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High rates of thrombosis are present in patients with SARS-CoV-2 infection. Deeper insight into the prothrombotic state is essential to provide the best thromboprophylaxis care. We aimed to explore associations among platelet indices, conventional hemostasis parameters, and viscoelastometry data. 21 patients with severe COVID-19 and 21 age-matched controls were enrolled. Each patient received 100 mg aspirin therapy at the time of blood sampling. To monitor the aspirin therapy, a platelet function test from hirudin anticoagulated whole blood was performed using the ASPI test by Multiplate analyser. High on-aspirin platelet reactivity (n = 8) was defined with an AUC > 40 cut-off value by ASPI tests. Furthermore, vitro viscoelastometric tests were carried out using a ClotPro analyser in COVID-associated thromboembolic events nor the survival rate showed significant associations with high on-aspirin platelet reactivity status. Patients presented with higher levels of inflammatory markers, along with evidence of hypercoagulability by ClotPro. H-IPF (%) was significantly higher among non-survivors (n = 18) compared to survivors (P = 0.011), and a negative correlation (P = 0.002) was found between H-IPF and plasminogen level in the total population. The platelet count was significantly higher among patients with high on-aspirin platelet reactivity (P = 0.03). ECA-A10 (P = 0.008), and ECA-MCF (P = 0.016) were significantly higher, while the tPA-CFT (P < 0.001) was significantly lower among patients with high on-aspirin platelet reactivity. However, only fibrinogen proved to be an independent predictor of hypofibrinolysis in severe COVID-19 patients. Surprisingly, a faster developing, more solid clot formation was observed in aspirin taking COVID-19 patients. In conclusion, an individually tailored thromboprophylaxis is needed to prevent thrombotic complications, particularly in the hypofibrinolytic cluster.

Background The concept of frailty provides an age-independent, easy-to-use tool for risk stratification. We aimed to summarize the evidence on the efficacy of frailty tools in risk assessment in COVID-19 patients. Methods The protocol was registered (CRD42021241544). Studies reporting on frailty in COVID-19 patients were eligible. The main outcomes were mortality, length of hospital stay (LOH) and intensive care unit (ICU) admission in frail and non-frail COVID-19 patients. Frailty was also compared in survivors and non-survivors. Five databases were searched up to 24th September 2021. The QUIPS tool was used for the risk of bias assessment. Odds ratios (OR) and weighted mean differences (WMD) were calculated with 95% confidence intervals (CI) using a random effect model. Heterogeneity was assessed using the I2 and χ2 tests. Results From 3640 records identified, 54 were included in the qualitative and 42 in the quantitative synthesis. Clinical Frailty Scale (CFS) was used in 46 studies, the Hospital Frailty Risk Score (HFRS) by 4, the Multidimensional Prognostic Index (MPI) by 3 and three studies used other scores. We found that patients with frailty (CFS 4–9 or HFRS ≥ 5) have a higher risk of mortality (CFS: OR: 3.12; CI 2.56–3.81; HFRS OR: 1.98; CI 1.89–2.07). Patients with frailty (CFS 4–9) were less likely to be admitted to ICU (OR 0.28, CI 0.12–0.64). Quantitative synthesis for LOH was not feasible. Most studies carried a high risk of bias. Conclusions As determined by CFS, frailty is strongly associated with mortality; hence, frailty-based patient management should be included in international COVID-19 treatment guidelines. Future studies investigating the role of frailty assessment on deciding ICU admission are strongly warranted.

Exploration of novel and effective antiplatelet strategies for the secondary prevention of ischemic stroke is utmost. Some platelet derived microparticles (PMVs) in convalescent stroke subjects were found to be predictive for the next vascular event. Patients with high-on-treatment platelet reactivity (HTPR) had a significantly higher risk for ischemic stroke. Here, we aimed to explore associations among circulating microparticles and responsivness to antiplatelet (clopidogrel) therapy.A total of 18 patients on clopidogrel therapy due to secondary stroke prevention were rospectively recruited into this study. Twenty age-matched healthy subjects served as controls. Flow cytometric measurements of microparicles (MVs) and data analysis were performed on Beckman-Coulter FC-500 cytometer with CXP software. Besides, platelet aggregometry data were revealed. Both measurements were performed in whole blood and from the lower and upper blood fractions separated after 1-hour gravity sedimentation by the analogy with erythrocyte sedimentation rate.The total number of circulating MVs, and particularly the platelet derived CD42+ and PAC-1+ were significantly higher in post-stroke patients (Circulating MVs may allow to monitor the response to antiplatelet therapy in post-stroke patients. In addition, the link between platelet derived MVs and neutrophil granulocytes might become therapeutic targets in the future.

Absztrakt

Acute-onset cerebrovascular diseases are connected to a number of immunological changes. Here, we summarize immune responses participating in the evolution of atherosclerotic plaques and poststroke local immune responses in the injured CNS as well as in the systemic circulation. Ischemic injury of the CNS alters the balanced neuroimmune modulation resulting in CIDS, the central nervous system injury-induced immune deficiency syndrome. Due to the immunodepression and reduced pro-inflammatory immune responses, the susceptibility for infection is increased; indeed, poststroke infection plays a major role in stroke-related mortality. On the other hand, CIDS may protect against damaging autoimmune responses elicited by exposed CNS antigens. Investigation of immune responses related to ischemic stroke may result in novel therapies indicated by an increasing number of experimental and clinical trials altering poststroke immune responses and preventing infections.