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1.
Acta Neuropathol Commun ; 10(1): 14, 2022 02 01.
Article in English | MEDLINE | ID: covidwho-1690864

ABSTRACT

Coronavirus disease 2019 (COVID-19) is associated with an increased risk of thrombotic events. Ischemic stroke in COVID-19 patients entails high severity and mortality rates. Here we aimed to analyze cerebral thrombi of COVID-19 patients with large vessel occlusion (LVO) acute ischemic stroke to expose molecular evidence for SARS-CoV-2 in the thrombus and to unravel any peculiar immune-thrombotic features. We conducted a systematic pathological analysis of cerebral thrombi retrieved by endovascular thrombectomy in patients with LVO stroke infected with COVID-19 (n = 7 patients) and non-covid LVO controls (n = 23). In thrombi of COVID-19 patients, the SARS-CoV-2 docking receptor ACE2 was mainly expressed in monocytes/macrophages and showed higher expression levels compared to controls. Using polymerase chain reaction and sequencing, we detected SARS-CoV-2 Clade20A, in the thrombus of one COVID-19 patient. Comparing thrombus composition of COVID-19 and control patients, we noted no overt differences in terms of red blood cells, fibrin, neutrophil extracellular traps (NETs), von Willebrand Factor (vWF), platelets and complement complex C5b-9. However, thrombi of COVID-19 patients showed increased neutrophil density (MPO+ cells) and a three-fold higher Neutrophil-to-Lymphocyte Ratio (tNLR). In the ROC analysis both neutrophils and tNLR had a good discriminative ability to differentiate thrombi of COVID-19 patients from controls. In summary, cerebral thrombi of COVID-19 patients can harbor SARS-CoV2 and are characterized by an increased neutrophil number and tNLR and higher ACE2 expression. These findings suggest neutrophils as the possible culprit in COVID-19-related thrombosis.


Subject(s)
Brain Ischemia/immunology , COVID-19/immunology , Immunity, Cellular/physiology , Intracranial Thrombosis/immunology , Neutrophils/immunology , Stroke/immunology , Aged , Aged, 80 and over , Angiotensin-Converting Enzyme 2/blood , Angiotensin-Converting Enzyme 2/genetics , Angiotensin-Converting Enzyme 2/immunology , Brain Ischemia/blood , Brain Ischemia/genetics , COVID-19/blood , COVID-19/genetics , Female , Humans , Intracranial Thrombosis/blood , Intracranial Thrombosis/genetics , Male , Mechanical Thrombolysis/methods , Middle Aged , Neutrophils/metabolism , Prospective Studies , SARS-CoV-2/genetics , SARS-CoV-2/immunology , SARS-CoV-2/metabolism , Stroke/blood , Stroke/genetics
2.
Front Immunol ; 12: 720363, 2021.
Article in English | MEDLINE | ID: covidwho-1376702

ABSTRACT

Severe coronavirus disease 2019 (COVID-19) can manifest as a viral-induced hyperinflammation with multiorgan dysfunction. It has been documented that severe COVID-19 is associated with higher levels of inflammatory mediators than a mild disease, and tracking these markers may allow early identification or even prediction of disease progression. It is well known that C-reactive protein (CRP) is the acute-phase protein and the active regulator of host innate immunity, which is highly predictive of the need for mechanical ventilation and may guide escalation of treatment of COVID-19-related uncontrolled inflammation. There are numerous causes of an elevated CRP, including acute and chronic responses, and these can be infectious or non-infectious in etiology. CRP are normally lacking in viral infections, while adaptive immunity appears to be essential for COVID-19 virus clearance, and the macrophage activation syndrome may explain the high serum CRP contents and contribute to the disease progression. Nevertheless, for the assessment of host inflammatory status and identification of viral infection in other pathologies, such as bacterial sepsis, the acute-phase proteins, including CRP and procalcitonin, can provide more important information for guiding clinical diagnosis and antibiotic therapy. This review is aimed to highlight the current and most recent studies with regard to the clinical significance of CRP in severe COVID-19 and other viral associated illnesses, including update advances on the implication of CRP and its form specifically on the pathogenesis of these diseases. The progressive understanding in these areas may be translated into promising measures to prevent severe outcomes and mitigate appropriate treatment modalities in critical COVID-19 and other viral infections.


Subject(s)
C-Reactive Protein/metabolism , COVID-19/blood , COVID-19/complications , Diabetes Mellitus, Type 2/blood , Diabetes Mellitus, Type 2/complications , Humans , Inflammation/blood , Influenza A Virus, H1N1 Subtype , Influenza, Human/blood , Influenza, Human/complications , Stroke/blood , Virus Diseases
3.
Rev Neurosci ; 32(3): 341-349, 2021 04 27.
Article in English | MEDLINE | ID: covidwho-1021723

ABSTRACT

Coronavirus disease 2019 (COVID-19), due to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged in Wuhan city, China in December 2019 and rapidly spread to other countries. The most common reported symptoms are fever, dry cough, myalgia and fatigue, headache, anorexia, and breathlessness. Anosmia and dysgeusia as well as gastrointestinal symptoms including nausea and diarrhea are other notable symptoms. This virus also can exhibit neurotropic properties and may also cause neurological diseases, including epileptic seizures, cerebrovascular accident, Guillian barre syndrome, acute transverse myelitis, and acute encephalitis. In this study, we discuss stroke as a complication of the new coronavirus and its possible mechanisms of damage.


Subject(s)
COVID-19/physiopathology , Endothelium, Vascular/physiopathology , Hypoxia/physiopathology , Stroke/physiopathology , Thrombophilia/physiopathology , Angiotensin-Converting Enzyme 2/metabolism , Blood Viscosity , COVID-19/blood , COVID-19/complications , COVID-19/metabolism , Humans , Hypoxia/complications , Myocarditis/complications , Myocarditis/physiopathology , Renin-Angiotensin System , Risk , SARS-CoV-2/metabolism , Stroke/blood , Stroke/etiology , Stroke/metabolism , Thrombophilia/blood , Thrombophilia/etiology
5.
Neurol India ; 68(3): 560-572, 2020.
Article in English | MEDLINE | ID: covidwho-640338

ABSTRACT

COVID-19, in most patients, presents with mild flu-like illness. Elderly patients with comorbidities, like hypertension, diabetes, or lung and cardiac disease, are more likely to have severe disease and deaths. Neurological complications are frequently reported in severely or critically ill patients with comorbidities. In COVID-19, both central and peripheral nervous systems can be affected. The SARS-CoV-2 virus causes the disease COVID-19 and has the potential to invade the brain. The SARS-CoV-2 virus enters the brain either via a hematogenous route or olfactory system. Angiotensin-converting enzyme two receptors, present on endothelial cells of cerebral vessels, are a possible viral entry point. The most severe neurological manifestations, altered sensorium (agitation, delirium, and coma), are because of hypoxic and metabolic abnormalities. Characteristic cytokine storm incites severe metabolic changes and multiple organ failure. Profound coagulopathies may manifest with ischemic or hemorrhagic stroke. Rarely, SARS-CoV-2 virus encephalitis or pictures like acute disseminated encephalomyelitis or acute necrotizing encephalopathy have been reported. Nonspecific headache is a commonly experienced neurological symptom. A new type of headache "personal protection equipment-related headache" has been described. Complete or partial anosmia and ageusia are common peripheral nervous system manifestations. Recently, many cases of Guillain-Barré syndrome in COVID-19 patients have been observed, and a postinfectious immune-mediated inflammatory process was held responsible for this. Guillain-Barré syndrome does respond to intravenous immunoglobulin. Myalgia/fatigue is also common, and elevated creatine kinase levels indicate muscle injury. Most of the reports about neurological complications are currently from China. COVID-19 pandemic is spreading to other parts of the world; the spectrum of neurological complications is likely to widen further.


Subject(s)
Ageusia/physiopathology , Coronavirus Infections/physiopathology , Cytokine Release Syndrome/immunology , Encephalitis/physiopathology , Guillain-Barre Syndrome/physiopathology , Headache/physiopathology , Olfaction Disorders/physiopathology , Pneumonia, Viral/physiopathology , Stroke/physiopathology , Ageusia/etiology , Betacoronavirus , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/etiology , Blood-Brain Barrier , Brain Ischemia/blood , Brain Ischemia/etiology , Brain Ischemia/immunology , Brain Ischemia/physiopathology , COVID-19 , Coma/etiology , Coma/physiopathology , Coronavirus Infections/blood , Coronavirus Infections/complications , Coronavirus Infections/immunology , Delirium/etiology , Delirium/physiopathology , Encephalitis/etiology , Encephalitis/immunology , Encephalomyelitis, Acute Disseminated/etiology , Encephalomyelitis, Acute Disseminated/immunology , Encephalomyelitis, Acute Disseminated/physiopathology , Fatigue/etiology , Fatigue/physiopathology , Guillain-Barre Syndrome/etiology , Headache/etiology , Humans , Intracranial Hemorrhages/blood , Intracranial Hemorrhages/etiology , Intracranial Hemorrhages/physiopathology , Leukoencephalitis, Acute Hemorrhagic/etiology , Leukoencephalitis, Acute Hemorrhagic/immunology , Leukoencephalitis, Acute Hemorrhagic/physiopathology , Myalgia/etiology , Myalgia/physiopathology , Olfaction Disorders/etiology , Pandemics , Personal Protective Equipment/adverse effects , Pneumonia, Viral/blood , Pneumonia, Viral/complications , Pneumonia, Viral/immunology , SARS-CoV-2 , Stroke/blood , Stroke/etiology , Stroke/immunology
6.
Stroke ; 51(7): 2002-2011, 2020 07.
Article in English | MEDLINE | ID: covidwho-640230

ABSTRACT

BACKGROUND AND PURPOSE: With the spread of coronavirus disease 2019 (COVID-19) during the current worldwide pandemic, there is mounting evidence that patients affected by the illness may develop clinically significant coagulopathy with thromboembolic complications including ischemic stroke. However, there is limited data on the clinical characteristics, stroke mechanism, and outcomes of patients who have a stroke and COVID-19. METHODS: We conducted a retrospective cohort study of consecutive patients with ischemic stroke who were hospitalized between March 15, 2020, and April 19, 2020, within a major health system in New York, the current global epicenter of the pandemic. We compared the clinical characteristics of stroke patients with a concurrent diagnosis of COVID-19 to stroke patients without COVID-19 (contemporary controls). In addition, we compared patients to a historical cohort of patients with ischemic stroke discharged from our hospital system between March 15, 2019, and April 15, 2019 (historical controls). RESULTS: During the study period in 2020, out of 3556 hospitalized patients with diagnosis of COVID-19 infection, 32 patients (0.9%) had imaging proven ischemic stroke. Cryptogenic stroke was more common in patients with COVID-19 (65.6%) as compared to contemporary controls (30.4%, P=0.003) and historical controls (25.0%, P<0.001). When compared with contemporary controls, COVID-19 positive patients had higher admission National Institutes of Health Stroke Scale score and higher peak D-dimer levels. When compared with historical controls, COVID-19 positive patients were more likely to be younger men with elevated troponin, higher admission National Institutes of Health Stroke Scale score, and higher erythrocyte sedimentation rate. Patients with COVID-19 and stroke had significantly higher mortality than historical and contemporary controls. CONCLUSIONS: We observed a low rate of imaging-confirmed ischemic stroke in hospitalized patients with COVID-19. Most strokes were cryptogenic, possibly related to an acquired hypercoagulability, and mortality was increased. Studies are needed to determine the utility of therapeutic anticoagulation for stroke and other thrombotic event prevention in patients with COVID-19.


Subject(s)
Betacoronavirus , Brain Ischemia/epidemiology , Coronavirus Infections/epidemiology , Pandemics , Pneumonia, Viral/epidemiology , Stroke/epidemiology , Adult , Aged , Biomarkers , Blood Sedimentation , Brain Ischemia/blood , Brain Ischemia/etiology , Brain Ischemia/therapy , COVID-19 , Causality , Cerebral Small Vessel Diseases/complications , Cerebral Small Vessel Diseases/diagnostic imaging , Cerebral Small Vessel Diseases/epidemiology , Comorbidity , Coronavirus Infections/blood , Coronavirus Infections/complications , Female , Fibrin Fibrinogen Degradation Products/analysis , Humans , Incidence , Male , Middle Aged , Neuroimaging , New York City/epidemiology , Patient Admission/statistics & numerical data , Pneumonia, Viral/blood , Pneumonia, Viral/complications , Retrospective Studies , SARS-CoV-2 , Severity of Illness Index , Stroke/blood , Stroke/etiology , Stroke/therapy , Thrombophilia/etiology , Troponin/blood
8.
Neurologia (Engl Ed) ; 35(5): 295-302, 2020 Jun.
Article in English, Spanish | MEDLINE | ID: covidwho-612886

ABSTRACT

INTRODUCTION: Ischaemic stroke has been reported in patients with COVID-19, particularly in more severe cases. However, it is unclear to what extent this is linked to systemic inflammation and hypercoagulability secondary to the infection. METHODS: We describe the cases of 4 patients with ischaemic stroke and COVID-19 who were attended at our hospital. Patients are classified according to the likelihood of a causal relationship between the hypercoagulable state and ischaemic stroke. We also conducted a review of studies addressing the possible mechanisms involved in the aetiopathogenesis of ischaemic stroke in these patients. RESULTS: The association between COVID-19 and stroke was probably causal in 2 patients, who presented cortical infarcts and had no relevant arterial or cardioembolic disease, but did show signs of hypercoagulability and systemic inflammation in laboratory analyses. The other 2 patients were of advanced age and presented cardioembolic ischaemic stroke; the association in these patients was probably incidental. CONCLUSIONS: Systemic inflammation and the potential direct action of the virus may cause endothelial dysfunction, resulting in a hypercoagulable state that could be considered a potential cause of ischaemic stroke. However, stroke involves multiple pathophysiological mechanisms; studies with larger samples are therefore needed to confirm our hypothesis. The management protocol for patients with stroke and COVID-19 should include a complete aetiological study, with the appropriate safety precautions always being observed.


Subject(s)
Brain Ischemia/etiology , Coronavirus Infections/complications , Pneumonia, Viral/complications , Stroke/virology , Aged , Aged, 80 and over , Betacoronavirus/isolation & purification , COVID-19 , Central Nervous System/virology , Coronavirus Infections/blood , Coronavirus Infections/virology , Female , Humans , Male , Middle Aged , Pandemics , Pneumonia, Viral/blood , Pneumonia, Viral/virology , Risk Factors , SARS-CoV-2 , Stroke/blood , Thrombophilia/virology
9.
Stroke ; 51(7): 2219-2223, 2020 07.
Article in English | MEDLINE | ID: covidwho-428108

ABSTRACT

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.


Subject(s)
Betacoronavirus , Coronavirus Infections , Pandemics , Pneumonia, Viral , Stroke/epidemiology , Aged , Blood Cell Count , COVID-19 , China/epidemiology , Comorbidity , Coronavirus Infections/epidemiology , Female , Hospital Mortality , Hospitals, University/statistics & numerical data , Humans , Male , Middle Aged , Pneumonia, Viral/epidemiology , Procedures and Techniques Utilization , Propensity Score , Recurrence , Respiration, Artificial/statistics & numerical data , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/therapy , SARS-CoV-2 , Stroke/blood , Stroke/therapy , Treatment Outcome
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