Abstract 1122‐000231: A Review of Effect of Ticagrelor on Platelet Inhibition in Clopidogrel Non‐Responders Undergoing Neuroendovascular Procedure

Introduction : Neuroendovascular procedures are becoming more routine in the treatment of intracranial conditions such as aneurysms, arterial stenosis, and ischemic stroke. These patients are frequently treated with antiplatelet agents prior to the procedure to prevent thrombotic complications. The combination of aspirin and a P2Y12 inhibitor such as clopidogrel is often initiated days before elective procedures or as loading doses for emergent procedures. However, some patients may still experience post procedural thrombotic or hemorrhagic complications which may be related to platelet inhibition. Methods : A retrospective review of patients who underwent a neuroendovascular procedure from 1/2017 to 12/2019 in a single tertiary care academic hospital. Procedures included flow‐diverting stent placement for aneurysms, intracranial, and cervical carotid artery stenting. Patients undergoing elective procedure were started on Aspirin and Clopidogrel 75 mg daily. Patients undergoing emergent procedures were given loading doses of Aspirin (650 mg) and Clopidogrel (600 mg). P2Y12 assay was checked prior to receiving Platelet inhibitor and from 3–6 hours after Clopidogrel loading dose. Optimal platelet inhibition was classified as reduction in P2Y12 assay by at least 60%. Patients with suboptimal platelet inhibition <60% were given Ticagrelor loading dose (180 mg) and P2y12 assay was rechecked. Patients who did not have complete chart information, patients with AFib requiring DOAC and patients previously on ADP inhibitors, were excluded from analysis. Results : Total neuroendovascular procedures requiring stents were 687 over the period of 3 years. mean age of patients was 61 years. This neuroendovascular procedure consisted of aneurysm stenting (239), aneurysm stent‐assisted coiling 112, intracranial stent for failed mechanical thrombectomy 62, carotid artery stent 108. Suboptimal platelet inhibition was noted in 54% (282) of 523 patients after receiving Clopidogrel. After receiving Ticagrelor, optimal inhibition was noted in 80% (226) of 282 patients with median increase of 26%. 62 patients with suboptimal response to Ticagrelor, 47 were started on Prasugrel. Thrombotic complications were noted in 7 patients, 6 of them were noted to have <50% platelet inhibition. Hemorrhagic complications were noted in 17 patients, amongst them >70% platelet inhibition was noted in 14 patients with mean P2Y12 value of 59. Conclusions : Patients receiving P2Y12 ADP antiplatelet therapy may have suboptimal platelet inhibition which results in increased thrombotic risk. Patients who have significant platelet inhibition (>70%) after loading dose are at increased risk for hemorrhagic complications. Better platelet inhibition was achieved with Ticagrelor in Clopidogrel hypo‐response patients. In patients with Clopidogrel hyper‐response, dosing was changed to half the dose or alternate day to reduce hemorrhagic complications. As the use of endovascular therapies requiring dual anti‐platelet agents becomes more established, there is an increasing need to develop titration protocols that minimize the risk of thrombotic and hemorrhagic events based on platelet inhibition.

Download Full-text

Thrombosis in IBD in the Era of JAK Inhibition

Current Drug Targets ◽

10.2174/1389450121666200902164240 ◽

2020 ◽

Vol 22 (1) ◽

pp. 126-136

Author(s):

Virginia Solitano ◽

Gionata Fiorino ◽

Ferdinando D’Amico ◽

Laurent Peyrin-Biroulet ◽

Silvio Danese

Keyword(s):

Small Molecules ◽

Arterial Thrombosis ◽

Protective Role ◽

Jak Inhibitors ◽

Thrombotic Risk ◽

Increased Risk ◽

Bowel Diseases ◽

Thrombotic Complications ◽

Inflammatory Bowel ◽

Inflammatory Effect

: Patients with inflammatory bowel diseases (IBD) have an increased risk of thrombosis. The interaction between inflammation and coagulation has been extensively studied. It is well-known that some drugs can influence the haemostatic system, but several concerns on the association between therapies and increased risk of thrombosis remain open. While biologics seem to have a protective role against thrombosis via their anti-inflammatory effect, some concerns about an increased risk of thrombosis with JAK inhibitors have been raised. We conducted a literature review to assess the association between biologics/small molecules and venous/arterial thrombotic complications. An increased risk of venous and arterial thrombosis was found in patients treated with corticosteroids, whereas anti-TNF were considered protective agents. No thromboembolic adverse event was reported with vedolizumab and ustekinumab. In addition, thromboembolic events rarely occurred in patients with ulcerative colitis (UC) after therapy with tofacitinib. The overall risk of both venous and arterial thrombosis was not increased based on the available evidence. Finally, in the era of JAK inhibitors, treatment should be individualized by evaluating the pre-existing potential thrombotic risk balanced with the intrinsic risk of the medication used.

Download Full-text

Evidence of Endothelial Dysfunction and Activation of RhoA/Rho Kinase Pathway in Inflammatory Bowel Disease

Blood ◽

10.1182/blood-2019-126033 ◽

2019 ◽

Vol 134 (Supplement_1) ◽

pp. 3641-3641

Author(s):

Jaime Pereira ◽

Claudia G Saez ◽

Manuel Alvarez ◽

Felipe Silva ◽

Nixa Olivares ◽

...

Keyword(s):

Endothelial Dysfunction ◽

Disease Activity ◽

Adhesion Molecule ◽

Rho Kinase ◽

Thrombotic Risk ◽

Intestinal Microbes ◽

Increased Risk ◽

Thrombotic Complications ◽

Inflammatory Bowel ◽

Kinase Pathway

Background. Inflammatory bowel diseases (IBD) comprise two chronic relapsing intestinal disorders: Crohn's disease (CD) and ulcerative colitis (UC). IBD are the result of an abnormal inflammatory response to intestinal microbes in a genetically susceptible host. Clinically, rectal bleeding, severe diarrhea, weight loss and abdominal pain characterize IBD. Moreover, IBD are associated with a variety of extraintestinal manifestations (EIM). Increased risk of arterial and venous thrombosis in IBD patients, with a 3-fold higher risk for development venous thromboembolism is one of the most important EIM in terms of morbidity and mortality. Although the mechanisms underlying the increased thrombotic risk in IBD are not completely understood, there is evidence of abnormalities in coagulation, fibrinolysis and platelet function. However, in this context, the contribution of the vessel wall has been less explored. Endothelial dysfunction (ED) and abnormal activation of RhoA/Rho kinase (ROCK) pathway have been shown to participate in multiple pathological processes associated with thrombotic complications. We hypothesize that in IBD, the chronic inflammatory process settles the conditions for a chronic endothelial stimulation and increased ROCK activation contributing to the pathogenesis of thrombotic complications in IBD. Objectives. The main objective of this work was to demonstrate evidence of ED in patients with IBD and activation of RhoA/Rho kinase pathway. Methods. We studied 67 IBD patients (aged 18-77 years, mean age 37 years) who met inclusion criteria and age and healthy controls (aged 24-65 years, mean age 32 years). Diagnosis was based on standard clinical, radiological, endoscopic, and histological criteria. Activity of the disease was assessed by Mayo or Harvey Bradshaw Score (UC and CD, respectively). Endothelial cell damage was determined by enumerating circulating endothelial cells (CECs) and levels of circulating biomarkers: soluble intercellular adhesion molecule (sICAM) and vascular cell adhesion molecule (sVCAM) by ELISA. Rho-kinase activity was assessed by the levels of phosphorylated to total myosin light chain phosphatase 1 (MYPT1-P/T) in circulating leukocytes. Results. IBD patients showed significantly elevated number of CECs compared to the controls (23, 3±15 vs 9, 6±4, 4 cells/mL; p<0.01; respectively). Plasma levels of sICAM (170±83 ng/mL) and sVCAM (523±125 ng/mL) were also increased in IBD patients compared to the controls (136±52 and 489±52, respectively; p< 0.05). In the control subjects, leukocyte mean MYPT1-P/T ratio was 0.6 ± 0.1 whereas in IBD patients were significantly increased (1.2 ± 0.15; p: 0.009). Interestingly, the number of CECs was directly related to the degree of disease activity (20±3.0, 30±4.0 and 33±6.0 cells/mL for mild, moderate and severe, respectively; p: 0.006). Conclusions: We found that patients with IBD exhibit evidence of endothelial dysfunction related to the degree of disease activity and abnormal activation of the ROCK pathway. Collectively, these data suggest that activation of ROCK could contribute to the increased risk for thrombotic complications in IBD patients. Inhibition of ROCK has proven to be of potential therapeutic benefit for a variety of diseases. In the case of IBD, the use of ROCK inhibitors (e.g. statins) may provide a novel tool to target the thrombotic risk in patients with IBD. Disclosures No relevant conflicts of interest to declare.

Download Full-text

Clinical Trial Perspective: Optimizing Crossover From Ticagrelor to Clopidogrel in Patients with Acute Coronary Syndrome (CAPITAL OPTICROSS)

US Cardiology Review ◽

10.15420/ucs.2017:10:1 ◽

2017 ◽

Vol 11 (2) ◽

pp. 59

Author(s):

Donald E Cutlip ◽

Keyword(s):

Clinical Trial ◽

Acute Coronary Syndrome ◽

Platelet Inhibition ◽

Initial Therapy ◽

Loading Dose ◽

Platelet Activity ◽

Coronary Syndrome ◽

Risk Of Bleeding ◽

Recommended Treatment ◽

Increased Risk

Guideline-recommended treatment in patients with acute coronary syndrome is dual anti-platelet therapy (DAPT) with aspirin and a P2Y12 inhibitor, with clopidogrel or ticagrelor the preferred options for initial therapy. Ticagrelor has been demonstrated to have improved efficacy, and is preferred over clopidogrel in the absence of contraindications or the need for oral anticoagulation. However, it is not uncommon that patients are switched to clopidogrel after starting on ticagrelor. Reasons for this may be related to recognition of the increased risk of bleeding, the higher costs of ticagrelor, or adverse effects such as adenosine-mediated dyspnea. It is therefore important to understand the optimal dosing strategy in patients undergoing a switch from ticagrelor to clopidogrel. A loading dose of clopidogrel is standard when initiating therapy for acute coronary syndrome or before coronary stenting. However, whether this is required in patients who have already achieved adequate platelet inhibition with ticagrelor is unknown. Owing to the short half-life of the unbound active metabolite of clopidogrel at standard doses, there are concerns of high on-treatment platelet activity for a period of time following switching. However, this must be balanced against concerns of an increased risk of bleeding if a loading dose is used. To investigate this, the Optimizing Crossover From Ticagrelor To Clopidogrel In Patients With Acute Coronary Syndrome (CAPITAL OPTICROSS) clinical trial was conducted to compare a clopidogrel bolus dose with no bolus among patients currently treated with ticagrelor and whose treating physician had decided to switch therapy to clopidogrel. This review summarizes the CAPITAL OPTICROSS trial and its findings, and discusses the implications for clinical practice.

Download Full-text

Thrombotic Complications in a Canadian Population of Critically Ill Patients with COVID-19

Blood ◽

10.1182/blood-2020-141996 ◽

2020 ◽

Vol 136 (Supplement 1) ◽

pp. 41-42

Author(s):

Simard Camille ◽

Maral Koolian ◽

Diana Escobar ◽

Mark Blostein ◽

Jed Lipes ◽

...

Keyword(s):

Pulmonary Embolism ◽

Critically Ill ◽

Critically Ill Patients ◽

Tertiary Care ◽

The United States ◽

Hospital Death ◽

Thrombotic Complication ◽

Arterial Thromboembolism ◽

Increased Risk ◽

Thrombotic Complications

Introduction Coronavirus disease 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), a virus strain that appeared in Wuhan China in December 2019, that has since spread to become pandemic. An increased risk of venous and arterial thromboembolism has been consistently reported in critically ill patients with COVID-19 in several countries. The mechanism is thought to be multifactorial, largely mediated by the interplay between inflammation and the coagulation system, or thromboinflammation. We aim to report the risk of thrombosis in a Canadian patient population admitted to the intensive care unit (ICU) with COVID-19. Method We conducted a retrospective cohort study of all consecutive patients with COVID-19 admitted to the ICU between March 1st, 2020 and May 10th, 2020 at the Jewish General Hospital (JGH) in Montreal, Canada. The JGH is a tertiary care centre in Montreal, the epicenter of the COVID-19 pandemic in Canada, and the JGH was the first designated hospitalization centre in Montreal for COVID-19 patients. Patients were followed from date of ICU admission to the earliest of the following: objectively confirmed venous or arterial thrombosis; discharge from hospital; death; or study end date (May 24th, 2020). We determined risk of venous (pulmonary embolism (PE) and deep vein thrombosis (DVT)) and arterial (myocardial infarction, cerebrovascular accident, arterial limb ischemia, and mesenteric ischemia) thrombotic events. Results During the study period, a total of 90 patients admitted to the ICU with COVID-19 were included. The median age was 66 years (standard deviation (SD) 13.8), and 41.1% of patients were female. The median body mass index was 30 kg/m2(SD 5.1), and 64% of patients were mechanically ventilated and 10.1% received continuous renal replacement therapy. The median duration of follow-up was 17.1 days (SD 13.4). In all, 98.9% of patients were prescribed anticoagulation, among whom 78.2% were on a prophylaxis dose, 15.0% intermediate dose, and 6.9% therapeutic dose. In all, 11 (12.2%) patients developed a thrombotic complication among whom 9 patients had objectively diagnosed pulmonary embolism (PE) and 2 patients had an arterial thromboembolism. Both arterial events were cerebrovascular accidents. All PE episodes involved segmental arteries. One PE was incidental, and 3 patients had a concomitant diagnosis of DVT. Overall, death was observed in 16.7% of cohort patients and 12.2% of patients were still admitted to hospital at study end date. Conclusion In this first Canadian study of critically ill patients with COVID-19, we found a 12.2% risk of thrombotic complications despite almost 100% use of anticoagulation primarily with standard prophylaxis dosing. This risk is considerably lower than most reported estimates to date from critical care COVID-19 cohorts in Europe, China and the United States. Our results fuel the ongoing discussion of optimal dose of anticoagulation in these patients. Disclosures No relevant conflicts of interest to declare.

Download Full-text

Dual antiplatelet therapy after carotid artery stenting: trends and outcomes in a large national database

Journal of NeuroInterventional Surgery ◽

10.1136/neurintsurg-2020-016008 ◽

2020 ◽

Vol 13 (1) ◽

pp. 8-13

Author(s):

Eric S Sussman ◽

Michael Jin ◽

Arjun V Pendharkar ◽

Benjamin Pulli ◽

Austin Feng ◽

...

Keyword(s):

Ischemic Stroke ◽

Carotid Artery ◽

Antiplatelet Therapy ◽

Carotid Artery Stenting ◽

Dual Antiplatelet Therapy ◽

National Database ◽

Increased Risk ◽

Hemorrhagic Complications ◽

The Impact ◽

Large National Database

BackgroundWhile dual antiplatelet therapy (dAPT) is standard of care following carotid artery stenting (CAS), the optimal dAPT regimen and duration has not been established.MethodsWe canvassed a large national database (IBM MarketScan) to identify patients receiving carotid endarterectomy (CEA) or CAS for treatment of ischemic stroke or carotid artery stenosis from 2007 to 2016. We performed univariable and multivariable regression methods to evaluate the impact of covariates on post-CAS stroke-free survival, including post-discharge antiplatelet therapy.ResultsA total of 79 084 patients diagnosed with ischemic stroke or carotid stenosis received CEA (71 178; 90.0%) or CAS (7906; 10.0%). After adjusting for covariates, <180 days prescribed post-CAS P2Y12-inhibition was associated with increased risk for stroke (<90 prescribed days HR=1.421, 95% CI 1.038 to 1.946; 90–179 prescribed days HR=1.484, 95% CI 1.045 to 2.106). The incidence of hemorrhagic complications was higher during the period of prescribed P2Y12-inhibition (1.16% per person-month vs 0.49% per person-month after discontinuation, P<0.001). The rate of extracranial hemorrhage was nearly six-fold higher while on dAPT (6.50% per patient-month vs 1.16% per patient-month, P<0.001), and there was a trend towards higher rate of intracranial hemorrhage that did not reach statistical significance (5.09% per patient-month vs 3.69% per patient-month, P=0.0556). Later hemorrhagic events beyond 30 days post-CAS were significantly more likely to be extracranial (P=0.028).ConclusionsIncreased duration of post-CAS dAPT is associated with lower rates of readmissions for stroke, and with increased risk of hemorrhagic complications, particularly extracranial hemorrhage. The potential benefit of prolonging dAPT with regard to ischemic complications must be balanced with the corresponding increased risk of predominantly extracranial hemorrhagic complications.

Download Full-text

Challenges in Oral Antiplatelet Therapy

European Cardiology Review ◽

10.15420/ecr.2010.6.1.53 ◽

2010 ◽

Vol 6 (1) ◽

pp. 53

Author(s):

Pat Wong ◽

Umair Shafique ◽

◽

Keyword(s):

Antiplatelet Therapy ◽

Positive Impact ◽

Antiplatelet Agents ◽

Coronary Intervention ◽

Optimal Level ◽

Platelet Inhibition ◽

Individual Variability ◽

Platelet Response ◽

Coronary Syndromes ◽

Thrombotic Complications

The positive impact of oral antiplatelet therapy on the prevention and treatment of cardiovascular events is well-documented, especially in terms of reducing the risk of thrombotic complications in patients with acute coronary syndromes and those undergoing percutaneous coronary intervention. The oral antiplatelet agents aspirin and clopidogrel have become the mainstay of therapy. However, a major challenge still exists in the need to determine the optimal level of platelet inhibition that is required to obtain a balance between the prevention of ischaemic events and minimisation of the risk of bleeding in various clinical settings. In addition, clopidogrel is associated with inter-individual variability of platelet response and delayed onset and offset of action, which can influence the safety and/or efficacy of the treatment. These pharmacological limitations have led to the development of new oral antiplatelets, such as prasugrel, which has recently been approved, and ticagrelor, which is in late-stage clinical development. These newer agents are associated with improved rates of onset and/or offset of action, and offer more consistent antiplatelet effects.

Download Full-text

High-dose clopidogrel, prasugrel or ticagrelor: trying to unravel a skein into a ball

Drugs and Therapy Studies ◽

10.4081/dts.2011.e13 ◽

2011 ◽

Vol 1 (1) ◽

pp. 13

Author(s):

Alessandro Aprile ◽

Raffaella Marzullo ◽

Giuseppe Biondi Zoccai ◽

Maria Grazia Modena

Keyword(s):

Acute Coronary Syndromes ◽

Antiplatelet Agents ◽

Bleeding Risk ◽

Coronary Intervention ◽

Platelet Inhibition ◽

High Dose ◽

Comprehensive Overview ◽

Increased Risk ◽

Coronary Syndromes ◽

Artery Disease

Antiplatelet therapy is a mainstay in the management of coronary artery disease. Indeed, optimal and rapid inhibition of platelet function is a key therapeutic goal in patients with acute coronary syndromes and those undergoing percutaneous coronary intervention. Currently, dual antiplatelet treatment with aspirin and clopidogrel is the gold standard care in patients with acute coronary syndromes or receiving coronary stents without prohibitive bleeding risk. However, recent data show that the efficacy of clopidogrel is hampered by its slow and variable platelet inhibition, with ensuing increased risk of ischemic events, including death, myocardial infarction and stent thrombosis. Novel agents such as prasugrel and ticagrelor have been developed to clopidogrel limits and thus improve cardiovascular outcomes. This article presents a comprehensive overview of the benefits and limitations of current and shortly available antiplatelet agents, providing detailed arguments in favor and against prasugrel and ticagrelor.

Download Full-text

The expression pattern of c-mpl in megakaryocytes correlates with thrombotic risk in essential thrombocythemia

Blood ◽

10.1182/blood.v100.2.714 ◽

2002 ◽

Vol 100 (2) ◽

pp. 714-717 ◽

Cited By ~ 28

Author(s):

Luciana Teofili ◽

Francesco Pierconti ◽

Annalaura Di Febo ◽

Nicola Maggiano ◽

Nicola Vianelli ◽

...

Keyword(s):

Bone Marrow ◽

Expression Pattern ◽

Essential Thrombocythemia ◽

Staining Intensity ◽

Thrombotic Risk ◽

Significant Percentage ◽

Increased Risk ◽

Significant Difference ◽

Thrombotic Complications ◽

Strong Staining

Abstract Using immunohistochemistry, we investigated the expression of c-mpl in bone marrow megakaryocytes of 88 patients with essential thrombocythemia (ET), 6 patients with secondary thrombocytosis (ST), and 20 patients with lymphoma (controls). Considering both the pattern of expression and the staining intensity, we identified a uniform and a heterogeneous pattern of c-mplexpression. The uniform pattern was found in all the controls, all the patients with ST, and 28 of the patients with ET, with a strong staining intensity observed in most megakaryocytes (> 80%). In contrast, c-mpl expression was heterogeneous in 60 patients with ET, 18 of whom (30%) presented with thrombosis at diagnosis, a significant difference from patients with a uniform c-mpl pattern (2 of 28; 7%; P = .026). In particular, the overrepresentation of thrombotic complications in patients with a heterogeneous c-mpl expression pattern was found mainly among patients with a significant percentage (10% to 40%) of weakly stained or c-mpl–negative megakaryocytes (heterogeneous-weak pattern; 13 of 30; 43%;P = .002). Accordingly, this pattern was associated with a 6.1-fold increased risk of thrombosis compared with that of patients with a uniform c-mpl pattern. In conclusion, the presence of a heterogeneous pattern of c-mpl distribution in bone marrow megakaryocytes could be a useful diagnostic criterion in the differential diagnosis of thrombocytosis. Furthermore, detection of a significant percentage of weakly stained or c-mpl–negative megakaryocytes can identify patients with a higher risk of thrombosis.

Download Full-text

Clinical, laboratory, and genetic risk factors for thrombosis in sickle cell disease

Blood Advances ◽

10.1182/bloodadvances.2019001384 ◽

2020 ◽

Vol 4 (9) ◽

pp. 1978-1986 ◽

Cited By ~ 1

Author(s):

Andrew Srisuwananukorn ◽

Rasha Raslan ◽

Xu Zhang ◽

Binal N. Shah ◽

Jin Han ◽

...

Keyword(s):

Risk Factors ◽

Sickle Cell Disease ◽

Sickle Cell ◽

Genetic Risk ◽

Clinical Laboratory ◽

Genetic Risk Factors ◽

Cell Disease ◽

Thrombotic Risk ◽

Increased Risk ◽

Thrombotic Complications

Abstract Sickle cell disease (SCD) patients are at a four- to 100-fold increased risk for thrombosis compared with the general population, although the mechanisms and risk factors are not clear. We investigated the incidence and predictors for thrombosis in a retrospective, longitudinal cohort of 1193 pediatric and adult SCD patients treated at our institution between January 2008 and December 2017. SCD diagnosis and thrombotic complications were identified using International Classification of Diseases coding and verified through medical chart review. Clinical and laboratory data were extracted from the medical records. With a median follow-up of 6.4 years, 208 (17.4%) SCD patients experienced 352 thrombotic events (64 strokes, 288 venous thromboembolisms [VTE]). Risk factors for stroke included older age and HbSS/Sβ0-genotype and a lower hemoglobin (Hb) F% in the subset of HbSS/Sβ0-genotype patients (P < .05). VTE risk was independently associated with lower estimated glomerular filtration rate, hydroxyurea (HU) use, HbSS/Sβ0 genotype, and higher white blood cell (WBC) counts and Hb (P ≤ .03). Two thrombomodulin gene variants previously associated with thrombosis in the general African American population, THBD rs2567617 (minor allele frequency [MAF] 0.25; odds ratio [OR], 1.5; P = .049) and THBD rs1998081 (MAF, 0.24; OR, 1.5; P = .059), were associated with thrombosis in this cohort. In summary, thrombotic complications are common, and several traditional and SCD-specific risk factors are associated with thrombotic risk. Future studies integrating clinical, laboratory, and genetic risk factors may improve our understanding of thrombosis and guide intervention practices in SCD.

Download Full-text

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

Vascular Medicine ◽

10.1177/1358863x211012754 ◽

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.

Download Full-text