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1.
J Stroke Cerebrovasc Dis ; 30(8): 105860, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1240473

ABSTRACT

OBJECTIVES: Amongst all the global catastrophe due to Coronavirus disease 2019, a significant bright spot is a reduction in air pollution as countries undergo lockdowns to limit the spread of infection. Another reduction that has been reported is in the number of strokes presenting to hospitals, despite the virus implicated in causing a hypercoagulable state. Acute exposure to air pollution has been linked to increase in stroke incidence and the improvement in air quality may be responsible for the decrease in stroke presentations. MATERIALS AND METHODS: To explore this hypothesis, we compared the air quality index (AQI) of Karachi, the largest cosmopolitan city of Pakistan, during the lockdown period in 2020 to the same period in the previous year. RESULTS: We found a significant drop in AQI depicting an improvement in air quality. Simultaneously, we identified a drop in number of stroke admissions to less than half from 2019 to 2020 at one of the largest tertiary care hospitals of the city, during this period of interest. CONCLUSION: We hypothesize that one important reason for this drop in stroke admissions, may be an actual reduction in stroke incidence brought about by an improvement in air quality.


Subject(s)
Air Pollutants/adverse effects , Air Pollution/adverse effects , COVID-19 , Environmental Exposure/prevention & control , Ischemic Stroke/epidemiology , Patient Admission/trends , Urban Health/trends , Aged , Environmental Exposure/adverse effects , Environmental Monitoring , Female , Humans , Incidence , Ischemic Stroke/diagnosis , Ischemic Stroke/prevention & control , Male , Middle Aged , Pakistan/epidemiology , Risk Assessment , Risk Factors , Time Factors
2.
Clin Appl Thromb Hemost ; 27: 10760296211002274, 2021.
Article in English | MEDLINE | ID: covidwho-1191430

ABSTRACT

The purpose of this article is to address several challenging questions in the management of young patients (those age 60 and under) who present with ischemic stroke. Do genetic thrombophilic states, strongly associated with venous thrombosis, independently cause arterial events in adults? Should cases of patent foramen ovale be closed with mechanical devices in patients with cryptogenic stroke? What are the optimal treatments for cerebral vein thrombosis, carotid artery dissection, and antiphospholipid syndrome and are DOACs acceptable treatment for these indications? What is the mechanism underlying large vessel stroke in patients with COVID-19? This is a narrative review. We searched PubMed and Embase and American College of physicians Journal club database for English language articles since 2000 looking mainly at randomized clinical trials, Meta analyses, Cochran reviews as well as some research articles viewed to be cutting edge regarding anticoagulation and cerebrovascular disease. Searches were done entering cerebral vein thrombosis, carotid dissection, anticoagulation therapy and stroke, antiphospholipid antibody and stroke, stroke in young adults, cryptogenic stroke and anticoagulation, patent foramen ovale and cryptogenic stroke, COVID-19 and stroke.


Subject(s)
COVID-19/complications , Ischemic Stroke/etiology , Ischemic Stroke/therapy , SARS-CoV-2 , Adult , Aneurysm, Dissecting/complications , Anticoagulants/adverse effects , Anticoagulants/therapeutic use , Antiphospholipid Syndrome/complications , Cervical Vertebrae/blood supply , Female , Foramen Ovale, Patent/complications , Foramen Ovale, Patent/surgery , Humans , Intracranial Thrombosis/etiology , Intracranial Thrombosis/therapy , Ischemic Stroke/prevention & control , Male , Middle Aged , Pandemics , Prognosis , Risk Factors , Thrombophilia/complications
3.
J Stroke Cerebrovasc Dis ; 30(7): 105817, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-1179850

ABSTRACT

Hypercoagulability and virally-mediated vascular inflammation have become well-recognized features of the SARS-CoV-2 virus infection, COVID-19. Of growing concern is the apparent ineffectiveness of therapeutic anticoagulation in preventing thromboembolic events among some at-risk patient subtypes with COVID-19. We present a 43-year-old female with a history of seropositive-antiphospholipid syndrome and systemic lupus erythematosus who developed an acute ischemic stroke in the setting of mild COVID-19 infection despite adherence to chronic systemic anticoagulation. The clinical significance of SARS-CoV-2-mediated endothelial cell dysfunction and its potential to cause macrovascular events in spite of full anticoagulation warrants further investigation and likely represents another disease-defining pathology of COVID-19.


Subject(s)
Anticoagulants/therapeutic use , Antiphospholipid Syndrome/drug therapy , COVID-19/complications , Ischemic Stroke/etiology , Lupus Coagulation Inhibitor/blood , Adult , Antiphospholipid Syndrome/blood , Antiphospholipid Syndrome/complications , Antiphospholipid Syndrome/diagnosis , Biomarkers/blood , COVID-19/diagnosis , Female , Humans , Ischemic Stroke/diagnostic imaging , Ischemic Stroke/prevention & control , Risk Factors , Treatment Failure
4.
Int J Mol Med ; 47(3)2021 03.
Article in English | MEDLINE | ID: covidwho-1067806

ABSTRACT

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.


Subject(s)
COVID-19/physiopathology , Ischemic Stroke/etiology , Thrombophilia/etiology , COVID-19/complications , Humans , Ischemic Stroke/drug therapy , Ischemic Stroke/prevention & control
5.
Cardiol Rev ; 29(1): 43-47, 2021.
Article in English | MEDLINE | ID: covidwho-965899

ABSTRACT

The novel coronavirus (severe acute respiratory syndrome CoV-2 [SARS-CoV-2]), also known as COVID-19, is a single-stranded enveloped RNA virus that created a Public Health Emergency of International Concern in January 2020, with a global case burden of over 15 million in just 7 months. Infected patients develop a wide range of clinical manifestations-typically presenting with fever, cough, myalgia, and fatigue. Severely ill patients may fall victim to acute respiratory distress syndrome, acute heart injuries, neurological manifestations, or complications due to secondary infections. These critically ill patients are also found to have disrupted coagulation function, predisposing them to consumptive coagulopathies, and both venous and thromboembolic complications. Common laboratory findings include thrombocytopenia, elevated D-dimer, fibrin degradation products, and fibrinogen, all of which have been associated with greater disease severity. Many cases of pulmonary embolism have been noted, along with deep vein thrombosis, ischemic stroke, myocardial infarction, and systemic arterial embolism. The pathogenesis of coronavirus has not been completely elucidated, but the virus is known to cause excessive inflammation, endothelial injury, hypoxia, and disseminated intravascular coagulation, all of which contribute to thrombosis formation. These patients are also faced with prolonged immobilization while staying in the hospital or intensive care unit. It is important to have a high degree of suspicion for thrombotic complications as patients may rapidly deteriorate in severe cases. Evidence suggests that prophylaxis with anticoagulation may lead to a lower risk of mortality, although it does not eliminate the possibility. The risks and benefits of anticoagulation treatment should be considered in each case. Patients should be regularly evaluated for bleeding risks and thrombotic complications.


Subject(s)
Blood Coagulation Disorders/blood , COVID-19/blood , Embolism/blood , Thrombosis/blood , Anticoagulants/therapeutic use , Blood Coagulation Disorders/drug therapy , Blood Coagulation Disorders/etiology , Blood Coagulation Disorders/metabolism , COVID-19/complications , COVID-19/drug therapy , COVID-19/metabolism , Cytokine Release Syndrome/blood , Cytokine Release Syndrome/complications , Cytokine Release Syndrome/metabolism , Disseminated Intravascular Coagulation/blood , Disseminated Intravascular Coagulation/etiology , Disseminated Intravascular Coagulation/metabolism , Disseminated Intravascular Coagulation/prevention & control , Embolism/etiology , Embolism/metabolism , Embolism/prevention & control , Endothelium, Vascular/metabolism , Fibrin Fibrinogen Degradation Products/metabolism , Fibrinogen/metabolism , Humans , Hypoxia/blood , Hypoxia/etiology , Hypoxia/metabolism , Immobilization , Inflammation/blood , Inflammation/etiology , Inflammation/metabolism , Ischemic Stroke/blood , Ischemic Stroke/etiology , Ischemic Stroke/metabolism , Ischemic Stroke/prevention & control , Myocardial Infarction/blood , Myocardial Infarction/etiology , Myocardial Infarction/metabolism , Myocardial Infarction/prevention & control , Practice Guidelines as Topic , Pulmonary Embolism/blood , Pulmonary Embolism/etiology , Pulmonary Embolism/metabolism , Pulmonary Embolism/prevention & control , Severity of Illness Index , Thrombocytopenia/blood , Thrombocytopenia/etiology , Thrombosis/etiology , Thrombosis/metabolism , Thrombosis/prevention & control , Venous Thrombosis/blood , Venous Thrombosis/etiology , Venous Thrombosis/metabolism
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