Biomarkers of Coagulation and Inflammation in COVID-19-Associated Ischemic Stroke.
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ABSTRACT:
SUBMITTER: Esenwa C
PROVIDER: S-EPMC8547586 | biostudies-literature | 2021 Nov
REPOSITORIES: biostudies-literature
Publications
Biomarkers of Coagulation and Inflammation in COVID-19-Associated Ischemic Stroke.
Esenwa Charles C Cheng Natalie T NT Luna Jorge J Willey Joshua J Boehme Amelia K AK Kirchoff-Torres Kathryn K Labovitz Daniel D Liberman Ava L AL Mabie Peter P Moncrieffe Khadean K Soetanto Ainie A Lendaris Andrea A Seiden Johanna J Goldman Inessa I Altschul David D Holland Ryan R Benton Joshua J Dardick Joseph J Fernandez-Torres Jenelys J Flomenbaum David D Lu Jenny J Malaviya Avinash A Patel Nikunj N Toma Aureliana A Lord Aaron A Ishida Koto K Torres Jose J Snyder Thomas T Frontera Jennifer J Yaghi Shadi S
Stroke 20210825 11
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| S-EPMC8140646 | biostudies-literature
Project description:(1) Background: Cirrhotic patients have an increased risk for severe COVID-19. We investigated the renin-angiotensin-aldosterone system (RAS), parameters of endothelial dysfunction, inflammation, and coagulation/fibrinolysis in cirrhotic patients and in COVID-19 patients. (2) Methods: 127 prospectively characterized cirrhotic patients (CIRR), along with nine patients with mild COVID-19 (mild-COVID), 11 patients with COVID-19 acute respiratory distress syndrome (ARDS; ARDS-COVID), and 10 healthy subjects (HS) were included in the study. Portal hypertension (PH) in cirrhotic patients was characterized by hepatic venous pressure gradient (HVPG). (3) Results: With increased liver disease severity (Child-Pugh stage A vs. B vs. C) and compared to HS, CIRR patients exhibited higher RAS activity (angiotensin-converting enzyme (ACE), renin, aldosterone), endothelial dysfunction (von Willebrand-factor (VWF) antigen), inflammation (C-reactive protein (CRP), interleukin-6 (IL-6)), and a disturbed coagulation/fibrinolysis profile (prothrombin fragment F1,2, D-dimer, plasminogen activity, antiplasmin activity). Increased RAS activity (renin), endothelial dysfunction (vWF), coagulation parameters (D-dimer, prothrombin fragment F1,2) and inflammation (CRP, IL-6) were significantly altered in COVID patients and followed similar trends from mild-COVID to ARDS-COVID. In CIRR patients, ACE activity was linked to IL-6 (ρ = 0.26; p = 0.003), independently correlated with VWF antigen (aB: 0.10; p = 0.001), and was inversely associated with prothrombin fragment F1,2 (aB: -0.03; p = 0.023) and antiplasmin activity (aB: -0.58; p = 0.006), after adjusting for liver disease severity. (4) Conclusions: The considerable upregulation of the RAS in Child-Pugh B/C cirrhosis is linked to systemic inflammation, endothelial dysfunction, and abnormal coagulation profile. The cirrhosis-associated abnormalities of ACE, IL-6, VWF antigen, and antiplasmin parallel those observed in severe COVID-19.
| S-EPMC8709210 | biostudies-literature
Project description:Since the onset of the COVID-19 pandemic, a substantial proportion of COVID-19 patients had documented thrombotic complications and ischemic stroke. Several mechanisms related to immune-mediated thrombosis, the renin angiotensin system and the effect of SARS-CoV-2 in cardiac and brain tissue may contribute to the pathogenesis of ischemic stroke in patients with COVID-19. Simultaneously, significant strains on global healthcare delivery, including ischemic stroke management, have made treatment of stroke in the setting of COVID-19 particularly challenging. In this review, we summarize the current knowledge on epidemiology, clinical manifestation, and pathophysiology of ischemic stroke in patients with COVID-19 to bridge the gap from bench to bedside and clinical practice during the most challenging global health crisis of the last decades.
| S-EPMC8444875 | biostudies-literature
Project description:The outbreak of the novel coronavirus infectious disease 2019 (COVID-19) caused by the SARS-CoV-2 virus has rapidly spread around the world. Increasing evidence has suggested that patients with COVID-19 may present neurological symptoms, and cerebrovascular diseases are one of the most frequent comorbidities. The markedly elevated D-dimer levels in patients with acute ischemic stroke suggests that SARS-CoV-2 infection may induce an inflammatory response and trigger a hypercoagulation state, thus leading to acute ischemic stroke. Cardioembolism and atherosclerosis in patients with COVID-19 infection may also increase the risk of ischemic stroke. The reduction of the angiotensin-converting enzyme II (ACE2) caused by SARS-CoV-2 binding to the ACE2 receptor can lead to abnormally elevated blood pressure and increase the risk of hemorrhagic stroke. Additionally, the cytokine storm induced by the immune response against the viral infection increases the risk of acute stroke. The management for COVID-19 patients with stroke is not only based on the traditional guidelines, but also based on the experience and new instructions from healthcare workers worldwide who are combatting COVID-19.
| S-EPMC7652923 | biostudies-literature
Project description:BackgroundCardiac injury, as measured by troponin elevation, has been reported among hospitalized coronavirus disease 2019 (COVID-19) patients and portends a poor prognosis. However, how the dynamics of troponin elevation interplay with inflammation and coagulation biomarkers over time is unknown. We assessed longitudinal follow-up of cardiac injury, inflammation and coagulation markers in relation to disease severity and outcome.MethodsWe retrospectively assessed 2068 patients with laboratory-confirmed COVID-19 between January 29 and April 1, 2020 at Tongji Hospital in Wuhan, China. We defined cardiac injury as an increase in high sensitivity cardiac troponin-I (hs-cTnI) above the 99th of the upper reference limit. We explored the dynamics of elevation in hs-cTnI and the relationship with inflammation (interleukin [IL]-6, IL-8, IL-10, IL-2 receptor, tumor necrosis factor-α, C-reactive protein) and coagulation (d-dimer, fibrinogen, international normalized ratio) markers in non-critically ill versus critically ill patients longitudinally and further correlated these markers to survivors and non-survivors.ResultsMedian age was 63 years (first to third quartile 51-70 years), 51.4% of whom were women. When compared to non-critically ill patients (N = 1592, 77.0%), critically ill (defined as requiring mechanical ventilation, in shock or multiorgan failure) patients (N = 476, 23.0%), had more frequent cardiac injury on admission (30.3% vs. 2.3%, p < 0.001), with increased mortality during hospitalization (38.4% vs. 0%, p < 0.001). Among critically ill patients, non-survivors (N = 183) had a continuous increase in hs-cTnI levels during hospitalization, while survivors (N = 293) showed a decrease in hs-cTnI level between day 4 and 7 after admission. Specifically, cardiac injury is an independent marker of mortality among critically ill patients at admission, day 4-7 and 8-14. Consistent positive correlations between hs-cTnI and interleukin (IL)-6 on admission (r = 0.59), day 4-7 (r = 0.66) and day 8-14 (r = 0.61; all p < 0.001) and d-dimer (at the same timepoints r = 0.54; 0.65; 0.61, all p < 0.001) were observed. A similar behavior was observed between hs-cTnI and most of other biomarkers of inflammation and coagulation.ConclusionsCardiac injury commonly occurs in critically ill COVID-19 patients, with increased levels of hs-cTnI beyond day 3 since admission portending a poor prognosis. A consistent positive correlation of hs-cTnI with IL-6 and d-dimer at several timepoints along hospitalization could suggest nonspecific cytokine-mediated cardiotoxicity.
| S-EPMC7438272 | biostudies-literature
Project description:This review provides a summary of the protein and RNA biomarkers that have been studied for the diagnosis and assessment of ischemic stroke. Many of the biomarkers identified relate to the pathophysiology of ischemic stroke, including ischemia of CNS tissue, acute thrombosis and inflammatory response. These biomarkers are summarized by their intended clinical application in ischemic stroke including diagnosis, prediction of stroke severity and outcome, and stratification of patients for stroke therapy. Among the biomarkers discussed are recent whole genome studies using RNA expression profiles to diagnose ischemic stroke and stroke etiology. Though many candidate blood based biomarkers for ischemic stroke have been identified, none are currently used in clinical practice. With further well designed study and careful validation, the development of blood biomarkers to improve the care of patients with ischemic stroke may be achieved.
| S-EPMC3250275 | biostudies-other
Project description:The mechanisms and phenotype of ischemic stroke associated with coronavirus disease 2019 (COVID-19) remain uncertain. A retrospective study was conducted in patients with COVID-19 presenting with ischemic stroke from March 1 to May 25, 2020, and cases with large-vessel occlusion were identified. To provide baseline institutional stroke data within and outside the COVID-19 pandemic, all consecutive ischemic stroke and TIA admissions (COVID and non-COVID) to the hospital during a 10-week period from March 1 to May 10, 2020, were collected and compared with data from the same time period in 2019. Among 20 patients with COVID-19 and acute ischemic stroke, 15 (75%) had large-vessel occlusion. These patients were young (mean age, 46.5 years), male (93%), without major burden of traditional cardiovascular risk factors, and had a severe stroke presentation. Large-vessel occlusions were observed in multiple vessels (40%), uncommonly affected vessels, and atypical locations with a large thrombus burden. Systemic thrombosis separate from large-vessel occlusion was not uncommon (26%). At short-term follow-up, stroke etiology remained undetermined in 46% of patients and functional outcome was poor. The above findings raise the possibility of stroke related to mechanisms induced by the COVID-19 infection itself, including a hypercoagulable state and/or endothelial damage. In addition, they document the severe presentation and poor outcomes of large-vessel occlusion in COVID-19 ischemic stroke.
| S-EPMC7963240 | biostudies-literature
Project description:BackgroundCoronavirus disease 2019 (COVID-19), a contagious infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has spread across the world. Apart from respiratory complications, an increasing number of patients with ischemic stroke have been reporting.ObjectiveThis systematic review and meta-analysis aims to explore the characteristics of ischemic stroke after SARS-CoV-2 infection, and provides valuable reference materials for subsequent clinical treatment.Materials and methodsPubMed, Web of Science, and Ovid-Embase databases were searched up to 24th March 2021. We utilized the search strategy of medical subject headings combined with entry terms to search all related literatures. All studies identified with the electronic and manual searches were listed by citation, title, authors, and abstract. Only studies involving patients with COVID-19-related stroke were eligible. The references of included studies were also manually screened.ResultsThe meta-analysis was conducted following the PRISMA and MOOSE reporting guidelines. Bias risk was assessed using the Newcastle-Ottawa Scale (NOS). Ten articles, including 26,691 participants and 280 patients with ischemic stroke and COVID-19, were selected. The pooled prevalence of ischemic stroke in COVID-19 was 2% (95% CI 1-2%; p < 0.01). The pooled proportions of hypertension, hyperlipidemia and diabetes in COVID-19-related ischemic stroke was 66% (95% CI 51-81%; p < 0.01), 48% (95% CI 19-76%; p < 0.01) and 40% (95% CI 29-51%; p < 0.01), respectively. Notably, the pooled proportions of female was 36% (95% CI 21-50%; p < 0.01) in patients with COVID-19 and stroke. In addition, in TOAST classification, cryptogenic stroke subtype was associated with a high trend, and its pooled proportion was 35% (95% CI 12-59%; p < 0.01).ConclusionIschemic stroke caused by COVID-19 has its own unique clinical features. Although common high-risk factors can also be observed, its importance may have changed. The major inflammatory storm of COVID-19 is more likely to occur in male patients. The increase in the proportion of cryptogenic stroke has also made stroke related to COVID-19 complicated.
| S-EPMC8517946 | biostudies-literature
Project description:BACKGROUND:The outbreak of a novel coronavirus since December 2019, became an emergency of major international concern. As of June 21, 2020, the SARS-CoV-2 pandemic has caused 8,769,844 confirmed infections with 463,745 fatal cases worldwide. The SARS-CoV-2 outbreak is a major challenge for clinicians. In our clinic, we found a rare case that a COVID-19 patient combined with ischemic stroke. CASE PRESENTATION:A 79-year-old man was admitted to the Hubei Provincial Hospital of Traditional Chinese Medicine due to right limb weakness for 1?day and slight cough for 1?week. At presentation, his oxygen saturation was 94.2% on room air and body temperature was 37.3?°C (99.0?°F) with some moist rales. Neurological examination showed right limb weakness, and the limb muscle strength was grade 4. The left leg and arms were unaffected. In addition, runs of speech were not fluent enough with tongue deviation. Laboratory studies showed lymphopenia and eosinophilic granulocytopenia. Chest CT revealed bilateral pulmonary parenchymal ground-glass and consolidative pulmonary opacities, with a peripheral lung distribution. Real-time polymerase chain reaction (RT-PCR) from throat swab sample was positive for SARS-CoV-2 nucleic acid. This patient was treated with antiviral drugs and anti-inflammatory drugs with supportive care until his discharge. Clopidogrel (75?mg) and atorvastatin (20?mg) were administered orally to treat acute ischemic stroke. After 12 days of treatment, he can walk normally and communicate with near fluent language. CONCLUSION:We report an even more unusual case, a patient who was hospitalized for right limb weakness and was later diagnosed with COVID-19. Here, SARS-CoV-2 infection caused hypoxemia and excessive secretion of inflammatory cytokines, which contribute to the occurrence and development of ischemic stroke. Once COVID-19 patients show acute ischemic stroke, neurologists should cooperate with infectious disease doctors to help patients.
| S-EPMC7323364 | biostudies-literature
Project description:The novel coronavirus disease (COVID-19) pandemic has caused an unprecedented worldwide socio-economic and health impact. There is increasing evidence that a combination of inflammation and hypercoagulable state are the main mechanisms of respiratory failure in these patients. This narrative review aims to summarize currently available evidence on the complex interplay of immune dysregulation, hypercoagulability, and thrombosis in the pathogenesis of respiratory failure in COVID-19 disease. In addition, we will describe the experience of anticoagulation and anti-inflammatory strategies that have been tested. Profound suppression of the adaptive and hyperactivity of innate immune systems with macrophage activation appears to be a prominent feature in this infection. Immune dysregulation together with endotheliitis and severe hypercoagulability results in thromboinflammation and microvascular thrombosis in the pulmonary vasculature leading to severe respiratory distress. Currently, some guidelines recommend the use of prophylactic low molecular weight heparin in all hospitalized patients, with intermediate dose prophylaxis in those needing intensive care, and the use of therapeutic anticoagulation in patients with proven or suspected thrombosis. Strong recommendations cannot be made until this approach is validated by trial results. To target the inflammatory cascade, low-dose dexamethasone appears to be helpful in moderate to severe cases and trials with anti-interleukin agents (e.g., tocilizumab, anakinra, siltuximab) and non-steroidal anti-inflammatory drugs are showing early promising results. Potential newer agents (e.g., Janus kinase inhibitor such as ruxolitinib, baricitinib, fedratinib) are likely to be investigated in clinical trials. Unfortunately, current trials are mostly examining these agents in isolation and there may be a significant delay before evidence-based practice can be implemented. It is plausible that a combination of anti-viral drugs together with anti-inflammatory and anti-coagulation medicines will be the most successful strategy in managing severely affected patients with COVID-19.
| S-EPMC7446744 | biostudies-literature