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1.
Case Rep Cardiol ; 2022: 5640965, 2022.
Article in English | MEDLINE | ID: covidwho-1832688

ABSTRACT

Both COVID-19 disease and cocaine consumption have prothrombotic and hypercoagulable effects and are associated with increased risk of cardiovascular events. We report the case of a patient with acute myocardial infarction in the setting of active COVID-19 disease and recent cocaine consumption. We hypothesize that COVID-19 and cocaine synergistically provoke cardiovascular events. Identifying COVID-19 disease and/or cocaine abuse as potential triggers of acute myocardial infarction can be crucial due to distinctive therapeutic consequences.

2.
EuropePMC; 2022.
Preprint in English | EuropePMC | ID: ppcovidwho-330954

ABSTRACT

Background: Acute myocardial injury is associated with poor prognosis in respiratory tract infections. We aimed to highlight the differences in prevalence of myocardial injury and its impact on prognosis in patients with COVID-19 compared to those with seasonal influenza. Methods: : This was a single-center prospective cohort study with a historical control group. 300 age-/sex-matched SARS-CoV-2 and seasonal influenza positive patients were enrolled. Myocardial injury was assessed by electrocardiogram (ECG), transthoracic echocardiography and biomarkers including high-sensitivity troponin-I. All patients were followed-up for 30 days after enrollment for all-cause mortalitiy, admission to the intensive care unit (ICU) and mechanical ventilation. Results: : Right ventricular distress was more common in COVID-19 whereas pathological ECG findings and impaired left ventricular function were more prevalent among influenza patients. COVID-19 patients suffered from a higher percentage of hypertension and dyslipidaemia. Contrary to COVID-19, pericardial effusion at admission was associated with poor outcome in the influenza group. Severe course of disease and respiratory failure resulted in significantly higher rates of ICU treatment and mechanical ventilation in COVID-19 patients. Although distribution of myocardial injury was similar, significantly fewer cardiac catheterizations were performed in COVID-19 patients. However, number of cardiac catheterizations was low in both groups. Finally, 30-day mortality was significantly higher in COVID-19 compared to influenza patients. Conclusions: : In adults requiring hospitalization due to COVID-19 or seasonal influenza, cardiovascular risk factors and signs of myocardial distress differ significantly. Furthermore, cardiovascular comorbidities may impair prognosis in COVID-19 patients to a higher degree than in their influenza counterparts.

3.
EuropePMC; 2021.
Preprint in English | EuropePMC | ID: ppcovidwho-311512

ABSTRACT

Background: Some recipients of ChAdOx1 nCoV-19 COVID-19 Vaccine AstraZeneca develop antibody-mediated vaccine-induced thrombotic thrombocytopenia (VITT), associated with cerebral venous and other unusual thrombosis resembling autoimmune heparin-induced thrombocytopenia. A prothrombotic predisposition is also observed in Covid-19. We explored whether antibodies against the SARS-CoV-2 spike protein induced by Covid-19 cross-react with platelet factor 4 (PF4/CXLC4), the protein targeted in both VITT and autoimmune heparin-induced thrombocytopenia. Methods: Immunogenic epitopes of PF4 and SARS-CoV-2 spike protein were compared via prediction tools and 3D modelling software (IMED, SIM, MacMYPOL). Sera from 222 PCR-confirmed Covid-19 patients from five European centers were tested by PF4/heparin ELISA, heparin-dependent and PF4-dependent platelet activation assays. Immunogenic reactivity of purified anti-PF4 and anti-PF4/heparin antibodies from patients with VITT were tested against recombinant SARS-CoV-2 spike protein. Results: Three motifs within the spike protein sequence share a potential immunogenic epitope with PF4. Nineteen of 222 (8.6%) Covid-19 patient sera tested positive in the IgG-specific PF4/heparin ELISA, none of which showed platelet activation in the heparin-dependent activation assay, including 10 (4.5%) of the 222 Covid-19 patients who developed thromboembolic complications. Purified anti-PF4 and anti-PF4/heparin antibodies from two VITT patients did not show cross-reactivity to recombinant SARS-CoV-2 spike protein. Conclusions: The antibody responses to PF4 in SARS-CoV-2 infection and after vaccination with COVID-19 Vaccine AstraZeneca differ. Antibodies against SARS-CoV-2 spike protein do not cross-react with PF4 or PF4/heparin complexes through molecular mimicry. These findings make it very unlikely that the intended vaccine-induced immune response against SARS-CoV-2 spike protein would itself induce VITT.

4.
Hamostaseologie ; 2021 Dec 08.
Article in English | MEDLINE | ID: covidwho-1559127

ABSTRACT

SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection is associated with high risk of venous and arterial thrombosis. Thrombotic complications, especially pulmonary embolism, lead to increased all-cause mortality in both intensive care unit and noncritically ill patients. Damage and activation of vascular endothelium, platelet activation, followed by thrombotic and fibrinolytic imbalance as well as hypercoagulability are the key pathomechanisms in immunothrombosis leading to a significant increase in thromboembolism in coronavirus disease 2019 (COVID-19) compared with other acute illnesses. In this review article, we discuss the incidence and prognosis, diagnosis, prevention, and treatment of venous thromboembolism in patients with COVID-19 disease, based on clinical experience and research available to date.

5.
Blood Adv ; 6(1): 248-258, 2022 01 11.
Article in English | MEDLINE | ID: covidwho-1507130

ABSTRACT

Thromboembolic events are frequently reported in patients infected with the SARS-CoV-2 virus. The exact mechanisms of COVID-19-associated hypercoagulopathy, however, remain elusive. Recently, we observed that platelets (PLTs) from patients with severe COVID-19 infection express high levels of procoagulant markers, which were found to be associated with increased risk for thrombosis. In the current study, we investigated the time course as well as the mechanisms leading to procoagulant PLTs in COVID-19. Our study demonstrates the presence of PLT-reactive IgG antibodies that induce marked changes in PLTs in terms of increased inner-mitochondrial transmembrane potential (Δψ) depolarization, phosphatidylserine (PS) externalization, and P-selectin expression. The IgG-induced procoagulant PLTs and increased thrombus formation were mediated by ligation of PLT Fc-γ RIIA (FcγRIIA). In addition, contents of calcium and cyclic-adenosine-monophosphate (cAMP) in PLTs were identified to play a central role in antibody-induced procoagulant PLT formation. Most importantly, antibody-induced procoagulant events, as well as increased thrombus formation in severe COVID-19, were inhibited by Iloprost, a clinically approved therapeutic agent that increases the intracellular cAMP levels in PLTs. Our data indicate that upregulation of cAMP could be a potential therapeutic target to prevent antibody-mediated coagulopathy in COVID-19 disease.


Subject(s)
COVID-19 , Thrombosis , Calcium , Humans , SARS-CoV-2 , Thrombosis/etiology , Up-Regulation
6.
Hamostaseologie ; 41(5): 379-385, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1483188

ABSTRACT

In 2019 first reports about a new human coronavirus emerged, which causes common cold symptoms as well as acute respiratory distress syndrome. The virus was identified as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and severe thrombotic events including deep vein thrombosis, pulmonary embolism, and microthrombi emerged as additional symptoms. Heart failure, myocardial infarction, myocarditis, and stroke have also been observed. As main mediator of thrombus formation, platelets became one of the key aspects in SARS-CoV-2 research. Platelets may also directly interact with SARS-CoV-2 and have been shown to carry the SARS-CoV-2 virus. Platelets can also facilitate the virus uptake by secretion of the subtilisin-like proprotein convertase furin. Cleavage of the SARS-CoV-2 spike protein by furin enhances binding capabilities and virus entry into various cell types. In COVID-19 patients, platelet count differs between mild and serious infections. Patients with mild symptoms have a slightly increased platelet count, whereas thrombocytopenia is a hallmark of severe COVID-19 infections. Low platelet count can be attributed to platelet apoptosis and the incorporation of platelets into microthrombi (peripheral consumption) and severe thrombotic events. The observed excessive formation of thrombi is due to hyperactivation of platelets caused by the infection. Various factors have been suggested in the activation of platelets in COVID-19, such as hypoxia, vessel damage, inflammatory factors, NETosis, SARS-CoV-2 interaction, autoimmune reactions, and autocrine activation. COVID-19 does alter chemokine and cytokine plasma concentrations. Platelet chemokine profiles are altered in COVID-19 and contribute to the described chemokine storms observed in severely ill COVID-19 patients.


Subject(s)
Blood Platelets/physiology , Blood Platelets/virology , COVID-19/blood , Blood Platelets/immunology , COVID-19/complications , COVID-19/immunology , Chemokines/blood , Cytokine Release Syndrome/blood , Cytokine Release Syndrome/etiology , Host Microbial Interactions/immunology , Host Microbial Interactions/physiology , Humans , Models, Biological , Pandemics , Platelet Activation/immunology , Platelet Activation/physiology , SARS-CoV-2/pathogenicity , Thrombosis/blood , Thrombosis/etiology
7.
Hamostaseologie ; 41(5): 347-348, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1483172

ABSTRACT

The COVID-19 pandemic is still threatening us, our patients, and the global health care system. Since the first outbreak at the end of 2019 in China, it became rapidly clear that a new variant of a SARS virus, SARS-CoV-2, is threatening our human society worldwide. Since then, the scientific community has accumulated an incredibly large amount of knowledge about the pathophysiology of this virus, primarily affecting the respiratory tract and, in severe cases, subsequently resulting in acute respiratory distress syndrome and multiple organ failure due to uncontrolled systemic inflammatory response syndrome.1 2.


Subject(s)
COVID-19/physiopathology , SARS-CoV-2 , Biomarkers/metabolism , Blood Vessels/physiopathology , COVID-19/complications , Cardiovascular Diseases/etiology , Cardiovascular Diseases/physiopathology , Heart/physiopathology , Humans , Lung/physiopathology , Pandemics , SARS-CoV-2/pathogenicity
8.
Hamostaseologie ; 41(5): 400-402, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1397934

ABSTRACT

In this case report we present a previously healthy 21-year-old male with extensive thromboembolism in the setting of asymptomatic COVID-19 infection and heterozygous factor V Leiden mutation with no additional thrombophilic risk factors.


Subject(s)
COVID-19/complications , Factor V/genetics , SARS-CoV-2 , Thromboembolism/complications , Thromboembolism/genetics , Asymptomatic Infections , COVID-19/diagnosis , COVID-19/diagnostic imaging , Computed Tomography Angiography , Heterozygote , Humans , Male , Thromboembolism/therapy , Young Adult
9.
Cardiovasc Res ; 117(1): 224-239, 2021 01 01.
Article in English | MEDLINE | ID: covidwho-1387842

ABSTRACT

AIMS: To elucidate the prognostic role of monocytes in the immune response of patients with coronary artery disease (CAD) at risk for life-threatening heart and lung injury as major complications of SARS-CoV-2 infection. METHODS AND RESULTS: From February to April 2020, we prospectively studied a cohort of 96 participants comprising 47 consecutive patients with CAD and acute SARS-CoV-2 infection (CAD + SARS-CoV-2), 19 CAD patients without infections, and 30 healthy controls. Clinical assessment included blood sampling, echocardiography, and electrocardiography within 12 h of admission. Respiratory failure was stratified by the Horovitz Index (HI) as moderately/severely impaired when HI ≤200 mmHg. The clinical endpoint (EP) was defined as HI ≤200 mmHg with subsequent mechanical ventilation within a follow-up of 30 days. The numbers of CD14dimCD16+ non-classical monocytes in peripheral blood were remarkably low in CAD + SARS-CoV-2 compared with CAD patients without infection and healthy controls (P < 0.0001). Moreover, these CD14dimCD16 monocytes showed decreased expression of established markers of adhesion, migration, and T-cell activation (CD54, CD62L, CX3CR1, CD80, and HLA-DR). Decreased numbers of CD14dimCD16+ monocytes were associated with the occurrence of EP. Kaplan-Meier curves illustrate that CAD + SARS-CoV-2 patients with numbers below the median of CD14dimCD16+ monocytes (median 1443 cells/mL) reached EP significantly more often compared to patients with numbers above the median (log-rank 5.03, P = 0.025). CONCLUSION: Decreased numbers of CD14dimCD16+ monocytes are associated with rapidly progressive respiratory failure in CAD + SARS-CoV-2 patients. Intensified risk assessments comprising monocyte sub- and phenotypes may help to identify patients at risk for respiratory failure.


Subject(s)
COVID-19/complications , Coronary Artery Disease/complications , Lipopolysaccharide Receptors/analysis , Monocytes/physiology , Receptors, IgG/analysis , SARS-CoV-2 , Aged , Aged, 80 and over , COVID-19/immunology , Coronary Artery Disease/immunology , Female , GPI-Linked Proteins/analysis , Humans , Immunohistochemistry , Male , Middle Aged , Monocytes/immunology , Phenotype , Retrospective Studies
10.
Heart Lung ; 50(6): 914-918, 2021.
Article in English | MEDLINE | ID: covidwho-1336454

ABSTRACT

BACKGROUND: Acute respiratory distress syndrome (ARDS) is considered the main cause of COVID-19 associated morbidity and mortality. Early and reliable risk stratification is of crucial clinical importance in order to identify persons at risk for developing a severe course of disease. Deceleration capacity (DC) of heart rate as a marker of cardiac autonomic function predicts outcome in persons with myocardial infarction and heart failure. We hypothesized that reduced modulation of heart rate may be helpful in identifying persons with COVID-19 at risk for developing ARDS. METHODS: We prospectively enrolled 60 consecutive COVID-19 positive persons presenting at the University Hospital of Tuebingen. Arterial blood gas analysis and 24 h-Holter ECG recordings were performed and analyzed at admission. The primary end point was defined as development of ARDS with regards to the Berlin classification. RESULTS: 61.7% (37 of 60 persons) developed an ARDS. In persons with ARDS DC was significantly reduced when compared to persons with milder course of infection (3.2 ms vs. 6.6 ms, p < 0.001). DC achieved a good discrimination performance (AUC = 0.76) for ARDS in COVID-19 persons. In a multivariate analysis, decreased DC was associated with the development of ARDS. CONCLUSION: Our data suggest a promising role of DC to risk stratification in COVID-19.


Subject(s)
COVID-19 , Respiratory Distress Syndrome , Deceleration , Electrocardiography, Ambulatory , Humans , Respiratory Distress Syndrome/diagnosis , Respiratory Distress Syndrome/epidemiology , Respiratory Distress Syndrome/etiology , SARS-CoV-2
11.
Blood ; 138(14): 1269-1277, 2021 10 07.
Article in English | MEDLINE | ID: covidwho-1317119

ABSTRACT

Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a severe adverse effect of ChAdOx1 nCoV-19 COVID-19 vaccine (Vaxzevria) and Janssen Ad26.COV2.S COVID-19 vaccine, and it is associated with unusual thrombosis. VITT is caused by anti-platelet factor 4 (PF4) antibodies activating platelets through their FcγRIIa receptors. Antibodies that activate platelets through FcγRIIa receptors have also been identified in patients with COVID-19. These findings raise concern that vaccination-induced antibodies against anti-SARS-CoV-2 spike protein cause thrombosis by cross-reacting with PF4. Immunogenic epitopes of PF4 and SARS-CoV-2 spike protein were compared using in silico prediction tools and 3D modeling. The SARS-CoV-2 spike protein and PF4 share at least 1 similar epitope. Reactivity of purified anti-PF4 antibodies from patients with VITT was tested against recombinant SARS-CoV-2 spike protein. However, none of the affinity-purified anti-PF4 antibodies from 14 patients with VITT cross-reacted with SARS-CoV-2 spike protein. Sera from 222 polymerase chain reaction-confirmed patients with COVID-19 from 5 European centers were tested by PF4-heparin enzyme-linked immunosorbent assays and PF4-dependent platelet activation assays. We found anti-PF4 antibodies in sera from 19 (8.6%) of 222 patients with COVID-19. However, only 4 showed weak to moderate platelet activation in the presence of PF4, and none of those patients developed thrombotic complications. Among 10 (4.5%) of 222 patients who had COVID-19 with thrombosis, none showed PF4-dependent platelet-activating antibodies. In conclusion, antibodies against PF4 induced by vaccination do not cross-react with the SARS-CoV-2 spike protein, indicating that the intended vaccine-induced immune response against SARS-CoV-2 spike protein is not the trigger of VITT. PF4-reactive antibodies found in patients with COVID-19 in this study were not associated with thrombotic complications.


Subject(s)
Antibodies/adverse effects , COVID-19 Vaccines/adverse effects , Cross Reactions/immunology , Platelet Factor 4/immunology , Purpura, Thrombocytopenic, Idiopathic/etiology , Purpura, Thrombocytopenic, Idiopathic/immunology , Spike Glycoprotein, Coronavirus/immunology , Adult , Aged , Aged, 80 and over , Blood Platelets/immunology , COVID-19/immunology , Cohort Studies , Epitopes/immunology , Female , Heparin/metabolism , Humans , Immunoglobulin G/immunology , Male , Middle Aged , Protein Binding , Protein Domains , Purpura, Thrombocytopenic, Idiopathic/blood , Spike Glycoprotein, Coronavirus/chemistry , Young Adult
12.
Front Cardiovasc Med ; 8: 584108, 2021.
Article in English | MEDLINE | ID: covidwho-1278385

ABSTRACT

COVID-19 may lead to severe acute respiratory distress syndrome (ARDS) resulting in increased morbidity and mortality. Heart failure and/or pre-existing cardiovascular disease may correlate with poor outcomes and thus require special attention from treating physicians. The present study sought to investigate a possible impact of impaired myocardial function as well as myocardial distress markers on mortality or ARDS with need for mechanical ventilation in 157 consecutive patients with confirmed SARS-CoV-2 infection. All patients were admitted and treated at the University Hospital of Tübingen, Germany, during the first wave of the pandemic. Electrocardiography, echocardiography, and routine blood sampling were performed at hospital admission. Impaired left-ventricular and right-ventricular function, tricuspid regurgitation > grade 1, and elevated RV-pressure as well as thrombotic and myocardial distress markers (D-dimers, NT-pro-BNP, and troponin-I) were associated with mechanical ventilation and/or all-cause mortality. Impaired cardiac function is more frequent amidst ARDS, leading to subsequent need for mechanical ventilation, and thus denotes a poor outcome in COVID-19. Since a causal treatment for SARS-CoV-2 infection is still lacking, guideline-compliant cardiovascular evaluation and treatment remains the best approach to improve outcomes in COVID-19 patients with cardiovascular comorbidities.

14.
Thromb Haemost ; 121(11): 1417-1426, 2021 Nov.
Article in English | MEDLINE | ID: covidwho-1104586

ABSTRACT

BACKGROUND: Accumulating evidence indicates toward an association between severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and procoagulatory state in blood. Thromboelastographic investigations are useful point-of-care devices to assess coagulation and fibrinolysis. OBJECTIVES: We investigated the hypothesis that the procoagulatory state in COVID-19 patients is associated with impaired fibrinolysis system. METHODS: Altogether, 29 COVID-19 patients admitted to normal wards or to the intensive care unit (ICU) were included in this descriptive study. Whole blood samples were investigated by thromboelastography to assess coagulation and fibrinolysis. Additionally, standard routine coagulation testing and immunoassays for factors of fibrinolysis as plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (tPA), plasminogen activity and α2-antiplasmin (A2AP) were performed. RESULTS: A significantly increased lysis resistance and a significantly longer time of lysis after adding tissue plasminogen activator were observed in blood samples from ICU COVID-19 patients compared with healthy controls (maximal lysis: 3.25 ± 0.56 vs. 6.20 ± 0.89%, p = 0.0127; lysis time: 365.7 ± 44.6 vs. 193.2 ± 16.3 seconds, p = 0.0014). PAI-1 activity was significantly higher in plasma samples of ICU COVID-19 patients (PAI-1: 4.92 ± 0.91 vs. 1.28 ± 0.33 U/mL, p = 0.001). A positive correlation between the activity of PAI-1 and lysis time of the formed clot (r = 0.70, p = 0.0006) was observed. CONCLUSION: Our data suggest that severe SARS-CoV-2 infection is associated with impaired fibrinolytic activity in blood, where fibrinolytic inhibitors are elevated leading to an increased resistance to clot lysis. Thromboelastography could offer a tool to investigate the contribution of the fibrinolytic status to the procoagulatory condition in COVID-19.


Subject(s)
COVID-19/complications , Fibrinolysis , Thrombelastography , Thrombosis/etiology , Adolescent , Adult , Aged , Aged, 80 and over , Biomarkers/blood , COVID-19/blood , COVID-19/diagnosis , Child , Female , Humans , Male , Middle Aged , Predictive Value of Tests , Retrospective Studies , Risk Factors , Severity of Illness Index , Thrombosis/blood , Thrombosis/diagnosis , Time Factors , Young Adult
15.
BMC Cardiovasc Disord ; 20(1): 494, 2020 11 23.
Article in English | MEDLINE | ID: covidwho-1094026

ABSTRACT

BACKGROUND: Infective endocarditis has a relevant clinical impact due to its high morbidity and mortality rates. Right-sided endocarditis has lower complication rates than left-sided endocarditis. Common complications are multiple septic pulmonary embolisms, haemoptysis, and acute renal failure. Risk factors associated with right-sided infective endocarditis are commonly related to intravenous drug abuse, central venous catheters, or infections due to implantable cardiac devices. However, patients with congenital ventricular septal defects might be at high risk of endocarditis and haemodynamic complications. CASE PRESENTATION: In the following, we present the case of a 23-year-old man without a previous intravenous drug history with tricuspid valve Staphylococcus aureus endocarditis complicated by acute renal failure and haemoptysis caused by multiple pulmonary emboli. In most cases, right-sided endocarditis is associated with several common risk factors, such as intravenous drug abuse, a central venous catheter, or infections due to implantable cardiac devices. In this case, we found a small perimembranous ventricular septal defect corresponding to a type 2 Gerbode defect. This finding raised the suspicion of a congenital ventricular septal defect complicated by a postendocarditis aneurysmal transformation. CONCLUSIONS: Management of the complications of right-sided infective endocarditis requires a multidisciplinary approach. Echocardiographic approaches should include screening for ventricular septal defects in patients without common risk factors for tricuspid valve endocarditis. Patients with undiagnosed congenital ventricular septal defects are at high risk of infective endocarditis. Therefore, endocarditis prophylaxis after dental procedures and/or soft-tissue infections is highly recommended. An acquired ventricular septal defect is a very rare complication of infective endocarditis. Surgical management of small ventricular septal defects without haemodynamic significance is still controversial.


Subject(s)
Acute Kidney Injury/etiology , Coronary Circulation , Endocarditis, Bacterial/microbiology , Heart Septal Defects, Ventricular/physiopathology , Hemodynamics , Hemoptysis/etiology , Staphylococcal Infections/microbiology , Acute Kidney Injury/microbiology , Acute Kidney Injury/physiopathology , Anti-Bacterial Agents/therapeutic use , Conservative Treatment , Endocarditis, Bacterial/complications , Endocarditis, Bacterial/diagnosis , Endocarditis, Bacterial/drug therapy , Heart Septal Defects, Ventricular/complications , Heart Septal Defects, Ventricular/diagnostic imaging , Hemoptysis/microbiology , Hemoptysis/physiopathology , Humans , Male , Risk Factors , Staphylococcal Infections/complications , Staphylococcal Infections/diagnosis , Staphylococcal Infections/drug therapy , Treatment Outcome , Young Adult
16.
Blood ; 137(8): 1061-1071, 2021 02 25.
Article in English | MEDLINE | ID: covidwho-1013145

ABSTRACT

The pathophysiology of COVID-19-associated thrombosis seems to be multifactorial. We hypothesized that COVID-19 is accompanied by procoagulant platelets with subsequent alteration of the coagulation system. We investigated depolarization of mitochondrial inner transmembrane potential (ΔΨm), cytosolic calcium (Ca2+) concentration, and phosphatidylserine (PS) externalization. Platelets from COVID-19 patients in the intensive care unit (ICU; n = 21) showed higher ΔΨm depolarization, cytosolic Ca2+, and PS externalization compared with healthy controls (n = 18) and non-ICU COVID-19 patients (n = 4). Moreover, significant higher cytosolic Ca2+ and PS were observed compared with a septic ICU control group (ICU control; n = 5). In the ICU control group, cytosolic Ca2+ and PS externalization were comparable with healthy controls, with an increase in ΔΨm depolarization. Sera from COVID-19 patients in the ICU induced a significant increase in apoptosis markers (ΔΨm depolarization, cytosolic Ca2+, and PS externalization) compared with healthy volunteers and septic ICU controls. Interestingly, immunoglobulin G fractions from COVID-19 patients induced an Fcγ receptor IIA-dependent platelet apoptosis (ΔΨm depolarization, cytosolic Ca2+, and PS externalization). Enhanced PS externalization in platelets from COVID-19 patients in the ICU was associated with increased sequential organ failure assessment score (r = 0.5635) and D-dimer (r = 0.4473). Most importantly, patients with thrombosis had significantly higher PS externalization compared with those without. The strong correlations between markers for apoptosic and procoagulant platelets and D-dimer levels, as well as the incidence of thrombosis, may indicate that antibody-mediated procoagulant platelets potentially contributes to sustained increased thromboembolic risk in ICU COVID-19 patients.


Subject(s)
Apoptosis , Blood Platelets/pathology , COVID-19/pathology , Immunoglobulin G/metabolism , Adult , Aged , Blood Coagulation , Blood Platelets/metabolism , COVID-19/blood , COVID-19/complications , COVID-19/metabolism , Calcium/metabolism , Cohort Studies , Female , Humans , Male , Membrane Potential, Mitochondrial , Middle Aged , Phosphatidylserines/metabolism , SARS-CoV-2/isolation & purification , SARS-CoV-2/physiology , Thrombosis/blood , Thrombosis/etiology , Thrombosis/metabolism , Thrombosis/pathology
17.
Clin Res Cardiol ; 109(12): 1491-1499, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-597440

ABSTRACT

BACKGROUND: COVID-19 infection may cause severe respiratory distress and is associated with increased morbidity and mortality. Impaired cardiac function and/or pre-existing cardiovascular disease may be associated with poor prognosis. In the present study, we report a comprehensive cardiovascular characterization in the first consecutive collective of patients that was admitted and treated at the University Hospital of Tübingen, Germany. METHODS: 123 consecutive patients with COVID-19 were included. Routine blood sampling, transthoracic echocardiography and electrocardiography were performed at hospital admission. RESULTS: We found that impaired left-ventricular and right-ventricular function as well as tricuspid regurgitation > grade 1 were significantly associated with higher mortality. Furthermore, elevated levels of myocardial distress markers (troponin-I and NT pro-BNP) were associated with poor prognosis in this patient collective. CONCLUSION: Impaired cardiac function is associated with poor prognosis in COVID-19 positive patients. Consequently, treatment of these patients should include careful guideline-conform cardiovascular evaluation and treatment. Thus, formation of a competent Cardio-COVID-19 team may represent a major clinical measure to optimize therapy of cardiovascular patients during this pandemic.


Subject(s)
COVID-19/mortality , Tricuspid Valve Insufficiency/mortality , Ventricular Dysfunction, Left/mortality , Ventricular Dysfunction, Right/mortality , Ventricular Function, Left , Ventricular Function, Right , Aged , Aged, 80 and over , COVID-19/diagnosis , COVID-19/physiopathology , COVID-19/therapy , Female , Germany , Hospital Mortality , Hospitalization , Humans , Male , Middle Aged , Prognosis , Prospective Studies , Risk Assessment , Risk Factors , Time Factors , Tricuspid Valve Insufficiency/diagnosis , Tricuspid Valve Insufficiency/physiopathology , Tricuspid Valve Insufficiency/therapy , Ventricular Dysfunction, Left/diagnosis , Ventricular Dysfunction, Left/physiopathology , Ventricular Dysfunction, Left/therapy , Ventricular Dysfunction, Right/diagnosis , Ventricular Dysfunction, Right/physiopathology , Ventricular Dysfunction, Right/therapy
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