COVID­19 and ischemic stroke: Mechanisms of hypercoagulability (Review).

During the coronavirus disease 2019 (COVID­19) pandemic, some patients with severe COVID­19 exhibited complications such as acute ischemic stroke (AIS), which was closely associated with a poor prognosis. These patients often had an abnormal coagulation, namely, elevated levels of D­dimer and fibrinogen, and a low platelet count. Certain studies have suggested that COVID­19 induces AIS by promoting hypercoagulability. Nevertheless, the exact mechanisms through which COVID­19 leads to a hypercoagulable state in infected patients remain unclear. Understanding the underlying mechanisms of hypercoagulability is of utmost importance for the effective treatment of these patients. The present review aims to summarize the current status of research on COVID­19, hypercoagulability and ischemic stroke. The present review also aimed to shed light into the underlying mechanisms through which COVID­19 induces hypercoagulability, and to provide therapies for different mechanisms for the more effective treatment of patients with COVID­19 with ischemic stroke and prevent AIS during the COVID­19 pandemic.

COVID-19 associated thromboinflammation of renal capillary: potential mechanisms and treatment.

Coronavirus disease 2019 (COVID-19) infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global pandemic disease with high morbidity and mortality. Inflammatory and thrombosis are its main manifestations. As an important organ of hemofiltration metabolism, the kidney is prone to blockage and destruction when filter high inflammatory and high viscous blood of COVID-19, resulting in the loss of a large amount of protein, aggravating blood concentration, and then worsening COVID-19 hypercoagulability, which may explain the phenomenon of erythrocytes aggregation blocking the capillary lumen and the main reason why the kidney has become the second largest involvement organs. Therefore, this review discusses the effects of pathophysiological mechanisms such as inflammatory storm, endothelial injury, phosphatidylserine expression, extracellular traps release on renal capillary thrombosis caused by COVID-19 infection. Meanwhile, in view of the above mechanisms, we put forward the potential targets of antithrombotic therapy, and graded management of patients, reasonable use of drugs according to the severity of the disease and the choice of time. And we support the view of prevention of thrombus before admission, continuous anticoagulation and drug choice after discharge. It is suggested that the symptomatic and supportive treatment of renal disease in critically ill patients should be combined with the concept of antithrombotic therapy. The ultimate goal is to reduce the occurrence and development of kidney disease, provide direction for the current management of COVID-19 with kidney disease, and reduce the mortality of COVID-19.

Dysregulation of Immune Response in Patients With Coronavirus 2019 (COVID-19) in Wuhan, China.

BACKGROUND: In December 2019, coronavirus 2019 (COVID-19) emerged in Wuhan and rapidly spread throughout China. METHODS: Demographic and clinical data of all confirmed cases with COVID-19 on admission at Tongji Hospital from 10 January to 12 February 2020 were collected and analyzed. The data on laboratory examinations, including peripheral lymphocyte subsets, were analyzed and compared between patients with severe and nonsevere infection. RESULTS: Of the 452 patients with COVID-19 recruited, 286 were diagnosed as having severe infection. The median age was 58 years and 235 were male. The most common symptoms were fever, shortness of breath, expectoration, fatigue, dry cough, and myalgia. Severe cases tend to have lower lymphocyte counts, higher leukocyte counts and neutrophil-lymphocyte ratio (NLR), as well as lower percentages of monocytes, eosinophils, and basophils. Most severe cases demonstrated elevated levels of infection-related biomarkers and inflammatory cytokines. The number of T cells significantly decreased, and were more impaired in severe cases. Both helper T (Th) cells and suppressor T cells in patients with COVID-19 were below normal levels, with lower levels of Th cells in the severe group. The percentage of naive Th cells increased and memory Th cells decreased in severe cases. Patients with COVID-19 also have lower levels of regulatory T cells, which are more obviously decreased in severe cases. CONCLUSIONS: The novel coronavirus might mainly act on lymphocytes, especially T lymphocytes. Surveillance of NLR and lymphocyte subsets is helpful in the early screening of critical illness, diagnosis, and treatment of COVID-19.

Clinical Characteristics and Outcomes of COVID-19 Patients With a History of Stroke in Wuhan, China.

BACKGROUND AND PURPOSE: Information on stroke survivors infected with coronavirus disease 2019 (COVID-19) is limited. The aim of this study was to describe specific clinical characteristics and outcomes of patients with COVID-19 with a history of stroke. METHODS: All the confirmed cases of COVID-19 at Tongji Hospital from January 27 to March 5, 2020, were included in our cohort study. Clinical data were analyzed and compared between patients with and without a history of stroke. RESULTS: Of the included 1875 patients with COVID-19, 50 patients had a history of stroke. The COVID-19 patients with medical history of stroke were older with more comorbidities, had higher neutrophil count, and lower lymphocyte and platelet counts than those without history of stroke. The levels of D-dimers, cardiac troponin I, NT pro-brain natriuretic peptide, and interleukin-6 were also markedly higher in patients with history of stroke. Stroke survivors who underwent COVID-19 developed more acute respiratory distress syndrome and received more noninvasive mechanical ventilation. Data from propensity-matched analysis indicated a higher proportion of patients with COVD-19 with a history of stroke were admitted to the intensive care unit requiring mechanical ventilation and were more likely to be held in the unit or die, compared with non-stroke history COVID-19 patients. CONCLUSIONS: Patients with COVID-19 with a history of stroke had more severe clinical symptoms and poorer outcomes compared with those without a history of stroke.