COVID-19 and simultaneous thrombosis of two coronary arteries.
Ontology highlight
ABSTRACT:
SUBMITTER: Rey JR
PROVIDER: S-EPMC7287480 | biostudies-literature | 2020 Aug
REPOSITORIES: biostudies-literature
Publications
COVID-19 and simultaneous thrombosis of two coronary arteries.
Rey Juan R JR Jiménez Valero Santiago S Poveda Pinedo Dolores D Merino Jose L JL López-Sendón José Luis JL Caro-Codón Juan J
Revista espanola de cardiologia (English ed.) 20200611 8
Similar Datasets
Project description: Not available
| S-EPMC7218359 | biostudies-literature
Project description:We present a case of simultaneous coronary thrombosis of the left main, the left anterior descending artery and the right coronary artery in a patient, recently diagnosed with rheumatoid arthritis.
| S-EPMC4970577 | biostudies-literature
Project description: Not available
| S-EPMC8783786 | biostudies-literature
Project description: Not available
| S-EPMC7239221 | biostudies-literature
Project description:Coronavirus disease 2019 is characterized by its severe respiratory effects. Data early on indicated an increased risk of mortality in patients with cardiovascular comorbidities. Early reports highlighted the multisystem inflammatory syndrome, cytokine storm, and thromboembolic events as part of the disease processes. The aim of this review is to assess the association between COVID-19 and its thrombotic complications, specifically related to the cardiovascular system. The role of neutrophil extracellular traps (NETs) is explored in the pathogenesis of the disease. The structure and anatomy of the virus are pivotal to its virulence in comparison to other α and β Coronaviridae (HCoV-229E, HCoV-OC43, HCoV-229E, HCoV-NL63, HCoV-OC43, and HCoV-HKU1). In particular, the host interaction and response may explain the variability of severity in patients. Angio tensin-converting enzyme 2 (ACE2) activation may be implicated in the cardiovascular and throm bogenic potential of the disease. The virus may also have direct effects on the endothelial lining affecting hemostasis and resulting in thrombosis through several mechanisms. Dipyridamole may have a therapeutic benefit in NET suppression. Therapeutic avenues should be concentrated on the different pathophysiological steps involving the virus and the host.
| S-EPMC8945192 | biostudies-literature
Project description:Thrombotic complications are frequent in COVID-19 and contribute significantly to mortality and morbidity. We review several mechanisms of hypercoagulability in sepsis that may be upregulated in COVID-19. These include immune-mediated thrombotic mechanisms, complement activation, macrophage activation syndrome, antiphospholipid antibody syndrome, hyperferritinemia, and renin-angiotensin system dysregulation. We highlight biomarkers within each pathway with potential prognostic value in COVID-19. Lastly, recent observational studies have evaluated a role for the expanded use of therapeutic anticoagulation in COVID-19. We review strengths and weaknesses of these studies, and we also discuss the hypothetical benefit and anticipated challenges of fibrinolytic therapy in COVID-19.
| S-EPMC7674272 | biostudies-literature
Project description: Not available
| S-EPMC7235975 | biostudies-literature
Project description:ObjectivesPeripheral artery embolizations are often required for therapeutic purposes. The therapeutic embolizations are usually performed using embolization particles and coils. These procedures are also associated with complications. Coils and their delivery cables, and the expertise are not always available in all catheterization centers. Hence, a novel, simple controlled technique for arterial closure would be useful in emergency settings.ResultsFollowing is a report of seven cases where embolization was performed successfully on an emergency basis after stenting using coronary stents for better closure of the target artery. Six patients underwent bronchial artery embolization for recurrent massive hemoptysis, and one another patient had pseudoaneurysm following percutaneous nephrolithotomy, and presented with hematuria and persistent and increasing blood discharge in drainage catheter. The stents were deployed in the target artery using 6F Judkin's diagnostic catheter over the 014 wires, which are easily available in all cardiac catheterization laboratories. This is a novel method to establish a metal platform inside the target arteries using coronary stents for better closure of the target arteries in combination with embolization techniques. The procedures were performed as lifesaving measures when small coils and the delivery cables were not available at the time of the procedures.
| S-EPMC6029168 | biostudies-literature
Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections cause coronavirus disease 2019 (COVID-19) and are associated with inflammation and coagulopathy and high incidence of thrombosis. Myeloid cells (Mϕ) help coordinate the initial immune response in COVID-19. Although we appreciate that Mϕ lie at the nexus of inflammation and thrombosis, the mechanisms that unite the two in COVID-19 remain largely unknown. In this study, we employed systems biology approaches including proteomics, transcriptomics, and mass cytometry to define the circulating proteome and circulating immune cell phenotypes in subjects with COVID-19. In a cohort of COVID-19 subjects (n=35), circulating markers of inflammation (CCL23, IL-6) and vascular dysfunction (ACE2, tissue factor [TF]) were elevated in subjects with severe compared with mild COVID-19. Additionally, although the total white blood cell (WBC) counts were similar between COVID-19 groups, CD14+ monocytes from severe COVID-19 subjects expressed more TF. At baseline, transcriptomics demonstrated increased IL-6, CCL3, ACOD1, C5AR1, C5AR2, and TF in severe COVID-19 subjects compared with controls. Using “stress” transcriptomics, we found that circulating immune cells from severe COVID-19 subjects had evidence of profound immune paralysis with greatly reduced transcriptional activation and release of inflammatory markers in response to Toll-like receptor (TLR) activation. Finally, sera from severe (but not mild) COVID-19 subjects activated human monocytes and induced TF expression. Taken together, these observations further elucidate the pathological mechanisms that underlie immune dysfunction and coagulation abnormalities in COVID-19, contributing to our growing understanding of SARS-CoV-2 infections that could also be leveraged to develop novel diagnostic and therapeutic strategies.
2024-01-23 | GSE247186 | GEO
Project description:Severe coronavirus disease 2019 (COVID-19) increases the risk of myocardial injury that contributes to mortality. This study used multiparameter immunofluorescence to extensively examine heart autopsy tissue of 7 patients who died of COVID-19 compared to 12 control specimens, with or without cardiovascular disease. Consistent with prior reports, no evidence of viral infection or lymphocytic infiltration indicative of myocarditis was found. However, frequent and extensive thrombosis was observed in large and small vessels in the hearts of the COVID-19 cohort, findings that were infrequent in controls. The endothelial lining of thrombosed vessels typically lacked evidence of cytokine-mediated endothelial activation, assessed as nuclear expression of transcription factors p65 (RelA), pSTAT1, or pSTAT3, or evidence of inflammatory activation assessed by expression of intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), tissue factor, or von Willebrand factor (VWF). Intimal EC lining was also generally preserved with little evidence of cell death or desquamation. In contrast, there were frequent markers of neutrophil activation within myocardial thrombi in patients with COVID-19, including neutrophil-platelet aggregates, neutrophil-rich clusters within macrothrombi, and evidence of neutrophil extracellular trap (NET) formation. These findings point to alterations in circulating neutrophils rather than in the endothelium as contributors to the increased thrombotic diathesis in the hearts of COVID-19 patients.
| S-EPMC8479934 | biostudies-literature