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1.
Brain Behav Immun ; 87: 115-119, 2020 07.
Article in English | MEDLINE | ID: covidwho-1719345

ABSTRACT

OBJECTIVE: Acute stroke remains a medical emergency even during the COVID-19 pandemic. Most patients with COVID-19 infection present with constitutional and respiratory symptoms; while others present with atypical gastrointestinal, cardiovascular, or neurological manifestations. Here we present a series of four patients with COVID-19 that presented with acute stroke. METHODS: We searched the hospital databases for patients that presented with acute stroke and concomitant features of suspected COVID-19 infection. All patients who had radiographic evidence of stroke and PCR-confirmed COVID-19 infection were included in the study. Patients admitted to the hospital with PCR- confirmed COVID-19 disease whose hospital course was complicated with acute stroke while inpatient were excluded from the study. Retrospective patient data were obtained from electronic medical records. Informed consent was obtained. RESULTS: We identified four patients who presented with radiographic confirmation of acute stroke and PCR-confirmed SARS-CoV-2 infection. We elucidate the clinical characteristics, imaging findings, and the clinical course. CONCLUSIONS: Timely assessment and hyperacute treatment is the key to minimize mortality and morbidity of patients with acute stroke. Stroke teams should be wary of the fact that COVID-19 patients can present with cerebrovascular accidents and should dawn appropriate personal protective equipment in every suspected patient. Further studies are urgently needed to improve current understandings of neurological pathology in the setting of COVID-19 infection.


Subject(s)
Coronavirus Infections/complications , Pneumonia, Viral/complications , Stroke/metabolism , Aged , Aged, 80 and over , Betacoronavirus , COVID-19 , Coronavirus Infections/diagnostic imaging , Coronavirus Infections/metabolism , Female , Hospitalization , Humans , Male , Pandemics , Pneumonia, Viral/diagnostic imaging , Pneumonia, Viral/metabolism , Retrospective Studies , SARS-CoV-2 , Stroke/complications
2.
Pharmacol Res Perspect ; 10(2): e00926, 2022 04.
Article in English | MEDLINE | ID: covidwho-1694654

ABSTRACT

The chronic neurological aspects of traumatic brain injury, post-stroke syndromes, long COVID-19, persistent Lyme disease, and influenza encephalopathy having close pathophysiological parallels that warrant being investigated in an integrated manner. A mechanism, common to all, for this persistence of the range of symptoms common to these conditions is described. While TNF maintains cerebral homeostasis, its excessive production through either pathogen-associated molecular patterns or damage-associated molecular patterns activity associates with the persistence of the symptoms common across both infectious and non-infectious conditions. The case is made that this shared chronicity arises from a positive feedback loop causing the persistence of the activation of microglia by the TNF that these cells generate. Lowering this excess TNF is the logical way to reducing this persistent, TNF-maintained, microglial activation. While too large to negotiate the blood-brain barrier effectively, the specific anti-TNF biological, etanercept, shows promise when administered by the perispinal route, which allows it to bypass this obstruction.


Subject(s)
COVID-19/complications , Etanercept/therapeutic use , Stroke/complications , COVID-19/metabolism , COVID-19/pathology , Etanercept/administration & dosage , Humans , Injections, Spinal , Microglia/metabolism , Microglia/pathology , Stroke/metabolism , Syndrome , Tumor Necrosis Factor-alpha/metabolism
3.
J Thromb Haemost ; 20(4): 919-928, 2022 04.
Article in English | MEDLINE | ID: covidwho-1626880

ABSTRACT

BACKGROUND: Resistance to fibrinolysis, levels of procoagulant/antifibrinolytic neutrophil extracellular traps (NETs), and the severity of acute ischemic stroke (AIS) are increased by COVID-19. Whether NETs are components of AIS thrombi from COVID-19 patients and whether COVID-19 impacts the susceptibility of these thrombi to thrombolytic treatments remain unknown, however. OBJECTIVES: We aimed to characterize AIS thrombi from COVID-19 patients by immunohistology and to compare their response to thrombolysis to that of AIS thrombi from non-COVID-19 patients. PATIENTS/METHODS: For this monocentric cohort study, 14 thrombi from COVID-19 AIS patients and 16 thrombi from non-COVID-19 patients, all recovered by endovascular therapy, were analyzed by immunohistology or subjected to ex vivo thrombolysis by tissue-type plasminogen (tPA)/plasminogen. RESULTS: COVID-19 AIS thrombi were rich in neutrophils and contained NETs, but not spike protein. Thrombolysis assays revealed a mean resistance profile to tPA/plasminogen of COVID-19 AIS thrombi similar to that of non-COVID-19 AIS thrombi. The addition of DNase 1 successfully improved thrombolysis by potentiating fibrinolysis irrespective of COVID-19 status. Levels of neutrophil, NETs, and platelet markers in lysis supernatants were comparable between AIS thrombi from non-COVID-19 and COVID-19 patients. CONCLUSIONS: These results show that COVID-19 does not impact NETs content or worsen fibrinolysis resistance of AIS thrombi, a therapeutic hurdle that could be overcome by DNase 1 even in the context of SARS-CoV-2 infection.


Subject(s)
Brain Ischemia , COVID-19 , Ischemic Stroke , Stroke , Thrombosis , Brain Ischemia/drug therapy , COVID-19/drug therapy , Cohort Studies , Fibrinolysis , Humans , SARS-CoV-2 , Stroke/drug therapy , Stroke/metabolism , Thrombolytic Therapy , Thrombosis/metabolism , Tissue Plasminogen Activator/therapeutic use
4.
Stem Cells ; 39(10): 1335-1348, 2021 10.
Article in English | MEDLINE | ID: covidwho-1293333

ABSTRACT

Thromboembolic stroke remains a major cause of neurological disability and death. Current stroke treatments (aspirin, tissue plasminogen activator) are significantly limited by timing and risks for hemorrhage which have driven researchers to explore other approaches. Stem cell-based therapy appears to be an effective option for ischemic stroke. Besides trans-differentiation into neural cells, stem cells also provide acute protection via paracrine signaling pathways through which releasing neuroprotective factors. We previously reported that intraperitoneal administration of human placenta mesenchymal stem cell (hPMSC) therapy upon reperfusion significantly protected the brain against middle cerebral artery occlusion (MCAO)-induced injury. In the present study, we specifically investigated the role of hPMSC-derived angiotensin converting enzyme-2 (ACE-2) in protection of MCAO-induced brain injury by measurement of brain tissue viability, cerebral blood flow, and neurological score. Here, we report for the first time that hPMSC expressing substantial amount of ACE-2, which mediates hPMSC protection in the MCAO model. Strikingly, we found that the protective effects of hPMSC in MCAO-induced brain injury could be attenuated by pretreatment of hPMSCs with MLN-4760, a specific inhibitor of ACE-2 activity, or by transfection of hPMSCs with ACE-2-shRNA-lentivirus. The hPMSC-derived ACE-2 specific protective mechanism was further demonstrated by administration of PD123319, an Angiotensin type-2 receptor antagonist, or A779, a MasR antagonist. Importantly, our study demonstrated that the protective effects of hPMSC in experimental stroke are ACE-2/MasR dependent and this signaling pathway represents an innovative and highly promising approach for targeted stroke therapy.


Subject(s)
Brain Injuries , Ischemic Stroke , Mesenchymal Stem Cells , Stroke , Female , Humans , Mesenchymal Stem Cells/metabolism , Peptidyl-Dipeptidase A/genetics , Placenta , Pregnancy , Stroke/metabolism , Tissue Plasminogen Activator/metabolism
5.
Platelets ; 32(8): 1009-1017, 2021 Nov 17.
Article in English | MEDLINE | ID: covidwho-1258665

ABSTRACT

Platelets may be a target of bacteria and viruses, which can directly or indirectly activate them so promoting thrombosis. In accordance with this, community-acquired pneumonia (CAP) is complicated by ischemia-related vascular disease (myocardial infarction and stroke) in roughly 10% of patients while the incidence of venous thrombosis is uncertain. In CAP platelet biosynthesis of TxA2 is augmented and associated with myocardial infarction; however, a cause-effect relationship is still unclear as unclear is if platelet activation promotes thrombosis or functional changes of coronary tree such vasospasm. Retrospective studies suggested a potential role of aspirin in reducing mortality but the impact on vascular disease is still unknown. Coronavirus disease 2019 (Covid-19) is complicated by thrombosis in roughly 20% of patients with an almost equivalent localization in arterial and venous circulation. Platelet activation seems to have a pivot role in the thrombotic process in Covid-19 as consistently evidenced by its involvement in promoting Tissue Factor up-regulation via leucocyte interaction. Until now, antiplatelet treatment has been scarcely considered for the treatment of Covid-19; interventional trials, however, are in progress to explore this issue. The aim of this review is 1) to compare the type of vascular diseases complicating CAP and Covid-19 2) to assess the different role of platelets in both diseases and 3) to discuss if antiplatelet treatment is potentially useful to improve clinical outcomes.


Subject(s)
Aspirin/therapeutic use , Blood Platelets/metabolism , COVID-19 , Myocardial Infarction , SARS-CoV-2/metabolism , Stroke , Thrombosis , COVID-19/drug therapy , COVID-19/metabolism , COVID-19/mortality , Humans , Myocardial Infarction/drug therapy , Myocardial Infarction/metabolism , Myocardial Infarction/mortality , Stroke/drug therapy , Stroke/metabolism , Stroke/mortality , Thrombosis/drug therapy , Thrombosis/metabolism , Thrombosis/mortality
6.
Stem Cells ; 39(7): 904-912, 2021 07.
Article in English | MEDLINE | ID: covidwho-1126519

ABSTRACT

We have shown previously that transplanted bone marrow mononuclear cells (BM-MNC), which are a cell fraction rich in hematopoietic stem cells, can activate cerebral endothelial cells via gap junction-mediated cell-cell interaction. In the present study, we investigated such cell-cell interaction between mesenchymal stem cells (MSC) and cerebral endothelial cells. In contrast to BM-MNC, for MSC we observed suppression of vascular endothelial growth factor uptake into endothelial cells and transfer of glucose from endothelial cells to MSC in vitro. The transfer of such a small molecule from MSC to vascular endothelium was subsequently confirmed in vivo and was followed by suppressed activation of macrophage/microglia in stroke mice. The suppressive effect was absent by blockade of gap junction at MSC. Furthermore, gap junction-mediated cell-cell interaction was observed between circulating white blood cells and MSC. Our findings indicate that gap junction-mediated cell-cell interaction is one of the major pathways for MSC-mediated suppression of inflammation in the brain following stroke and provides a novel strategy to maintain the blood-brain barrier in injured brain. Furthermore, our current results have the potential to provide a novel insight for other ongoing clinical trials that make use of MSC transplantation aiming to suppress excess inflammation, as well as other diseases such as COVID-19 (coronavirus disease 2019).


Subject(s)
Cell Communication , Gap Junctions , Human Umbilical Vein Endothelial Cells/metabolism , Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells , Stroke , Allografts , Animals , COVID-19/metabolism , COVID-19/pathology , Gap Junctions/metabolism , Gap Junctions/pathology , Human Umbilical Vein Endothelial Cells/pathology , Humans , Mesenchymal Stem Cells/metabolism , Mesenchymal Stem Cells/pathology , Mice , SARS-CoV-2/metabolism , Stroke/metabolism , Stroke/pathology , Stroke/therapy
7.
J Cereb Blood Flow Metab ; 41(6): 1179-1192, 2021 06.
Article in English | MEDLINE | ID: covidwho-1061015

ABSTRACT

Cerebrovascular events have emerged as a central feature of the clinical syndrome associated with Sars-CoV-2 infection. This increase in infection-related strokes is marked by atypical presentations including stroke in younger patients and a high rate of hemorrhagic transformation after ischemia. A variety of pathogenic mechanisms may underlie this connection. Efforts to identify synergism in the pathophysiology underlying stroke and Sars-CoV-2 infection can inform the understanding of both conditions in novel ways. In this review, the molecular cascades connected to Sars-CoV-2 infection are placed in the context of the cerebral vasculature and in relationship to pathways known to be associated with stroke. Cytokine-mediated promotion of systemic hypercoagulability is suggested while direct Sars-CoV-2 infection of cerebral endothelial cells may also contribute. Endotheliopathy resulting from direct Sars-CoV-2 infection of the cerebral vasculature can modulate ACE2/AT1R/MasR signaling pathways, trigger direct viral activation of the complement cascade, and activate feed-forward cytokine cascades that impact the blood-brain barrier. All of these pathways are already implicated as independent mechanisms driving stroke and cerebrovascular injury irrespective of Sars-CoV-2. Recognizing the overlap of molecular pathways triggered by Sars-CoV-2 infection with those implicated in the pathogenesis of stroke provides an opportunity to identify future therapeutics targeting both Sars-CoV-2 and stroke thereby reducing the impact of the global pandemic.


Subject(s)
COVID-19/pathology , Cerebrovascular Disorders/etiology , Stroke/etiology , Angiotensin-Converting Enzyme 2/metabolism , Blood-Brain Barrier/metabolism , COVID-19/complications , COVID-19/virology , Cerebrovascular Disorders/metabolism , Complement Activation , Humans , Renin-Angiotensin System , Spike Glycoprotein, Coronavirus/metabolism , Stroke/metabolism , Virus Internalization
8.
Int J Stroke ; 16(2): 137-149, 2021 02.
Article in English | MEDLINE | ID: covidwho-1027186

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) has become a global pandemic, affecting millions of people. However, the relationship between COVID-19 and acute cerebrovascular diseases is unclear. AIMS: We aimed to characterize the incidence, risk factors, clinical-radiological manifestations, and outcome of COVID-19-associated stroke. METHODS: Three medical databases were systematically reviewed for published articles on acute cerebrovascular diseases in COVID-19 (December 2019-September 2020). The review protocol was previously registered (PROSPERO ID = CRD42020185476). Data were extracted from articles reporting ≥5 stroke cases in COVID-19. We complied with the PRISMA guidelines and used the Newcastle-Ottawa Scale to assess data quality. Data were pooled using a random-effect model. SUMMARY OF REVIEW: Of 2277 initially identified articles, 61 (2.7%) were entered in the meta-analysis. Out of 108,571 patients with COVID-19, acute CVD occurred in 1.4% (95%CI: 1.0-1.9). The most common manifestation was acute ischemic stroke (87.4%); intracerebral hemorrhage was less common (11.6%). Patients with COVID-19 developing acute cerebrovascular diseases, compared to those who did not, were older (pooled median difference = 4.8 years; 95%CI: 1.7-22.4), more likely to have hypertension (OR = 7.35; 95%CI: 1.94-27.87), diabetes mellitus (OR = 5.56; 95%CI: 3.34-9.24), coronary artery disease (OR = 3.12; 95%CI: 1.61-6.02), and severe infection (OR = 5.10; 95%CI: 2.72-9.54). Compared to individuals who experienced a stroke without the infection, patients with COVID-19 and stroke were younger (pooled median difference = -6.0 years; 95%CI: -12.3 to -1.4), had higher NIHSS (pooled median difference = 5; 95%CI: 3-9), higher frequency of large vessel occlusion (OR = 2.73; 95%CI: 1.63-4.57), and higher in-hospital mortality rate (OR = 5.21; 95%CI: 3.43-7.90). CONCLUSIONS: Acute cerebrovascular diseases are not uncommon in patients with COVID-19, especially in those whom are severely infected and have pre-existing vascular risk factors. The pattern of large vessel occlusion and multi-territory infarcts suggests that cerebral thrombosis and/or thromboembolism could be possible causative pathways for the disease.


Subject(s)
Brain Ischemia/diagnostic imaging , Brain Ischemia/epidemiology , COVID-19/diagnostic imaging , COVID-19/epidemiology , Stroke/diagnostic imaging , Stroke/epidemiology , Brain Ischemia/metabolism , COVID-19/metabolism , Humans , Observational Studies as Topic/methods , Risk Factors , Stroke/metabolism
9.
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
10.
Neurosci Lett ; 742: 135529, 2021 01 18.
Article in English | MEDLINE | ID: covidwho-971460
12.
Neuroepidemiology ; 54(5): 370-374, 2020.
Article in English | MEDLINE | ID: covidwho-713643

ABSTRACT

The severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) causes the coronavirus disease 2019 (COVID-19). It quickly became pandemic, and so did a new concern about COVID-19 infections increasing the risk for cerebrovascular diseases. There is an association between COVID-19 illness in people and acute stroke. Several chemical, mechanical, and/or inflammatory central nervous system pathologies are proposed to explain how this viral infection might induce acute cerebrovascular disease. Timely available evaluation and/or intervention is imperative for patients with concerns about acute cerebrovascular issues.


Subject(s)
Betacoronavirus , Brain/virology , Cerebrovascular Circulation/physiology , Coronavirus Infections/complications , Pneumonia, Viral/complications , Stroke/etiology , Stroke/virology , Betacoronavirus/metabolism , Brain/metabolism , Brain Ischemia/etiology , Brain Ischemia/metabolism , Brain Ischemia/virology , COVID-19 , Coronavirus Infections/metabolism , Humans , Pandemics , Pneumonia, Viral/metabolism , SARS-CoV-2 , Stroke/metabolism
13.
Biochem Biophys Res Commun ; 528(3): 413-419, 2020 07 30.
Article in English | MEDLINE | ID: covidwho-436643

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a worldwide pandemic. It has a high transmission rate among humans, and is a threat to global public health. However, there are no effective prophylactics or therapeutics available. It is necessary to identify vulnerable and susceptible groups for adequate protection and care against this disease. Recent studies have reported that COVID-19 has angiotensin-converting enzyme 2 (ACE2) as a functional receptor, which may lead to the development of severe cerebrovascular diseases (CVD), including strokes, in patients with risk factors for CVD such as diabetes and smoking. Thus, the World Health Organization (WHO) advised caution against COVID-19 for smokers and patients with underlying clinical symptoms, including cardiovascular diseases. Here, we observed ACE2 expression in the brain of rat middle cerebral artery occlusion (MCAO) model and evaluated the effects of cigarette smoke extract (CSE) and diabetes on ACE2 expression in vessels. We showed that the levels of ACE2 expression was increased in the cortex penumbra after ischemic injuries. CSE treatment significantly elevated ACE2 expression in human brain vessels. We found that ACE2 expression was upregulated in primary cultured human blood vessels with diabetes compared to healthy controls. This study demonstrates that ACE2 expression is increased in ischemic brains and vessels exposed to diabetes or smoking, makes them vulnerable to COVID-19 infection.


Subject(s)
Betacoronavirus/metabolism , Brain Ischemia/virology , Brain/blood supply , Diabetes Mellitus , Peptidyl-Dipeptidase A/biosynthesis , Receptors, Virus/biosynthesis , Smokers , Stroke/virology , Up-Regulation , Angiotensin-Converting Enzyme 2 , Animals , Betacoronavirus/pathogenicity , Brain/drug effects , Brain Ischemia/genetics , Brain Ischemia/metabolism , COVID-19 , Coronavirus Infections/genetics , Coronavirus Infections/metabolism , Coronavirus Infections/virology , Diabetes Mellitus/genetics , Diabetes Mellitus/metabolism , Disease Models, Animal , Disease Susceptibility , Infarction, Middle Cerebral Artery/complications , Male , Mice , Mice, Inbred C57BL , Pandemics , Peptidyl-Dipeptidase A/genetics , Pneumonia, Viral/genetics , Pneumonia, Viral/metabolism , Pneumonia, Viral/virology , Rats , Rats, Sprague-Dawley , Receptors, Virus/genetics , SARS-CoV-2 , Smoke/adverse effects , Stroke/genetics , Stroke/metabolism , Up-Regulation/drug effects
14.
J Stroke Cerebrovasc Dis ; 29(8): 104941, 2020 Aug.
Article in English | MEDLINE | ID: covidwho-380483

ABSTRACT

Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a global health threat. Some COVID-19 patients have exhibited widespread neurological manifestations including stroke. Acute ischemic stroke, intracerebral hemorrhage, and cerebral venous sinus thrombosis have been reported in patients with COVID-19. COVID-19-associated coagulopathy is increasingly recognized as a result of acute infection and is likely caused by inflammation, including inflammatory cytokine storm. Recent studies suggest that axonal transport of SARS-CoV-2 to the brain can occur via the cribriform plate adjacent to the olfactory bulb that may lead to symptomatic anosmia. The internalization of SARS-CoV-2 is mediated by the binding of the spike glycoprotein of the virus to the angiotensin-converting enzyme 2 (ACE2) on cellular membranes. ACE2 is expressed in several tissues including lung alveolar cells, gastrointestinal tissue, and brain. The aim of this review is to provide insights into the clinical manifestations and pathophysiological mechanisms of stroke in COVID-19 patients. SARS-CoV-2 can down-regulate ACE2 and, in turn, overactivate the classical renin-angiotensin system (RAS) axis and decrease the activation of the alternative RAS pathway in the brain. The consequent imbalance in vasodilation, neuroinflammation, oxidative stress, and thrombotic response may contribute to the pathophysiology of stroke during SARS-CoV-2 infection.


Subject(s)
Betacoronavirus/pathogenicity , Brain/physiopathology , Coronavirus Infections/physiopathology , Encephalitis, Viral/physiopathology , Pneumonia, Viral/physiopathology , Stroke/physiopathology , Angiotensin-Converting Enzyme 2 , Betacoronavirus/metabolism , Blood Coagulation , Brain/metabolism , Brain/virology , COVID-19 , Coronavirus Infections/epidemiology , Coronavirus Infections/metabolism , Coronavirus Infections/virology , Encephalitis, Viral/epidemiology , Encephalitis, Viral/metabolism , Encephalitis, Viral/virology , Host Microbial Interactions , Humans , Inflammation Mediators/metabolism , Oxidative Stress , Pandemics , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/epidemiology , Pneumonia, Viral/metabolism , Pneumonia, Viral/virology , Renin-Angiotensin System , SARS-CoV-2 , Signal Transduction , Spike Glycoprotein, Coronavirus/metabolism , Stroke/epidemiology , Stroke/metabolism , Stroke/virology , Vasodilation , Virulence
15.
J Clin Neurosci ; 77: 227-229, 2020 Jul.
Article in English | MEDLINE | ID: covidwho-186658

ABSTRACT

Coronaviruses are revealed to target the human respiratory system mainly. However, they also have neuro-invasive abilities and might spread from the respiratory system to the central nervous system. Herein, we report four patients with COVID-19 simultaneously diagnosed with acute ischemic stroke. There were four stroke cases with simultaneously diagnosis of Covid-19 till the April 14, 2020 in the city of Sakarya, Turkey. They were aged between 45 and 77 years. All four cases were likely to have contracted the virus in Sakarya. The patients had all commonly reported symptoms of Covid-19. Three patients have elevated D-dimer levels, and two of them had high C-reactive protein (CRP) levels. They were managed symptomatically for both the infection and the stroke. Our findings suggest that ischemic cerebrovascular diseases may simultaneously develop in the course of Covid-19 independently of the critical disease process. Increased inflammation predicted by CRP and D-dimer levels may play a role in the formation of ischemia. In particular, elder patients with prothrombotic risk factors should also be considered for the signs of cerebrovascular events in addition to infectious symptoms.


Subject(s)
Brain Ischemia/complications , Coronavirus Infections/complications , Pneumonia, Viral/complications , Stroke/complications , Aged , Betacoronavirus , Biomarkers/metabolism , Brain Ischemia/metabolism , C-Reactive Protein/metabolism , COVID-19 , Female , Fibrin Fibrinogen Degradation Products/metabolism , Humans , Inflammation/complications , Inflammation/metabolism , Male , Middle Aged , Pandemics , Risk Factors , SARS-CoV-2 , Stroke/metabolism , Turkey
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