Stroke as a Potential Complication of COVID-19-Associated Coagulopathy: A Narrative and Systematic Review of the Literature
Open Access
- 28 September 2020
- journal article
- review article
- Published by MDPI AG in Journal of Clinical Medicine
- Vol. 9 (10), 3137
- https://doi.org/10.3390/jcm9103137
Abstract
Coronavirus disease 2019 (COVID-19) is the most overwhelming medical threat of the past few decades. The infection, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can cause serious illness leading to respiratory insufficiency, and, in severely ill patients, it can progress to multiple organ failure leading to death. It has been noted from the earliest reports that the disease influences the hemostasis system and a hallmark of severe infection is elevated D-dimer levels. The profound coagulation changes in COVID-19 seem to be linked to inflammation-related events and severe endothelial cell injury. Besides the high incidence of venous thromboembolic events in SARS-CoV-2 infections, arterial events, including cerebrovascular events, were found to be associated with the disease. In this review, we aimed to summarize the available literature on COVID-19-associated coagulopathy and thrombosis. Furthermore, we performed a systematic search of the literature to identify the characteristics of stroke in COVID-19. Our findings showed that acute ischemic stroke (AIS) is the most frequent type of stroke occurring in infected patients. In most cases, stroke was severe (median NIHSS:16) and most of the patients had one or more vascular risk factors. Laboratory findings in AIS patients were consistent with COVID-19-associated coagulopathy, and elevated D-dimer levels were the most common finding. The outcome was unfavorable in most cases, as a large proportion of the reported patients died or remained bedridden. Limited data are available as yet on outcomes after acute vascular interventions in COVID-19 patients. In the future, well-designed studies are needed to better understand the risk of stroke in COVID-19, to optimize treatment, and to improve stroke care.Funding Information
- European Regional Development Fund (GINOP-2.3.2-15-2016-00043)
This publication has 47 references indexed in Scilit:
- Failure of Anticoagulant ThromboprophylaxisCritical Care Medicine, 2015
- Delayed induction of proinflammatory cytokines and suppression of innate antiviral response by the novel Middle East respiratory syndrome coronavirus: implications for pathogenesis and treatmentJournal of General Virology, 2013
- Thrombosis as an intravascular effector of innate immunityNature Reviews Immunology, 2012
- Isolation of a Novel Coronavirus from a Man with Pneumonia in Saudi ArabiaThe New England Journal of Medicine, 2012
- Angiotensin II, tissue factor and the thrombotic paradox of hypertensionExpert Review of Cardiovascular Therapy, 2010
- Treatment of Sepsis-Induced Acquired Protein C Deficiency Reverses Angiotensin-Converting Enzyme-2 Inhibition and Decreases Pulmonary Inflammatory ResponseThe Journal of pharmacology and experimental therapeutics, 2008
- HLH‐2004: Diagnostic and therapeutic guidelines for hemophagocytic lymphohistiocytosisPediatric Blood & Cancer, 2006
- Complement Activation in Angiotensin II–Induced Organ DamageCirculation Research, 2005
- Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesisThe Journal of Pathology, 2004
- Epidemiology and cause of severe acute respiratory syndrome (SARS) in Guangdong, People's Republic of China, in February, 2003The Lancet, 2003