scholarly journals SARS-CoV-2 Receptors are Expressed on Human Platelets and the Effect of Aspirin on Clinical Outcomes in COVID-19 Patients

2020 ◽  
Author(s):  
Aditya Sahai ◽  
Rohan Bhandari ◽  
Milka Koupenova ◽  
Jane Freedman ◽  
Mathew Godwin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Venous Thromboembolism ◽  
Confocal Microscopy ◽  
Cell Surface ◽  
Cerebrovascular Accident ◽  
Human Platelets ◽  
Thrombotic Risk ◽  
Increased Risk ◽  
Inflammatory Drugs

Abstract Coronavirus disease-2019 (COVID-19) caused by SARS-CoV-2 is an ongoing viral pandemic marked by increased risk of thrombotic events. However, the role of platelets in the elevated observed thrombotic risk in COVID-19 and utility of anti-platelet agents in attenuating thrombosis is unknown. We aimed to determine if human platelets express the known SARS-CoV-2 receptor-protease axis on their cell surface and assess whether the anti-platelet effect of aspirin may mitigate risk of myocardial infarction (MI), cerebrovascular accident (CVA), and venous thromboembolism (VTE) in COVID-19. Expression of ACE2 and TMPRSS2 on human platelets were detected by immunoblotting and confirmed by confocal microscopy. We evaluated 22,072 symptomatic patients tested for COVID-19. Propensity-matched analyses were performed to determine if treatment with aspirin or non-steroidal anti-inflammatory drugs (NSAIDs) affected thrombotic outcomes in COVID-19. Neither aspirin nor NSAIDs affected mortality in COVID-19. However, both aspirin and NSAID therapies were associated with increased risk of the combined thrombotic endpoint of (MI), (CVA), and (VTE). Thus, while platelets clearly express ACE2-TMPRSS2 receptor-protease axis for SARS-CoV-2 infection, aspirin does not prevent thrombosis and death in COVID-19. The mechanisms of thrombosis in COVID-19, therefore, appears distinct and the role of platelets as direct mediators of SARS-CoV-2-mediated thrombosis warrants further investigation.

scholarly journals Effect of aspirin on short-term outcomes in hospitalized patients with COVID-19

2021 ◽  
pp. 1358863X2110127
Author(s):  
Aditya Sahai ◽  
Rohan Bhandari ◽  
Matthew Godwin ◽  
Thomas McIntyre ◽  
Mina K Chung ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Venous Thromboembolism ◽  
Cerebrovascular Accident ◽  
Antiplatelet Agents ◽  
Hospitalized Patients ◽  
Short Term ◽  
Thrombotic Risk ◽  
Increased Risk ◽  
Inflammatory Drugs

Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 is an ongoing viral pandemic marked by increased risk of thrombotic events. However, the role of platelets in the elevated observed thrombotic risk in COVID-19 and utility of antiplatelet agents in attenuating thrombosis is unknown. We aimed to determine if the antiplatelet effect of aspirin may mitigate risk of myocardial infarction, cerebrovascular accident, and venous thromboembolism in COVID-19. We evaluated 22,072 symptomatic patients tested for COVID-19. Propensity-matched analyses were performed to determine if treatment with aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) affected thrombotic outcomes in COVID-19. Neither aspirin nor NSAIDs affected mortality in COVID-19. Thus, aspirin does not appear to prevent thrombosis and death in COVID-19. The mechanisms of thrombosis in COVID-19, therefore, appear distinct and the role of platelets as direct mediators of SARS-CoV-2-mediated thrombosis warrants further investigation.

Allele 4G of gene PAI-1 associated with prothrombin mutation G20210A increases the risk for venous thrombosis

2003 ◽  
Vol 90 (12) ◽  
pp. 1061-1064 ◽  
Author(s):  
Doris Barcellona ◽  
Lara Fenu ◽  
Cristiana Cauli ◽  
Giulia Pisu ◽  
Francesco Marongiu
Keyword(s):  
Risk Factor ◽  
Venous Thromboembolism ◽  
Odds Ratio ◽  
Final Conclusion ◽  
Thrombotic Risk ◽  
G20210a Mutation ◽  
Increased Risk ◽  
Prothrombin Mutation ◽  
Pai 1

SummarySeveral studies have tried to clarify the role of polymorphism 4G/5G of the PAI-1 gene in venous thromboembolism without reaching any final conclusion. It has been demonstrated that this polymorphism may induce an increased risk for venous thromboembolism (VTE) in patients with thrombophilic defects. We studied the association of prothrombin mutation G20210A with 4G/5G polymorphism in 402 VTE patients and 466 healthy controls. Patients affected by prothrombin mutation G20210A, with or without the concomitant presence of allele 4G, had a 3.7 thrombotic risk (C.I. 95% 2.3–6.0; p<0.0001). Moreover, genotype 4G/4G is a mild risk factor for VTE, irrespectively of whether the prothrombin mutation was present.Logistic regression analysis showed that patients carrying the G20210A prothrombin mutation with allele 4G gave an odds ratio for VTE of 6.1 (C.I. 95% 3.2 – 11.4; p<0.001). The risk increased up to 13.0 (C.I. 95% 3.0 – 60.4; p<0.001) when we considered the association of the prothrombin mutation with genotype 4G/4G. The G20210A mutation without allele 4G (5G/5G) was not a risk factor for VTE. In conclusion, we believe that patients affected by VTE with concomitant presence of the G20210A prothrombin mutation could be tested for genotype 4G/4G to better define their thrombotic risk.

scholarly journals POS1131 THE INCIDENCE AND PREVALENCE OF CARDIOVASCULAR DISEASES IN GOUT: A SYSTEMATIC REVIEW AND META-ANALYSIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 844.2-845
Author(s):  
P. Cox ◽  
S. Gupta ◽  
S. S. Zhao ◽  
D. Hughes
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Cardiovascular Disease ◽  
Cardiovascular Risk ◽  
Venous Thromboembolism ◽  
Cardiovascular Diseases ◽  
Cerebrovascular Accident ◽  
Meta Analysis ◽  
Pooled Prevalence ◽  
Increased Risk

Background:Gout is an inflammatory crystal arthropathy characterised by hyperuricaemia and sodium urate crystal deposition. Both gout and subclinical hyperuricaemia are associated with adverse cardiovascular outcomes. Several studies have found gout to cause an increased risk of cardiovascular disease, but the evidence is not unanimous. The conflicting evidence has made it difficult to establish the extent of the cardiovascular risk to patients with gout.Objectives:To describe the incidence and prevalence of cardiovascular disease in gout, compare these results with non-gout controls.Methods:PubMed, Scopus and Web of Science were systematically searched in January 2021 for studies reporting prevalence of any cardiovascular disease in a gout population. Studies with non-representative sampling, where a cohort had been used in another study, small sample size (< 100) and where gout could not be distinguished from other rheumatic conditions were excluded. Sample size, prevalence of the investigated cardiovascular disease, definition of gout and cardiovascular disease, demographic data, data source and any comparisons with non-gout controls were extracted from each study. Where prevalence data was reported in ≥3 cohorts meta-analysis was performed using random-effect models.Results:Of the 6164 titles identified, 105 full texts were assessed for eligibility with 30 included in the review, producing a gout population of 1,125,988. Pooled prevalence estimates were calculated for six cardiovascular diseases: heart failure (8.73%; 95% confidence interval (CI), 2.85 – 23.76), cerebrovascular accident (4.27%; 95% CI, 1.83 – 9.67), myocardial infarction (2.82%; 95% CI, 1.58 – 5.01), venous thromboembolism (2.05%; 95% CI, 1.22 – 3.43), hypertension (63.94%; 95% CI, 24.51 – 90.64) and cardiovascular mortality (4.75%; 95% CI, 3.56 – 6.31). Twenty studies reported comparisons with non-gout controls, illustrating an increased risk in the gout group across all cardiovascular diseases, particularly for myocardial infarction.Conclusion:Cardiovascular diseases are more prevalent in patients with gout and should prompt vigilance from clinicians to the need to assess and stratify cardiovascular risk. These results are in line with other studies which have shown an increased cardiovascular risk for sufferers of hyperuricaemia, highlighting the need for future research to explain this finding. There are limited studies in the literature investigating less common cardiovascular conditions, illustrating the need for future work if a more thorough picture of prevalence is to be established.Figure 1.Forest plots of pooled prevalence of: (A) 8.73% for heart failure, (B) 4.27% for cerebrovascular accident, (C) 2.82% for myocardial infarction, (D) 2.05% for venous thromboembolism, (E) 63.94% for hypertension and (F) 4.75% for cardiovascular mortality.Disclosure of Interests:None declared.

scholarly journals MiR-126-3p and MiR-223-3p as Biomarkers for Prediction of Thrombotic Risk in Patients with Acute Myocardial Infarction and Primary Angioplasty

2021 ◽  
Vol 11 (6) ◽  
pp. 508
Author(s):  
Milan Hromadka ◽  
Zuzana Motovska ◽  
Ota Hlinomaz ◽  
Petr Kala ◽  
Frantisek Tousek ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Predictive Accuracy ◽  
Cardiovascular Death ◽  
Primary Angioplasty ◽  
Bleeding Complications ◽  
Clinical Predictors ◽  
Thrombotic Risk ◽  
Increased Risk ◽  
One Year

Aim. This study was designed to evaluate the relationship between microRNAs (miRNAs), miR-126-3p and miR-223-3p, as new biomarkers of platelet activation, and predicting recurrent thrombotic events after acute myocardial infarction (AMI). Methods and Results. The analysis included 598 patients randomized in the PRAGUE-18 study (ticagrelor vs. prasugrel in AMI). The measurements of miRNAs were performed by using a novel miRNA immunoassay method. The association of miRNAs with the occurrence of the ischemic endpoint (EP) (cardiovascular death, nonfatal MI, or stroke) and bleeding were analyzed. The miR-223-3p level was significantly related to an increased risk of occurrence of the ischemic EP within 30 days (odds ratio (OR) = 15.74, 95% confidence interval (CI): 2.07–119.93, p = 0.008) and one year (OR = 3.18, 95% CI: 1.40–7.19, p = 0.006), respectively. The miR-126-3p to miR-223-3p ratio was related to a decreased risk of occurrence of EP within 30 days (OR = 0.14, 95% CI: 0.03–0.61, p = 0.009) and one year (OR = 0.37, 95% CI: 0.17–0.82, p = 0.014), respectively. MiRNAs were identified as independent predictors of EP even after adjustment for confounding clinical predictors. Adding miR-223-3p and miR-126-3p to miR-223-3p ratios as predictors into the model calculating the ischemic risk significantly increased the predictive accuracy for combined ischemic EP within one year more than using only clinical ischemic risk parameters. No associations between miRNAs and bleeding complications were identified. Conclusion. The miR-223-3p and the miR-126-3p are promising independent predictors of thrombotic events and can be used for ischemic risk stratification after AMI.

scholarly journals Role of diuretics on long-term mortality may differ in volume status in patients with acute myocardial infarction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
T Kawai ◽  
D Nakatani ◽  
T Yamada ◽  
T Watanabe ◽  
T Morita ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Propensity Score ◽  
Plasma Volume ◽  
Cox Regression ◽  
Volume Status ◽  
Increased Risk ◽  
Long Term Mortality

Abstract Background Diuretics has been reported to have a potential for an activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system, leading to a possibility of poor clinical outcome in patients with cardiovascular disease. However, few data are available on clinical impact of diuretics on long-term outcome in patients with acute myocardial infarction (AMI) based on plasma volume status. Methods To address the issue, a total of 3,416 survived patients with AMI who were registered to a large database of the Osaka Acute Coronary Insufficiency Study (OACIS) were studied. Plasma volume status was assessed with the estimated plasma volume status (ePVS) that was calculated at discharge as follows: actual PV = (1 − hematocrit) × [a + (b × body weight)] (a=1530 in males and a=864 in females, b=41.0 in males and b=47.9 in females); ideal PV = c × body weight (c=39 in males and c=40 in females), and ePVS = [(actual PV − ideal PV)/ideal PV] × 100 (%). Multivariable Cox regression analysis and propensity score matching were performed to account for imbalances in covariates. The endpoint was all-cause of death (ACD) within 5 years. Results During a median follow-up period of 855±656 days, 193 patients had ACD. In whole population, there was no significant difference in long-term mortality risk between patients with and without diuretics in both multivariate cox regression model and propensity score matching population. When patients were divided into 2 groups according to ePVS with a median value of 4.2%, 46 and 147 patients had ACD in groups with low ePVS and high ePVS, respectively. Multivariate Cox analysis showed that use of diuretics was independently associated with an increased risk of ACD in low ePVS group, (HR: 2.63, 95% confidence interval [CI]: 1.22–5.63, p=0.01), but not in high ePVS group (HR: 0.70, 95% CI: 0.44–1.10, p=0.12). These observations were consistent in the propensity-score matched cohorts; the 5-year mortality rate was significantly higher in patients with diuretics than those without among low ePVS group (4.7% vs 1.7%, p=0.041), but not among high ePVS group (8.0% vs 10.3%, p=0.247). Conclusion Prescription of diuretics at discharge was associated with increased risk of 5-year mortality in patients with AMI without PV expansion, but not with PV expansion. The role of diuretics on long-term mortality may differ in plasma volume status. Therefore, prescription of diuretics after AMI may be considered based on plasma volume status. Funding Acknowledgement Type of funding source: None

scholarly journals Investigating Association of rs5918 Human Platelets Antigen 1 and rs1800790 Fibrinogen β Chain as Critical Players with Recurrent Pregnancy Loss

2018 ◽  
Vol 6 (4) ◽  
pp. 98 ◽  
Author(s):  
Fatemeh Karami ◽  
Maliheh Askari ◽  
Mohammad Modarressi
Keyword(s):  
Pregnancy Loss ◽  
Recurrent Pregnancy Loss ◽  
Human Platelets ◽  
P Value ◽  
Increased Risk ◽  
History Of ◽  
Polymerase Chain ◽  
Β Chain ◽  
Larger Sample

Thrombophilia gene variants have been shown to be associated with higher risk of recurrent pregnancy loss (RPL). Due to the role of human platelets antigen 1 (HPA-1) and fibrinogen β chain (FGB) as critical players in the coagulation process, their most important variants including rs5918 T > C and rs1800790 G > A were selected to be studied in women affected by RPL. Three milliliters of peripheral blood were drawn from 110 women with history of at least two consecutive spontaneous abortion and 110 healthy women controls. rs5918 T > C and rs1800790 G > A of HPA-1 and FGB genes, respectively, were selected to be analyzed through polymerase chain reaction-restriction fragment length polymorphism (PCR_RFLP) following DNA isolation using QIAamp DNA Blood Mini Kit. Heterozygote genotype (TC) of HPA-1 gene rs5918 polymorphism was significantly associated with risk of RPL (p-value = 0.02). Although, rs1800790 G > A of FGB gene was not associated with RPL, its combination with rs5918 polymorphism was associated with increased risk of RPL. Owing to the critical roles of FGB and HPA-1 genes in coagulation, and thrombosis and several confinements on the meaningful association between the combination of those polymorphism with risk of RPL, including them in the thrombophilia panel may increase detection rate of hereditary thrombophilia patients. However, further studies with larger sample sizes are required to shed light on the exact role of the studied gene polymorphism, especially rs1800790 G > A of FGB gene variant in pathogenesis of RPL.

scholarly journals The Role of Stroke as a Trigger for Incident Venous Thromboembolism: Results from a Population-based Case-Crossover Study

TH Open ◽  
2019 ◽  
Vol 03 (01) ◽  
pp. e50-e57
Author(s):  
Vânia Morelli ◽  
Joakim Sejrup ◽  
Birgit Småbrekke ◽  
Ludvig Rinde ◽  
Gro Grimnes ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Acute Stroke ◽  
Crossover Study ◽  
Conditional Logistic Regression ◽  
Population Based ◽  
Red Blood Cell Transfusion ◽  
Odds Ratios ◽  
Case Crossover ◽  
Increased Risk

AbstractStroke is associated with a short-term increased risk of subsequent venous thromboembolism (VTE). It is unclear to what extent this association is mediated by stroke-related complications that are potential triggers for VTE, such as immobilization and infection. We aimed to investigate the role of acute stroke as a trigger for incident VTE while taking other concomitant VTE triggers into account. We conducted a population-based case-crossover study with 707 VTE patients. Triggers were registered during the 90 days before a VTE event (hazard period) and in four preceding 90-day control periods. Conditional logistic regression was used to estimate odds ratios with 95% confidence intervals (CIs) for VTE according to triggers. Stroke was registered in 30 of the 707 (4.2%) hazard periods and in 6 of the 2,828 (0.2%) control periods, resulting in a high risk of VTE, with odds ratios of 20.0 (95% CI: 8.3–48.1). After adjustments for immobilization and infection, odds ratios for VTE conferred by stroke were attenuated to 6.0 (95% CI: 1.6–22.1), and further to 4.0 (95% CI: 1.1–14.2) when other triggers (major surgery, red blood cell transfusion, trauma, and central venous catheter) were added to the regression model. A mediation analysis revealed that 67.8% of the total effect of stroke on VTE risk could be mediated through immobilization and infection. Analyses restricted to ischemic stroke yielded similar results. In conclusion, acute stroke was a trigger for VTE, and the association between stroke and VTE risk appeared to be largely mediated by immobilization and infection.

Antiphospholipid antibodies and myocardial infarction

Lupus ◽  
1998 ◽  
Vol 7 (2_suppl) ◽  
pp. 132-134 ◽  
Author(s):  
O Vaarala
Keyword(s):  
Myocardial Infarction ◽  
Heart Disease ◽  
Antiphospholipid Antibodies ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Epidemiological Data ◽  
Oxidative Modification ◽  
Increased Risk ◽  
Different Types

In prospective studies, increased levels of cardiolipin-biding antibodies and autoantibodies to oxidized low-density lipoprotein (LDL) have been observed in patients with myocardial infarction (MI). These findings suggest that antiphospholipid antibodies may contribute to the development of MI. The ‘oxidative-modification hypothesis’ in the pathogenesis of atherosclerotic heart disease is based on the oxidation of LDL, its accumulation into arterial wall, and the development of chronic inflammation in the atheroma. Evidence of enhanced lipid peroxidation and its association with antiphospholipid antibodies has been recently reported in SLE patients. There is also epidemiological data showing a remarkably increased risk of MI in SLE. In this review, the role of different types of antiphospholipid antibodies in the development of atherosclerotic heart disease is evaluated with particular attention to their potential pathogenic mechanisms and the possibilities in the prevention of MI associated with antiphospholipid antibodies.

Elevated venous thromboembolism risk in preeclampsia: molecular mechanisms and clinical impact

2015 ◽  
Vol 43 (4) ◽  
pp. 696-701 ◽  
Author(s):  
Karl Egan ◽  
Barry Kevane ◽  
Fionnuala Ní Áinle
Keyword(s):  
Venous Thromboembolism ◽  
Molecular Mechanisms ◽  
Endothelial Activation ◽  
Extracellular Traps ◽  
Increased Risk ◽  
Consensus Statements ◽  
Maternal Hypertension ◽  
The Subject ◽  
Developed World

Venous thromboembolism (VTE) remains a leading cause of maternal death and morbidity in the developed world. Strategies for prevention of VTE in pregnancy have been the subject of recent guidelines and consensus statements. These guidelines recommend thrombosis prevention in women who have risk factors associated with an elevated VTE risk. Preeclampsia is characterized by maternal hypertension and proteinuria developing after 20 weeks gestation, complicating up to 7% of pregnancies and is associated with a massive annual morbidity and mortality burden. Women with preeclampsia have been shown to be at increased risk of VTE with studies to date suggesting that this risk may be up to 5-fold greater than the risk of pregnancy-associated VTE in the general population. Despite the fact that preeclampsia is so common and potentially devastating, our understanding of its pathogenesis and potential therapeutic strategies remain poor. In addition, the mechanisms underlying the prothrombotic phenotype in preeclampsia are also poorly characterized although a number of potential mechanisms have been postulated. Derangements of platelet and endothelial activation and impairment of endogenous anti-coagulant pathways have been reported and may contribute to the observed VTE risk. Recently, evidence for the role of neutrophil extracellular traps (NETs) and cell-free DNA in the pathogenesis of VTE has emerged and some evidence exists to suggest that this may be of relevance in preeclampsia. Future studies aimed at understanding the diagnostic and potential therapeutic relevance of this procoagulant state are likely to be of enormous clinical benefit for pregnant women affected with this potentially devastating condition.

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