MedPath

Prasugrel in Severe COVID-19 Pneumonia

Phase 3
Conditions
COVID19
Thrombosis
Interventions
Registration Number
NCT04445623
Lead Sponsor
Azienda Ospedaliera Universitaria Integrata Verona
Brief Summary

Inflammatory diseases favour the onset of venous thromboembolic events in hospitalized patients. Thromboprophylaxis with a fixed dose of heparin/low molecular weight heparin (LMWH) is recommended if concomitant inflammatory disease. In severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) pneumonia an inflammation-dependent thrombotic process occurs and platelet activation may promote thrombosis and amplify inflammation, as indicated by previous experimental evidence , and the similarities with atherothrombosis and thrombotic microangiopathies. Antiplatelet agents represent the cornerstone in the prevention and treatment of atherosclerotic arterial thromboembolism, with limited efficacy in the context of venous thromboembolism. The use of purinergic receptor P2Y12 inhibitors in pneumococcal pneumonia may improve inflammation and respiratory function in humans. There are no validated protocols for thrombosis prevention in Covid-19. There is scientific rationale to consider a P2Y12 inhibitor for the prevention of thrombosis in the pulmonary circulation and attenuation of inflammation. This is supported by numerous demonstrations of the anti-inflammatory activity of P2Y12 inhibitors and the evidence of improvement in respiratory function both in human and experimental pathology. Prasugrel could be considered as an ideal candidate drug for Covid-19 patients because of higher efficacy and limited Interactions with drugs used in the treatment of Sars-CoV2. The hypothesis underlying the present study project is that in Covid-19 platelet activation occurs through an inflammation-dependent mechanism and that early antithrombotic prophylaxis in non-critical patients could reduce the incidence of pulmonary thrombosis and respiratory and multi-organ failure improving clinical outcome in patients with SARS-CoV2 pneumonia. The prevention of thrombogenic platelet activity with a P2Y12 inhibitor could be superior to fixed dose enoxaparin alone. The proposed treatment is feasible in all coronavirus disease 2019 (COVID-19) patients, regardless of the treatment regimen (antivirals, anti-inflammatory drugs, antibiotics), except for specific contraindications.

Detailed Description

Severe respiratory failure and multi-organ damage in coronavirus disease 2019 (COVID-19) patients have not a unitary pathophysiological interpretation. There is evidence of an association between the clinical entity of the disease and its severity with the plasma levels of D-dimer and inflammatory indexes. On the basis of retrospective investigations there is accumulating evidence of alterations in the haemostatic parameters that with increased D-dimer values, increased coagulation time and platelets may be predictors of worse prognosis. A systematic survey conducted in the coronavirus disease 2019 (COVID-19) Centre of the AOUI Verona, as part of the Database and Study on the role of platelets in the clinical manifestations of COVID-19 (Ethics Committee CESC Verona and Rovigo approved) revealed by means of computerized tomography (CT) angiograph in patients with a persistent respiratory deficit and very high D-dimer values mainly multiple, bilateral vascular occlusions involving the segmental and subsegmental branches of the pulmonary arteries. This finding is suggestive of a frequent and clinically relevant thrombotic process in a appreciable number (approximately 20%) of patients with COVID-19 pneumonia hospitalized in medical wards. It is a well-established clinical notion that acute and chronic inflammatory diseases may favour the onset of venous thromboembolic events in hospitalized patients. Thromboprophylaxis with a fixed dose of heparin/low molecular weight heparin (LMWH) is recommended for medical patient with concomitant neoplasia or inflammatory disease. It is conceivable that under conditions, such as SARS-CoV2 pneumonia, an inflammation-dependent thrombotic process takes place and that platelet activation may play a pathogenic role both in the thrombotic process and in the amplification of the inflammatory process. In fact, there is experimental evidence that platelet activation in inflammation would lead to accelerated coagulation and a thrombotic vascular occlusion, with similarities to what is widely documented in atherothrombosis and thrombotic microangiopathies. The administration of antiplatelet drugs represents the cornerstone for the prevention and treatment of arterial thromboembolism in atherosclerotic disease and has also shown some limited efficacy also in the context of venous and arterial thromboembolism associated with atrial fibrillation. Preliminary observations indicate that the use of purinergic receptor P2Y12 inhibitors during pneumococcal pneumonia may improve the inflammatory process and respiratory function in humans. There are currently no validated protocols for thrombosis prevention in the field of pulmonary viral diseases, in particular COVID-19. There is adequate scientific rationale to consider the use of a P2Y12 inhibitor antiplatelet drug for the prevention of thrombosis in the pulmonary circulation and the attenuation of pulmonary inflammation. The use of a P2Y12 inhibitor is motivated by numerous experimental demonstrations of the anti-inflammatory activity of P2Y12 inhibitors and by the evidence of improvement of respiratory function parameters both in humans and experimental models. Prasugrel could be considered as an ideal candidate drug for administration in Covid-19 patients because of its higher efficacy in acute coronary syndrome compared to clopidogrel. Interactions of prasugrel with drugs used for the treatment of SARS-CoV2 are limited. The hypothesis underlying the present study project is that in Covid-19 platelet activation occurs via an inflammation-dependent mechanism and that early antithrombotic prophylaxis in non-critical patients, like those admitted to medical wards, could reduce the incidence of pulmonary thrombosis as well as respiratory and multi-organ failure, contributing to improve clinical outcome of the patients with pneumonia caused by SARS-CoV2 viruses. The anticoagulant activity exerted by a fixed dose of enoxaparin (4000U/day), recommended in patients with the clinical features described, according to a note of the "Italian Medicines Agency" (AIFA), together with the prevention of thrombogenic activity of platelets by means of a P2Y12 inhibitor could prevent aggravation of COVID-19 patients to a greater extent than enoxaparin alone given at the same dose. Early initiation of treatment should mitigate the presentation of pneumonia. The proposed treatment is feasible in all COVID-19 patients, regardless of the treatment regimen used for their condition (antivirals, anti-inflammatory drugs, antibiotics), except for specific contraindications to the use of prasugrel, or placebo if patients are treated with antiplatelet drugs.

Recruitment & Eligibility

Status
UNKNOWN
Sex
All
Target Recruitment
128
Inclusion Criteria
  • Covid-19 pneumonia
  • Age over 18 years
  • Willingness to express consent
Exclusion Criteria
  • Active neoplasia or in maintenance therapy
  • Pregnancy and breastfeeding
  • Any absolute contraindication to the use of antiplatelet drugs
  • Pathological bleeding in progress.
  • Recent major bleeding at any location
  • Need to use therapeutic doses of oral anticoagulants or heparins
  • Need to use antiplatelet in combination for clinical indication
  • Hypersensitivity to the active substance prasugrel or any of the excipients
  • Clinical history of stroke or transient ischemic attack (TIA).
  • Severe liver failure (Child-Pugh class C).

Study & Design

Study Type
INTERVENTIONAL
Study Design
PARALLEL
Arm && Interventions
GroupInterventionDescription
placeboPlacebofilm-coated tablets of placebo (10 mg daily dose after loading dose of 60 mg)
prasugrel hydrochloridePrasugrel Hydrochloride 10 MG Oral Tabletfilm-coated tablets of prasugrel hydrochloride (10 mg daily dose after loading dose of 60 mg)
Primary Outcome Measures
NameTimeMethod
P/F ratio at day 7day 7

PaO2/FiO2 ratio (arterial oxygen tension divided by the fraction of inspired oxygen) detected after 7 days of treatment

Secondary Outcome Measures
NameTimeMethod
Clinical progression of the disease SOFA scoreday 15 and day 30

Clinical progression of the disease evaluated by SOFA score (Units 0-6 better outcome, 15-24 worse outcome) by day 15 and day 30

Clinical progression of the disease APACHE IIday 15 and day 30

Clinical progression of the disease evaluated by Acute Physiology And Chronic Health Evaluation (APACHE II) score (Units 1-5 better outcome, over 30 worse outcome) by day 15 and day 30

Venous thrombosis/ pulmonary embolism/thrombosisday 15 and day 30

Number of patients with venous thrombosis/ pulmonary embolism/thrombosis by day 15 and day 30

Daily total blood count Leukocytes15 days

Total blood count measured in venous blood for 15 days, Leukocytes (cell/mcL)

Indices of inflammation C-reactive proteinday 1, 2, 7, 15

C-reactive protein microg/L in venous blood

Daily progression at imaging (chest-X-ray)15 days

progression of lung infiltrates as detected by chest-X-ray by treatment arm

Total bleedingday 1, 2, 7, 15, 30

Total bleeding according to International Society of Thrombosis and Haemostasis (ISTH bleeding) scale (Unit 0 better outcome, 4 worse outcome, 11 items) during treatment.

Unexpected clinical or laboratory findingsday 1, 2, 7, 15

Number of unexpected changes in clinical or laboratory findings not included in the predefined list of outcomes during treatment. .

Indices of inflammation D-dimerday 1, 2, 7, 15

D-dimer microg/L in venous blood

Indices of inflammation IL-1day 1, 2, 7, 15

Interleukin (IL)-1 pg/mL in venous blood by treatment arm

Death15 day and day 30

death by day 15 and day 30 by treatment arm

Daily total blood count Red Blood Cells15 days

Total blood count measured in venous blood for 15 days, Red Blood cells (cell/mcL)

Daily P/F ratio15 days

PaO2/FiO2 ratio (arterial oxygen tension divided by the fraction of inspired oxygen) detected daily for 15 days

Daily blood pressure15 days

Blood pressure measured twice daily for 15 days, mmHg

Daily indices of organ damage Liver15 days

ALT U/L in venous blood

Indices of inflammation IL-6day 1, 2, 7, 15

Interleukin (IL)-6 pg/mL in venous blood by treatment arm

Daily need for oxygen supply15 days

daily need for oxygen supply for 15 days

MOFday 15 and day 30

Multi-organ failure (MOF) by day 15 and day 30 assessed using sequential organ failure assessment score (SOFA) score (Units 0-4 better outcome, over 30 worse outcome) by treatment arm

Indices of haemostasis PTday 1, 2, 7,15

PT ratio in venous blood by treatment arm

Need for ICUday 15 and day 30

Number of patients requiring transfer to the intensive care unit (ICU) by treatment arm

Dischargeday 15 and day 30

Number of patients discharged after improvement by day 15 and day 30 by treatment arm

Need for CT imagingday 15

Number of patients requiring computerized tomography (CT) imaging due to worsening of respiratory function by treatment arm

Daily Temperature15 days

Body temperature measured twice daily for 15 days, C°

Daily total blood count Hemoglobin15 days

Total blood count measured in venous blood for 15 days, Hemoglobin, g/L (cell/mcL

Daily total blood count Platelets15 days

Total blood count measured in venous blood for 15 days, platelets (cell/mcL)

Major bleedingday 1, 2, 7, 15, 30

Major and/or clinically relevant bleeding according to International Society of Thrombosis and Haemostasis (ISTH) bleeding scale (Unit 0 better outcome, 4 worse outcome, 11 items) during treatment.

Indices of inflammation Fibrinogenday 1, 2, 7, 15

Fibrinogen g/L in venous blood

Haemostasis aPTTday 1, 2, 7,15

aPTT ratio by treatment arm

Haemostasis VASP PRIday 1, 2, 7,15

Vasodilator stimulated phosphoprotein (VASP) phosphorylation (PRI) % by treatment arm

Haemostasis platelet-leukocytes aggregatesday 1, 2, 7,15

Platelet-leukocytes aggregates % in peripheral by treatment arm

Daily indices of organ damage heart15 days

troponin t ng/L by treatment arm

Daily indices of organ damage kidney15 days

serum creatinine micromol/L by treatment arm

Trial Locations

Locations (1)

Azienda Ospedaliera Universitaria Integrata Verona

🇮🇹

Verona, Italy

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