribution was tested by simulating PCV and VCV at same inflation volumes. The compartmental distributions of the tidal volume were compared during CMV and PCV in different configurations obtained by changing the elastic and viscoelastic properties in each compartment, but maintaining the same total values of respiratory mechanics measured in patients. In all instances PCV resulted in a slightly higher air-trapping than in VCV mode. Heterogeneous elastic properties diverted most of the tidal volume towards the less compromised compartment. However, both ventilatory modes provided similar compartmental gas distribution, but during VCV compartmental peak pressures were higher in the sicker compartment respect to PCV. The use of PCV could grant a less remarkable pressure variability able to reduce the potential ventilator-associated lung injury. Moreover, the parameters measured during an end-inspiratory pause could not pinpoint unique characteristics for each configuration.