Late‐onset hematological complications post <scp>COVID</scp>‐19: An emerging medical problem for the hematologist

Korompoki, Eleni; Gavriatopoulou, Maria; Fotiou, Despina; Ntanasis‐Stathopoulos, Ioannis; Dimopoulos, Meletios A.; Terpos, Evangelos

doi:10.1002/ajh.26384

Cited by 53 publications

(51 citation statements)

References 76 publications

(105 reference statements)

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“…Long-COVID-19 emerges as a new aspect of the public health crisis triggered by the pandemic [32]. Delayed arterial thrombosis or venous thromboembolism post-COVID-19 is an emerging health problem [33][34][35]. The data presented herein allow to propose that evaluation of blood hypercoagulability (using D-dimer for instance) and endothelial cell activation could offer the possibility of prompt identification of COVID-19 survivors at risk of post-COVID-19 vascular complications.…”

Section: Discussionmentioning

confidence: 92%

Persisting Endothelial Cell Activation and Hypercoagulability after COVID-19 Recovery—The Prospective Observational ROADMAP-Post COVID-19 Study

Gerotziafas

Dreden

Sergentanis

et al. 2022

Hemato

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Background. Hypercoagulable state and endothelial cell activation are common alterations in patients with COVID-19. Nevertheless, the hypothesis of persistent hypercoagulability and endothelial cell activation following recovery from COVID-19 remains an unresolved issue. Objectives. To investigate the persistence of endothelial cell activation and hypercoagulability after recovery from COVID-19. Patients/Methods. COVID-19 survivors (n = 208) and 30 healthy individuals were enrolled in this study. The following biomarkers were measured: procoagulant phospholipid-dependent clotting time (PPL-ct), D-Dimer, fibrin monomers (FM), free Tissue factor pathway inhibitor (free-TFP)I, heparinase, and soluble thrombomodulin (sTM). Antibodies against SARS-CoV-2 (IgG and IgA) were also measured. Results. The median interval between symptom onset and screening for SARS-CoV-2 antibodies was 62 days (IQR = 22 days). Survivors showed significantly higher levels of D-Dimers, FM, TFPI, and heparanase as compared to that of the control group. Survivors had significantly shorter PPL-ct. Elevated D-dimer was associated with older age. Elevated FM was associated with female gender. Elevated heparanase was independently associated with male gender. Decreased Procoag-PPL clotting time was associated with female gender. One out of four of COVID-19 survivors showed increase at least one biomarker of endothelial cell activation or hypercoagulability. Conclusions. Two months after onset of COVID-19, a significant activation of endothelial cells and in vivo thrombin generation persists in at least one out of four survivors of COVID-19. The clinical relevance of these biomarkers in the diagnosis and follow-up of patients with long COVID-19 merits to be evaluated in a prospective clinical study.

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Section: Discussionmentioning

confidence: 92%

Persisting Endothelial Cell Activation and Hypercoagulability after COVID-19 Recovery—The Prospective Observational ROADMAP-Post COVID-19 Study

Gerotziafas

Dreden

Sergentanis

et al. 2022

Hemato

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“…Korompoki et al. also summarized available evidence on post-acute COVID-19 hematological complications ( Korompoki et al., 2022 ). Overall, these studies have shown that persistent coagulation abnormalities and thrombosis are common in long covid.…”

Section: Long Covid Coagulation Abnormalitiesmentioning

confidence: 99%

Long COVID: The Nature of Thrombotic Sequelae Determines the Necessity of Early Anticoagulation

Wang

Jing

et al. 2022

Front. Cell. Infect. Microbiol.

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Many discharged COVID-19 patients affected by sequelae experience reduced quality of life leading to an increased burden on the healthcare system, their families and society at large. Possible pathophysiological mechanisms of long COVID include: persistent viral replication, chronic hypoxia and inflammation. Ongoing vascular endothelial damage promotes platelet adhesion and coagulation, resulting in the impairment of various organ functions. Meanwhile, thrombosis will further aggravate vasculitis contributing to further deterioration. Thus, long COVID is essentially a thrombotic sequela. Unfortunately, there is currently no effective treatment for long COVID. This article summarizes the evidence for coagulation abnormalities in long COVID, with a focus on the pathophysiological mechanisms of thrombosis. Extracellular vesicles (EVs) released by various types of cells can carry SARS-CoV-2 through the circulation and attack distant tissues and organs. Furthermore, EVs express tissue factor and phosphatidylserine (PS) which aggravate thrombosis. Given the persistence of the virus, chronic inflammation and endothelial damage are inevitable. Pulmonary structural changes such as hypertension, embolism and fibrosis are common in long COVID. The resulting impaired lung function and chronic hypoxia again aggravates vascular inflammation and coagulation abnormalities. In this article, we also summarize recent research on antithrombotic therapy in COVID-19. There is increasing evidence that early anticoagulation can be effective in improving outcomes. In fact, persistent systemic vascular inflammation and dysfunction caused by thrombosis are key factors driving various complications of long COVID. Early prophylactic anticoagulation can prevent the release of or remove procoagulant substances, thereby protecting the vascular endothelium from damage, reducing thrombotic sequelae, and improving quality of life for long-COVID patients.

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“…Nevertheless, these impaired vascular endothelial cells often serve as the initial site of thrombosis. At this time, activated vascular endothelial cells are often overlooked, but they are the vulnerable basis of long COVID after discharge ( 31 , 33 , 39 , 43 ). Although vascular endothelial damage is difficult to distinguish clinically, it can be used as a differentiating point in pathology.…”

Section: Pulmonary Vulnerabilitymentioning

confidence: 99%

“…With the enhanced permeability of the alveolar membrane, the pulmonary edema causes further hypoxemia and deterioration ( 23 , 24 ). Pulmonary (micro)thrombus is key to severe hypoxemia, multiple organ dysfunction, and prolonged COVID-19 syndrome ( 25 – 33 ). Microthrombi can block microvessels in the alveolar capillaries, making it difficult for red blood cells to pass through.…”

Section: Introductionmentioning

confidence: 99%

Persistent Lung Injury and Prothrombotic State in Long COVID

et al. 2022

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Lung injury may persist during the recovery period of COVID-19 as shown through imaging, six-minute walk, and lung function tests. The pathophysiological mechanisms leading to long COVID have not been adequately explained. Our aim is to investigate the basis of pulmonary susceptibility during sequelae and the possibility that prothrombotic states may influence long-term pulmonary symptoms of COVID-19. The patient’s lungs remain vulnerable during the recovery stage due to persistent shedding of the virus, the inflammatory environment, the prothrombotic state, and injury and subsequent repair of the blood-air barrier. The transformation of inflammation to proliferation and fibrosis, hypoxia-involved vascular remodeling, vascular endothelial cell damage, phosphatidylserine-involved hypercoagulability, and continuous changes in serological markers all contribute to post-discharge lung injury. Considering the important role of microthrombus and arteriovenous thrombus in the process of pulmonary functional lesions to organic lesions, we further study the possibility that prothrombotic states, including pulmonary vascular endothelial cell activation and hypercoagulability, may affect long-term pulmonary symptoms in long COVID. Early use of combined anticoagulant and antiplatelet therapy is a promising approach to reduce the incidence of pulmonary sequelae. Essentially, early treatment can block the occurrence of thrombotic events. Because impeded pulmonary circulation causes large pressure imbalances over the alveolar membrane leading to the infiltration of plasma into the alveolar cavity, inhibition of thrombotic events can prevent pulmonary hypertension, formation of lung hyaline membranes, and lung consolidation.

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Late‐onset hematological complications post COVID‐19: An emerging medical problem for the hematologist

Cited by 53 publications

References 76 publications

Persisting Endothelial Cell Activation and Hypercoagulability after COVID-19 Recovery—The Prospective Observational ROADMAP-Post COVID-19 Study

Persisting Endothelial Cell Activation and Hypercoagulability after COVID-19 Recovery—The Prospective Observational ROADMAP-Post COVID-19 Study

Long COVID: The Nature of Thrombotic Sequelae Determines the Necessity of Early Anticoagulation

Persistent Lung Injury and Prothrombotic State in Long COVID

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