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1.
Clin Appl Thromb Hemost ; 27: 10760296211069082, 2021.
Article in English | MEDLINE | ID: covidwho-1575453

ABSTRACT

BACKGROUND: The association between coronavirus infection 2019 (COVID-19) and thrombosis has been explicitly shown through numerous reports that demonstrate high rates of thrombotic complications in infected patients. Recently, much evidence has shown that patients who survived COVID-19 might have a high thrombotic risk after hospital discharge. This current systematic review and meta-analysis was conducted to better understand the incidence of thrombosis, bleeding, and mortality rates among patients discharged after COVID-19 hospitalization. METHODS: Using a search strategy that included terms for postdischarge, thrombosis, and COVID-19, 2 investigators independently searched for published articles indexed in the MEDLINE, Embase, and Scopus databases that were published before August 2021. Pooled incidences and 95% confidence intervals were calculated using the DerSimonian-Laird random-effects model with a double arcsine transformation. RESULTS: Twenty articles were included in the meta-analysis. They provided a total of 19 461 patients discharged after COVID-19 hospitalization. The weighted pooled incidence of overall thrombosis among the patients was 1.3% (95 CI, 0. 6-2; I2 90.5), with a pooled incidence of venous thrombosis of 0.7% (95 CI, 0. 4-1; I2 73.9) and a pooled incidence of arterial thrombosis of 0.6% (95 CI, 0. 2-1; I2 88.1). The weighted pooled incidences of bleeding and mortality were 0.9% (95 CI, 0. 1-1.9; I2 95.1) and 2.8% (95 CI, 0. 6-5; I2 98.2), respectively. CONCLUSIONS: The incidences of thrombosis and bleeding in patients discharged after COVID-19 hospitalization are comparable to those of medically ill patients.


Subject(s)
COVID-19/complications , Hemorrhage/etiology , Thrombosis/etiology , Aged , Aged, 80 and over , Female , Hemorrhage/physiopathology , Humans , Incidence , Male , Middle Aged , Patient Discharge , Risk Factors , Thrombosis/physiopathology
2.
Clin Appl Thromb Hemost ; 27: 10760296211042940, 2021.
Article in English | MEDLINE | ID: covidwho-1484251

ABSTRACT

The world is in a hard battle against COVID-19. Endothelial cells are among the most critical targets of SARS-CoV-2. Dysfunction of endothelium leads to vascular injury following by coagulopathies and thrombotic conditions in the vital organs increasing the risk of life-threatening events. Growing evidences revealed that endothelial dysfunction and consequent thrombotic conditions are associated with the severity of outcomes. It is not yet fully clear that these devastating sequels originate directly from the virus or a side effect of virus-induced cytokine storm. Due to endothelial dysfunction, plasma levels of some biomarkers are changed and relevant clinical manifestations appear as well. Stabilization of endothelial integrity and supporting its function are among the promising therapeutic strategies. Other than respiratory, COVID-19 could be called a systemic vascular disease and this aspect should be scrutinized in more detail in order to reduce related mortality. In the present investigation, the effects of COVID-19 on endothelial function and thrombosis formation are discussed. In this regard, critical players, laboratory findings, clinical manifestation, and suggestive therapies are presented.


Subject(s)
Blood Coagulation , COVID-19/virology , Endothelial Cells/virology , Endothelium, Vascular/virology , SARS-CoV-2/pathogenicity , Thrombosis/virology , Animals , COVID-19/blood , COVID-19/pathology , COVID-19/physiopathology , Endothelial Cells/metabolism , Endothelial Cells/pathology , Endothelium, Vascular/metabolism , Endothelium, Vascular/physiopathology , Host-Pathogen Interactions , Humans , Signal Transduction , Thrombosis/blood , Thrombosis/pathology , Thrombosis/physiopathology
3.
Cells ; 10(9)2021 08 26.
Article in English | MEDLINE | ID: covidwho-1458477

ABSTRACT

The enlightenment of the formation of neutrophil extracellular traps (NETs) as a part of the innate immune system shed new insights into the pathologies of various diseases. The initial idea that NETs are a pivotal defense structure was gradually amended due to several deleterious effects in consecutive investigations. NETs formation is now considered a double-edged sword. The harmful effects are not limited to the induction of inflammation by NETs remnants but also include occlusions caused by aggregated NETs (aggNETs). The latter carries the risk of occluding tubular structures like vessels or ducts and appear to be associated with the pathologies of various diseases. In addition to life-threatening vascular clogging, other occlusions include painful stone formation in the biliary system, the kidneys, the prostate, and the appendix. AggNETs are also prone to occlude the ductal system of exocrine glands, as seen in ocular glands, salivary glands, and others. Last, but not least, they also clog the pancreatic ducts in a murine model of neutrophilia. In this regard, elucidating the mechanism of NETs-dependent occlusions is of crucial importance for the development of new therapeutic approaches. Therefore, the purpose of this review is to address the putative mechanisms of NETs-associated occlusions in the pathogenesis of disease, as well as prospective treatment modalities.


Subject(s)
Embolism/immunology , Extracellular Traps/physiology , Thrombosis/immunology , Animals , Body Fluids/immunology , Body Fluids/physiology , Embolism/physiopathology , Extracellular Traps/immunology , Extracellular Traps/metabolism , Humans , Inflammation/pathology , Neutrophils/immunology , Prospective Studies , Thrombosis/physiopathology
4.
Open Heart ; 8(2)2021 10.
Article in English | MEDLINE | ID: covidwho-1455738

ABSTRACT

BACKGROUND: COVID-19 is a respiratory disease that results in a prothrombotic state manifesting as thrombotic, microthrombotic and thromboembolic events. As a result, several antithrombotic modalities have been implicated in the treatment of this disease. This study aimed to identify if therapeutic anticoagulation (TAC) or concurrent use of antiplatelet and anticoagulants was associated with an improved outcome in this patient population. METHODS: A retrospective observational cohort study of adult patients admitted to a single university hospital for COVID-19 infection was performed. The primary outcome was a composite of in-hospital mortality, intensive care unit (ICU) admission or the need for mechanical ventilation. The secondary outcomes were each of the components of the primary outcome, in-hospital mortality, ICU admission, or the need for mechanical ventilation. RESULTS: 242 patients were included in the study and divided into four subgroups: Therapeutic anticoagulation (TAC), prophylactic anticoagulation+antiplatelet (PACAP), TAC+antiplatelet (TACAP) and prophylactic anticoagulation (PAC) which was the reference for comparison. Multivariable Cox regression analysis and propensity matching were done and showed when compared with PAC, TACAP and TAC were associated with less in-hospital all-cause mortality with an adjusted HR (aHR) of 0.113 (95% CI 0.028 to 0.449) and 0.126 (95% CI 0.028 to 0.528), respectively. The number needed to treat in both subgroups was 11. Furthermore, PACAP was associated with a reduced risk of invasive mechanical ventilation with an aHR of 0.07 (95% CI 0.014 to 0.351). However, the was no statistically significant difference in the occurrence of major or minor bleeds, ICU admission or the composite outcome of in-hospital mortality, ICU admission or the need for mechanical ventilation. CONCLUSION: The use of combined anticoagulant and antiplatelet agents or TAC alone in hospitalised patients with COVID-19 was associated with a better outcome in comparison to PAC alone without an increase in the risk of major and minor bleeds. Sufficiently powered randomised controlled trials are needed to further evaluate the safety and efficacy of combining antiplatelet and anticoagulants agents or using TAC in the management of patients with COVID-19 infection.


Subject(s)
Anticoagulants/therapeutic use , COVID-19/therapy , Platelet Aggregation Inhibitors/therapeutic use , Adult , Aged , Aged, 80 and over , Blood Coagulation/drug effects , COVID-19/blood , COVID-19/complications , COVID-19/mortality , Female , Hospital Mortality , Humans , Inpatients , Intensive Care Units , Male , Middle Aged , Retrospective Studies , SARS-CoV-2 , Survival Analysis , Thromboembolism/drug therapy , Thromboembolism/physiopathology , Thrombosis/drug therapy , Thrombosis/physiopathology , Treatment Outcome
5.
Diabetes Metab Syndr ; 15(5): 102240, 2021.
Article in English | MEDLINE | ID: covidwho-1347578

ABSTRACT

AIMS: To evaluate calculated total plasma osmolality as a marker of outcome prediction, fluid and metabolic balance, thrombotic risk in severe COVID-19 patients. METHODS: Retrospective data of RT-PCR confirmed hospitalized severe COVID-19 patients (total: n = 175 patients, including diabetic subset: n = 102) were analyzed. Clinically applicable cut-offs were derived using receiver operating characteristic (ROC) curve analysis for calculated total osmolality, eGFR, and D-dimer, and their correlations were studied. RESULTS: Among 175 severe COVID-19 patients, a significant association with mortality was seen with respect to calculated total osmolality (p < 0.001), eGFR (p < 0.001), and D-dimer (p < 0.001). In the total cohort, applicable cut-offs based on ROC curve in predicting outcome were, for total osmolality 299 mosm/kg (area under the curve (AUC)-0.773, odds ratio (OR)-1.09), eGFR 61.5 ml/min/m2 (AUC-0.789, OR-0.96), D-dimer 5.13 (AUC-0.814, OR-2.65) respectively. In diabetic subset, the cut-offs for total osmolality were 298 mosm/kg (AUC-0.794, OR-1.12), eGFR 44.9 ml/min/m2 (AUC-0.774, OR-0.96) and D-dimer 1.59 (AUC-0.769, OR-1.52) respectively. CONCLUSIONS: Applicable cut-offs for calculated total plasma osmolality, eGFR, and D-dimer predicts clinical outcome in severe COVID-19 with and without diabetes. Correlation studies validated calculated total osmolality as a marker of the combined effect of fluid and metabolic imbalance, compromised renal function and hypercoagulability.


Subject(s)
COVID-19/diagnosis , Glomerular Filtration Rate/physiology , Plasma/chemistry , Biomarkers/blood , Blood Coagulation/physiology , COVID-19/blood , COVID-19/physiopathology , COVID-19/therapy , Cohort Studies , Diabetes Complications/blood , Diabetes Complications/diagnosis , Diabetes Complications/physiopathology , Diabetes Complications/therapy , Female , Fibrin Fibrinogen Degradation Products/analysis , Fibrin Fibrinogen Degradation Products/metabolism , Humans , India , Male , Middle Aged , Osmolar Concentration , Patient Admission/statistics & numerical data , Prognosis , Retrospective Studies , Risk Factors , Severity of Illness Index , Thrombosis/blood , Thrombosis/diagnosis , Thrombosis/etiology , Thrombosis/physiopathology , Water-Electrolyte Balance/physiology
7.
Int J Mol Sci ; 22(11)2021 May 31.
Article in English | MEDLINE | ID: covidwho-1256566

ABSTRACT

Cells convey information among one another. One instrument employed to transmit data and constituents to specific (target) cells is extracellular vesicles (EVs). They originate from a variety of cells (endothelial, immune cells, platelets, mesenchymal stromal cells, etc.), and consequently, their surface characteristics and cargo vary according to the paternal cell. The cargo could be DNA, mRNA, microRNA, receptors, metabolites, cytoplasmic proteins, or pathological molecules, as a function of which EVs exert different effects upon endocytosis in recipient cells. Recently, EVs have become important participants in a variety of pathologies, including atherogenesis and coronavirus disease 2019 (COVID-19)-associated thrombosis. Herein, we summarize recent advances and some of our own results on the role of EVs in atherosclerotic cardiovascular diseases, and discuss their potential to function as signaling mediators, biomarkers and therapeutic agents. Since COVID-19 patients have a high rate of thrombotic events, a special section of the review is dedicated to the mechanism of thrombosis and the possible therapeutic potential of EVs in COVID-19-related thrombosis. Yet, EV mechanisms and their role in the transfer of information between cells in normal and pathological conditions remain to be explored.


Subject(s)
Atherosclerosis/metabolism , COVID-19/metabolism , Extracellular Vesicles/metabolism , Thrombosis/metabolism , Atherosclerosis/physiopathology , Atherosclerosis/therapy , Atherosclerosis/virology , Biomarkers/metabolism , COVID-19/complications , COVID-19/physiopathology , COVID-19/therapy , Endothelial Cells/metabolism , Humans , Inflammation/immunology , Inflammation/metabolism , Inflammation/virology , Mesenchymal Stem Cells/metabolism , Signal Transduction/immunology , Thrombosis/complications , Thrombosis/physiopathology , Thrombosis/virology
8.
Clin Appl Thromb Hemost ; 27: 10760296211021498, 2021.
Article in English | MEDLINE | ID: covidwho-1249538

ABSTRACT

Today the coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has become a global health problem. After more than a year with the pandemic, although our knowledge has progressed on COVID-19, there are still many unknowns in virological, pathophysiological and immunological aspects. It is obvious that the most efficient solution to end this pandemic are safe and efficient vaccines. This manuscript summarizes the pathophysiological and thrombotic features of COVID-19 and the safety and efficacy of currently approved COVID-19 vaccines with an aim to clarify the recent concerns of thromboembolic events after COVID-19 vaccination. The influx of newer information is rapid, requiring periodic updates and objective assessment of the data on the pathogenesis of COVID-19 variants and the safety and efficacy of currently available vaccines.


Subject(s)
COVID-19 Vaccines/adverse effects , COVID-19/prevention & control , SARS-CoV-2 , Thrombosis/etiology , Autoantibodies/biosynthesis , COVID-19/epidemiology , COVID-19/physiopathology , COVID-19 Vaccines/genetics , COVID-19 Vaccines/immunology , Clinical Trials as Topic , Disseminated Intravascular Coagulation/epidemiology , Disseminated Intravascular Coagulation/etiology , Drug Approval , Female , Genetic Vectors , Glycosaminoglycans/immunology , Humans , Male , Models, Cardiovascular , Pandemics/prevention & control , Platelet Factor 4/immunology , SARS-CoV-2/genetics , SARS-CoV-2/immunology , SARS-CoV-2/pathogenicity , Safety , Sinus Thrombosis, Intracranial/epidemiology , Sinus Thrombosis, Intracranial/etiology , Thrombosis/epidemiology , Thrombosis/physiopathology , Vaccines, Inactivated/adverse effects , Vaccines, Inactivated/genetics , Vaccines, Inactivated/immunology , Vaccines, Synthetic/adverse effects , Vaccines, Synthetic/genetics , Vaccines, Synthetic/immunology
9.
Microcirculation ; 28(7): e12718, 2021 10.
Article in English | MEDLINE | ID: covidwho-1236400

ABSTRACT

Recently, accumulating evidence has highlighted the role of endothelial dysfunction in COVID-19 progression. Coronary microvascular dysfunction (CMD) plays a pivotal role in cardiovascular disease (CVD) and CVD-related risk factors (eg, age, gender, hypertension, diabetes mellitus, and obesity). Equally, these are also risk factors for COVID-19. The purpose of this review was to explore CMD pathophysiology in COVID-19, based on recent evidence. COVID-19 mechanisms were reviewed in terms of imbalanced renin-angiotensin-aldosterone-systems (RAAS), systemic inflammation and immune responses, endothelial dysfunction, and coagulatory disorders. Based on these mechanisms, we addressed CMD pathophysiology within the context of COVID-19, from five perspectives. The first was the disarrangement of local RAAS and Kallikrein-kinin-systems attributable to SARS-Cov-2 entry, and the concomitant decrease in coronary microvascular endothelial angiotensin I converting enzyme 2 (ACE2) levels. The second was related to coronary microvascular obstruction, induced by COVID-19-associated systemic hyper-inflammation and pro-thrombotic state. The third was focused on how pneumonia/acute respiratory distress syndrome (ARDS)-related systemic hypoxia elicited oxidative stress in coronary microvessels and cardiac sympathetic nerve activation. Fourthly, we discussed how autonomic nerve dysfunction mediated by COVID-19-associated mental, physical, or physiological factors could elicit changes in coronary blood flow, resulting in CMD in COVID-19 patients. Finally, we analyzed reciprocity between the coronary microvascular endothelium and perivascular cellular structures due to viremia, SARS-CoV-2 dissemination, and systemic inflammation. These mechanisms may function either consecutively or intermittently, finally culminating in CMD-mediated cardiovascular symptoms in COVID-19 patients. However, the underlying molecular pathogenesis remains to be clarified.


Subject(s)
COVID-19/physiopathology , Coronary Vessels/physiopathology , SARS-CoV-2 , COVID-19/complications , COVID-19/immunology , Cardiovascular Diseases/etiology , Cardiovascular Diseases/physiopathology , Disease Progression , Endothelium, Vascular/physiopathology , Female , Humans , Inflammation/physiopathology , Male , Microcirculation/physiology , Models, Cardiovascular , Renin-Angiotensin System/physiology , Risk Factors , Thrombosis/etiology , Thrombosis/physiopathology
10.
J Thorac Imaging ; 35(6): 344-345, 2020 Nov 01.
Article in English | MEDLINE | ID: covidwho-1219915

ABSTRACT

In this hypothesis paper, we suggest that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may induce intravascular pulmonary thrombosis, which may result in the rapid worsening of clinical conditions and, eventually, exitus. Previously published papers have demonstrated that increased levels of D-dimer at hospital admission correlate with a more severe disease (0.5 mg/L) or occurrence of death (1 mg/L). The potential prothrombotic action of the SARS-CoV-2 is supported by the topographical involvement of the lung regions with a predilection for the lower lobe with peripheral involvement. If this hypothesis is demonstrated, this could suggest the benefit of using antithrombotic/coagulation regimens for SARS-CoV-2 and, at the same time, the urgency to identify drugs that could alter the inflammatory storm, thus protecting the vessel wall.


Subject(s)
COVID-19/complications , COVID-19/physiopathology , Thrombosis/etiology , Thrombosis/physiopathology , COVID-19/blood , Fibrin Fibrinogen Degradation Products/metabolism , Humans , Lung/physiopathology , Lung Diseases/blood , Lung Diseases/etiology , Lung Diseases/physiopathology , SARS-CoV-2 , Thrombosis/blood
11.
Stroke ; 52(5): 1885-1894, 2021 05.
Article in English | MEDLINE | ID: covidwho-1166635

ABSTRACT

The severe acute respiratory syndrome coronavirus 2 or coronavirus disease 2019 (COVID-19) pandemic has raised concerns about the correlation with this viral illness and increased risk of stroke. Although it is too early in the pandemic to know the strength of the association between COVID-19 and stroke, it is an opportune time to review the relationship between acute viral illnesses and stroke. Here, we summarize pathophysiological principles and available literature to guide understanding of how viruses may contribute to ischemic stroke. After a review of inflammatory mechanisms, we summarize relevant pathophysiological principles of vasculopathy, hypercoagulability, and hemodynamic instability. We will end by discussing mechanisms by which several well-known viruses may cause stroke in an effort to inform our understanding of the relationship between COVID-19 and stroke.


Subject(s)
Brain Ischemia/complications , Brain Ischemia/physiopathology , COVID-19/complications , COVID-19/epidemiology , Ischemic Stroke/complications , Ischemic Stroke/physiopathology , Acute Disease , Blood Coagulation , Brain Ischemia/virology , Hemodynamics , Herpesvirus 3, Human , Humans , Inflammation/physiopathology , Ischemic Stroke/virology , Pandemics , Plaque, Atherosclerotic/physiopathology , Risk , Thrombophilia/physiopathology , Thrombosis/physiopathology , Vascular Diseases/physiopathology , Virus Diseases/physiopathology
12.
Cardiol Rev ; 29(3): 143-149, 2021.
Article in English | MEDLINE | ID: covidwho-1148006

ABSTRACT

The coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 has affected the health of people across the globe. Cardiovascular diseases (CVDs) have a significant relationship with COVID-19, both as a risk factor and prognostic indicator, and as a complication of the disease itself. In addition to predisposing to CVD complications, the ongoing pandemic has severely affected the delivery of timely and appropriate care for cardiovascular conditions resulting in increased mortality. The etiology behind the cardiac injury associated with severe acute respiratory syndrome coronavirus-2 is likely varied, including coronary artery disease, microvascular thrombosis, myocarditis, and stress cardiomyopathy. Further large-scale investigations are needed to better determine the underlying mechanism of myocardial infarction and other cardiac injury in COVID-19 patients and to determine the incidence of each type of cardiac injury in this patient population. Telemedicine and remote monitoring technologies can play an important role in optimizing outcomes in patients with established CVD. In this article, we summarize the various impacts that COVID-19 has on the cardiovascular system, including myocardial infarction, myocarditis, stress cardiomyopathy, thrombosis, and stroke.


Subject(s)
COVID-19/physiopathology , Cardiovascular Diseases/physiopathology , COVID-19/complications , COVID-19/epidemiology , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/etiology , Comorbidity , Coronary Artery Disease/epidemiology , Coronary Artery Disease/etiology , Coronary Artery Disease/physiopathology , Coronary Thrombosis/etiology , Coronary Thrombosis/physiopathology , Heart Disease Risk Factors , Humans , Ischemic Stroke/epidemiology , Ischemic Stroke/etiology , Ischemic Stroke/physiopathology , Microvessels , Myocardial Infarction/epidemiology , Myocardial Infarction/etiology , Myocardial Infarction/physiopathology , Myocarditis/etiology , Myocarditis/physiopathology , SARS-CoV-2 , Stroke/epidemiology , Stroke/etiology , Stroke/physiopathology , Takotsubo Cardiomyopathy/etiology , Takotsubo Cardiomyopathy/physiopathology , Thrombosis/etiology , Thrombosis/physiopathology
13.
Eur J Clin Invest ; 51(5): e13546, 2021 May.
Article in English | MEDLINE | ID: covidwho-1142880
14.
Glob Heart ; 16(1): 14, 2021 02 12.
Article in English | MEDLINE | ID: covidwho-1143732

ABSTRACT

Background: Infection caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) exhibits a strong infectivity but less virulence compared to severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS). In terms of cardiovascular morbidity, susceptible population include elderly and patients with certain cardiovascular conditions. This infection has been associated with cardiac injury, cardiovascular complications and higher mortality. Objectives: The main objective of the CARDIO COVID 19-20 Registry is to determine the presence of cardiovascular comorbidities and cardiovascular complications in COVID-19 infected patients that required in-hospital treatment in different Latin American institutions. Methods: The CARDIO COVID 19-20 Registry is an observational, multicenter, ambispective, and hospital-based registry of patients with confirmed COVID-19 infection who required in-hospital treatment in Latin America. Enrollment of patients started on May 01, 2020 and was initially planned to last three months; based on the progression of pandemic in Latin America, enrollment was extended until December 2020, and could be extended once again based on the pandemic course in our continent at that moment. Conclusions: The CARDIO COVID 19-20 Registry will characterize the in-hospital population diagnosed with COVID-19 in Latin America in order to identify risk factors for worsening of cardiovascular comorbidities or for the appearance of cardiovascular complications during hospitalization and during the 30-day follow up period.


Subject(s)
COVID-19/epidemiology , Cardiovascular Diseases/epidemiology , Registries , Arrhythmias, Cardiac/epidemiology , Arrhythmias, Cardiac/etiology , Arrhythmias, Cardiac/physiopathology , COVID-19/complications , COVID-19/physiopathology , Cardiovascular Diseases/etiology , Cardiovascular Diseases/physiopathology , Comorbidity , Coronary Disease/epidemiology , Coronary Disease/etiology , Coronary Disease/physiopathology , Heart Failure/epidemiology , Heart Failure/etiology , Heart Failure/physiopathology , Humans , Latin America , Myocarditis/epidemiology , Myocarditis/etiology , Myocarditis/physiopathology , SARS-CoV-2 , Thrombosis/epidemiology , Thrombosis/etiology , Thrombosis/physiopathology
15.
Cancer Res ; 81(5): 1209-1211, 2021 03 01.
Article in English | MEDLINE | ID: covidwho-1133379

ABSTRACT

Patients with cancer are more susceptible to be infected by SARS-CoV-2 and develop severe outcomes including ICU admittance, mechanical ventilator support, and a high rate of mortality. Like mid-to late-stage cancer, SARS-CoV-2 infection is associated with platelet hyperactivity, systemic inflammation, thrombotic complications, and coagulopathy. Platelets also promote cancer cell growth, survival in circulation, and angiogenesis at sites of metastases. In this article, we will discuss the potential for platelets in the development of systemic inflammation and thrombosis in SARS-CoV-2-infected patients with cancer, with the concern that the platelet-induced pathogenic events are likely magnified in cancer patients with COVID-19.


Subject(s)
COVID-19/physiopathology , Neoplasms/physiopathology , Platelet Activation/physiology , SARS-CoV-2/isolation & purification , Blood Platelets/physiology , COVID-19/diagnosis , COVID-19/virology , Humans , Inflammation/physiopathology , Neoplasms/diagnosis , Risk Assessment/methods , Risk Assessment/statistics & numerical data , Risk Factors , SARS-CoV-2/physiology , Thrombosis/physiopathology
16.
Crit Care ; 25(1): 95, 2021 03 08.
Article in English | MEDLINE | ID: covidwho-1123662

ABSTRACT

Endothelial cells play a key role in maintaining intravascular patency through their anticoagulant properties. They provide a favorable environment for plasma anticoagulant proteins, including antithrombin, tissue factor pathway inhibitor, and protein C. Under septic conditions, however, the anticoagulant properties of endothelial cells are compromised. Rather, activated/injured endothelial cells can provide a scaffold for intravascular coagulation. For example, the expression of tissue factor, an important initiator of the coagulation pathway, is induced on the surface of activated endothelial cells. Phosphatidylserine, a high-affinity scaffold for gamma-carboxyglutamate domain containing coagulation factors, including FII, FVII, FIX, and FX, is externalized to the outer leaflet of the plasma membrane of injured endothelial cells. Hemodilution decreases not only coagulation factors but also plasma anticoagulant proteins, resulting in unleashed activation of coagulation on the surface of activated/injured endothelial cells. The aberrant activation of coagulation can be suppressed in part by the supplementation of recombinant antithrombin and recombinant thrombomodulin. This review aims to overview the physiological and pathological functions of endothelial cells along with proof-of-concept in vitro studies. The pathophysiology of COVID-19-associated thrombosis is also discussed.


Subject(s)
COVID-19/complications , Disseminated Intravascular Coagulation/physiopathology , Endothelial Cells/pathology , Sepsis/physiopathology , COVID-19/physiopathology , Clinical Trials, Phase III as Topic , Humans , Randomized Controlled Trials as Topic , Thrombosis/physiopathology , Thrombosis/virology
17.
J Med Case Rep ; 15(1): 112, 2021 Mar 02.
Article in English | MEDLINE | ID: covidwho-1115251

ABSTRACT

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 infection can lead to a constellation of viral and immune symptoms called coronavirus disease 2019. Emerging literature increasingly supports the premise that severe acute respiratory syndrome coronavirus 2 promotes a prothrombotic milieu. However, to date there have been no reports of acute aortic occlusion, itself a rare phenomenon. We report a case of fatal acute aortic occlusion in a patient with coronavirus disease 2019. CASE REPORT: A 59-year-old Caucasian male with past medical history of peripheral vascular disease presented to the emergency department for evaluation of shortness of breath, fevers, and dry cough. His symptoms started 5-7 days prior to the emergency department visit, and he received antibiotics in the outpatient setting without any effect. He was found to be febrile, tachypneic, and hypoxemic. He was placed on supplemental oxygen via a non-rebreather mask. Chest X-ray showed multifocal opacifications. Intravenous antibiotics for possible pneumonia were initiated. Hydroxychloroquine was initiated to cover possible coronavirus disease 2019 pneumonia. During the hospitalization, the patient became progressively hypoxemic, for which he was placed on bilevel positive airway pressure. D-dimer, ferritin, lactate dehydrogenase, and C-reactive protein were all elevated. Severe acute respiratory syndrome coronavirus 2 reverse transcription polymerase chain reaction was positive. On day 3, the patient was upgraded to the intensive care unit. Soon after he was intubated, he developed a mottled appearance of skin, which extended from his bilateral feet up to the level of the subumbilical plane. Bedside ultrasound revealed an absence of flow from the mid-aorta to both common iliac arteries. The patient was evaluated emergently by vascular surgery. After a discussion with the family, it was decided to proceed with comfort-directed care, and the patient died later that day. DISCUSSION: Viral infections have been identified as a source of prothrombotic states due to direct injury of vascular tissue and inflammatory cascades. Severe acute respiratory syndrome coronavirus 2 appears to follow a similar pattern, with numerous institutions identifying elevated levels of thrombotic complications. We believe that healthcare providers should be aware of both venous and arterial thrombotic complications associated with coronavirus disease 2019, including possible fatal outcome.


Subject(s)
Aortic Diseases , Arterial Occlusive Diseases , SARS-CoV-2 , Thrombosis , Ultrasonography/methods , Aorta, Abdominal/diagnostic imaging , Aortic Diseases/diagnosis , Aortic Diseases/etiology , Aortic Diseases/physiopathology , Arterial Occlusive Diseases/diagnosis , Arterial Occlusive Diseases/etiology , Arterial Occlusive Diseases/physiopathology , Blood Coagulation , COVID-19/blood , COVID-19/complications , COVID-19/physiopathology , COVID-19/therapy , COVID-19 Nucleic Acid Testing/methods , Clinical Deterioration , Fatal Outcome , Humans , Male , Middle Aged , Patient Comfort , Point-of-Care Testing , SARS-CoV-2/isolation & purification , SARS-CoV-2/pathogenicity , Thrombosis/diagnostic imaging , Thrombosis/etiology , Thrombosis/physiopathology
18.
ACS Chem Neurosci ; 12(4): 573-580, 2021 02 17.
Article in English | MEDLINE | ID: covidwho-1065791

ABSTRACT

Long-COVID is a postviral illness that can affect survivors of COVID-19, regardless of initial disease severity or age. Symptoms of long-COVID include fatigue, dyspnea, gastrointestinal and cardiac problems, cognitive impairments, myalgia, and others. While the possible causes of long-COVID include long-term tissue damage, viral persistence, and chronic inflammation, the review proposes, perhaps for the first time, that persistent brainstem dysfunction may also be involved. This hypothesis can be split into two parts. The first is the brainstem tropism and damage in COVID-19. As the brainstem has a relatively high expression of ACE2 receptor compared with other brain regions, SARS-CoV-2 may exhibit tropism therein. Evidence also exists that neuropilin-1, a co-receptor of SARS-CoV-2, may be expressed in the brainstem. Indeed, autopsy studies have found SARS-CoV-2 RNA and proteins in the brainstem. The brainstem is also highly prone to damage from pathological immune or vascular activation, which has also been observed in autopsy of COVID-19 cases. The second part concerns functions of the brainstem that overlap with symptoms of long-COVID. The brainstem contains numerous distinct nuclei and subparts that regulate the respiratory, cardiovascular, gastrointestinal, and neurological processes, which can be linked to long-COVID. As neurons do not readily regenerate, brainstem dysfunction may be long-lasting and, thus, is long-COVID. Indeed, brainstem dysfunction has been implicated in other similar disorders, such as chronic pain and migraine and myalgic encephalomyelitis or chronic fatigue syndrome.


Subject(s)
Brain Diseases/physiopathology , Brain Stem/physiopathology , COVID-19/complications , Inflammation/physiopathology , Thrombosis/physiopathology , Angiotensin-Converting Enzyme 2/metabolism , Brain Diseases/metabolism , Brain Diseases/virology , Brain Stem/blood supply , Brain Stem/metabolism , Brain Stem/virology , COVID-19/metabolism , COVID-19/physiopathology , Humans , Inflammation/metabolism , Inflammation/virology , Neuropilin-1/metabolism , RNA, Viral/isolation & purification , RNA, Viral/metabolism , Receptors, Coronavirus/metabolism , SARS-CoV-2/genetics , SARS-CoV-2/pathogenicity , Thrombosis/metabolism , Thrombosis/virology , Viral Tropism
20.
Int J Cardiovasc Imaging ; 37(5): 1539-1550, 2021 May.
Article in English | MEDLINE | ID: covidwho-1002114

ABSTRACT

During the COVID-19 pandemic, transesophageal echocardiography (TEE) for left atrial appendage thrombosis (LAAT) detection should be limited to situations of absolute necessity. We sought to identify the main conventional and functional echocardiographic parameters associated with LAAT on TEE in non-valvular atrial fibrillation (NVAF) patients planned for electrical cardioversion (ECV). This retrospective study included 125 consecutive NVAF patients (71.5±7.8 yrs, 75 males), who underwent TEE at our Institution between April 2016 and January 2020, to exclude LAAT before scheduled ECV. All patients underwent a transthoracic echocardiography (TTE) implemented with speckle tracking echocardiography (STE) analysis of left atrial (LA) strain and strain rate (SR) parameters. 28% of patients were diagnosed with LAAT, while 72% without LAAT. Compared to controls, patients with LAAT had significantly higher CHA2DS2-Vasc Score and average E/e' ratio, and significantly lower left ventricular ejection fraction (LVEF). Moreover, LA-peak positive global atrial strain (GSA+) and LA-SR parameters were significantly reduced in patients with LAAT. Multivariate logistic regression revealed that, differently from CHA2DS2-Vasc Score, LVEF (OR 0.88, 95%CI 0.81-0.97, p = 0.01), average E/e' ratio (OR 2.36, 95%CI 1.41-3.98, p = 0.001), and LA-GSA+ (OR 0.57, 95%CI 0.36-0-90, p = 0.01) were independently associated with LAAT. LA-GSA+ (optimal cut-off ≤ 9.1%, AUC 0.95) showed the highest diagnostic performance. Finally, a strong linear correlation of LA peak-to-peak SR with both LA appendage filling (r = 0.86) and emptying (r = 0.83) velocities was demonstrated. TTE implemented with STE analysis of LA mechanics improves thrombotic risk assessment of NVAF patients.


Subject(s)
Atrial Appendage/diagnostic imaging , Atrial Fibrillation/physiopathology , Risk Assessment , Thrombosis/diagnostic imaging , Aged , Atrial Appendage/physiopathology , Case-Control Studies , Echocardiography , Echocardiography, Transesophageal , Electric Countershock , Female , Humans , Male , Retrospective Studies , Stroke Volume/physiology , Thrombosis/physiopathology
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