Ignite Creation Date:
2024-05-06 @ 7:51 AM
Last Modification Date:
2024-10-26 @ 11:53 AM
Study NCT ID:
NCT02616497
Status:
COMPLETED
Last Update Posted:
2018-04-17
First Post:
2015-11-20
Brief Title:
ASpirin vs Triflusal for Event Reduction In Atherothrombosis Secondary Prevention ASTERIAS
Sponsor:
University of Ioannina
Organization:
University of Ioannina
Study Overview
Official Title:
Comparison of Triflusal With Aspirin in the Secondary Prevention of Atherothrombotic Events
Status:
COMPLETED
Status Verified Date:
2018-04
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
ASTERIAS
Brief Summary:
Investigation of the efficacy and safety of triflusal in comparison with aspirin in patients with stable coronary artery disease CAD and in those with a history of an acute non-cardioembolic ischemic stroke
Detailed Description:
Triflusal 2-acetyloxy-4-trifluoromethyl benzoic acid is an antiplatelet agent with a chemical structure similar to aspirin but with a different pharmacokinetic and pharmacodynamic profile The drug is administered orally and its bioavailability ranges from 83 to 100 It binds almost entirely 99 to plasma proteins and crosses readily organic barriers Triflusal is deacetylated in the liver forming its main metabolite 2-hydroxy-4-trifluoromethyl benzoic acid HTB In contrast to the inactive aspirin metabolite salicylic acid HTB exhibits antiplatelet activity and has a long plasma half-life of approximately 40h Triflusal irreversibly inhibits COX-1 and reduces TxA2 production but to a lesser extent compared with aspirin It inhibits COX-1 and AA metabolism selectively in platelets preserving PGI2 synthesis in vascular endothelial cells 1 Except of platelet COX-1 triflusal and in particular HTB inhibit phosphodiesterase the enzyme that degrades the cyclic nucleotides cyclic adenosine monophosphate c-AMP and cyclic guanosine monophosphate c-GMP both of which inhibit platelet function
Triflusal has similar to aspirin efficacy for the secondary prevention of vascular events in patients with acute myocardial infarction MI and stroke while it reduces the incidence of intracranial and gastrointestinal haemorrhage compared with aspirin It should be noted that triflusal is well tolerated in patients with aspirin-induced asthma
Aspirin acetyl salicylic acid remains for over 50 years the cornerstone of antiplatelet therapy due to its proven clinical benefit and very good cost effectiveness profile Aspirin selectively and irreversibly acetylates the hydroxyl group of a single serine residue at position 529 within the polypeptide chain of PGH synthase-1 Thus aspirin inhibits the COX-1 activity but it does not affect the hydroperoxidase activity PGH synthase-1 By blocking COX-1 the production of TXA2 is reduced leading to reduced platelet aggregation Aspirin improves clinical outcome in all cardiovascular syndromes in primary and secondary prevention including acute events In high-risk patients aspirin substantially reduces the risk of vascular death by 15 and non-fatal vascular events by 30 as it reported by a meta-analysis of over 100 large-scale randomized trials Several studies the last years have suggested that a proportion of patients 5 to 65 exhibit a hyporesponsiveness resistance to aspirin treatment which could be associated with recurrent ischemic events Aspirin resistance may result from several causes such as low compliance interference with non-steroid anti-inflammatory drugs NSAIDS and protein glycation occurring in type 2 diabetes mellitus Increased platelet turnover observed in various diseases such as ACS peripheral arterial disease and diabetic angiopathy associated with faster re-appearance of newly formed non aspirinated platelets may also account for aspirin resistance
Although triflusal is chemically related to aspirin and has similar effectiveness it appears to have a better tolerability profile than aspirin Results from large-scale clinical trials and a meta-analysis suggest that its use may be preferable to that of aspirin in several clinical settings where antiplatelet therapy is indicated Furthermore in selected populations such as in geriatric patients because of an increased risk of bleeding complications in patients suffering from asthma chronic sinusitis and nasal polyps or in cases of aspirin resistance triflusal may be a choice worth considering Furthermore when combination antiplatelet-fibrinolytic or antiplatelet-anticoagulant therapy is needed clinical data support triflusal use based on its efficacy and better safety than aspirin Unlike aspirin triflusal also less likely affect the efficacy of antihypertensive drugs especially angiotensin converting enzyme inhibitors The aim of the present trial is to investigate the efficacy and safety of triflusal in comparison with aspirin in patients with stable coronary artery disease CAD and in those with a history of an acute non-cardioembolic ischemic stroke
Triflusal has similar to aspirin efficacy for the secondary prevention of vascular events in patients with acute myocardial infarction MI and stroke while it reduces the incidence of intracranial and gastrointestinal haemorrhage compared with aspirin It should be noted that triflusal is well tolerated in patients with aspirin-induced asthma
Aspirin acetyl salicylic acid remains for over 50 years the cornerstone of antiplatelet therapy due to its proven clinical benefit and very good cost effectiveness profile Aspirin selectively and irreversibly acetylates the hydroxyl group of a single serine residue at position 529 within the polypeptide chain of PGH synthase-1 Thus aspirin inhibits the COX-1 activity but it does not affect the hydroperoxidase activity PGH synthase-1 By blocking COX-1 the production of TXA2 is reduced leading to reduced platelet aggregation Aspirin improves clinical outcome in all cardiovascular syndromes in primary and secondary prevention including acute events In high-risk patients aspirin substantially reduces the risk of vascular death by 15 and non-fatal vascular events by 30 as it reported by a meta-analysis of over 100 large-scale randomized trials Several studies the last years have suggested that a proportion of patients 5 to 65 exhibit a hyporesponsiveness resistance to aspirin treatment which could be associated with recurrent ischemic events Aspirin resistance may result from several causes such as low compliance interference with non-steroid anti-inflammatory drugs NSAIDS and protein glycation occurring in type 2 diabetes mellitus Increased platelet turnover observed in various diseases such as ACS peripheral arterial disease and diabetic angiopathy associated with faster re-appearance of newly formed non aspirinated platelets may also account for aspirin resistance
Although triflusal is chemically related to aspirin and has similar effectiveness it appears to have a better tolerability profile than aspirin Results from large-scale clinical trials and a meta-analysis suggest that its use may be preferable to that of aspirin in several clinical settings where antiplatelet therapy is indicated Furthermore in selected populations such as in geriatric patients because of an increased risk of bleeding complications in patients suffering from asthma chronic sinusitis and nasal polyps or in cases of aspirin resistance triflusal may be a choice worth considering Furthermore when combination antiplatelet-fibrinolytic or antiplatelet-anticoagulant therapy is needed clinical data support triflusal use based on its efficacy and better safety than aspirin Unlike aspirin triflusal also less likely affect the efficacy of antihypertensive drugs especially angiotensin converting enzyme inhibitors The aim of the present trial is to investigate the efficacy and safety of triflusal in comparison with aspirin in patients with stable coronary artery disease CAD and in those with a history of an acute non-cardioembolic ischemic stroke
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None