Aspirin Response in High Risk Patients With Coronary Artery Disease

Is a Reduced Biochemical Response to Aspirin Associated With Increased Cardiovascular Morbidity and Mortality in High Risk Patients With Coronary Artery Disease?

Status

UNKNOWN

Phases

Unknown

Study type

Observational

Source

ClinicalTrials.gov

Registry ID

NCT01383304

Enrollment

906

Registered

2011-06-28

Start date

2007-11-30

Completion date

2017-01-31

Last updated

2016-05-12

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Coronary Artery Disease, Diabetes Mellitus, Myocardial Infarction, Renal Insufficiency, Chronic

Keywords

Platelet aggregation, Aspirin, Drug resistance, Thromboxane B2, Pharmacologic Actions, Platelet Aggregation Inhibitors

Brief summary

Previous studies indicate that patients with cardiovascular disease have a variable response to aspirin. Despite treatment with aspirin a large number of patients suffer a myocardial infarction. This has given rise to the phenomenon aspirin low-responsiveness. Laboratory aspirin low-responsiveness can be defined as the failure of aspirin to inhibit platelet production of thromboxane A2 or inhibit thromboxane-dependent platelet aggregation. Whether a low platelet response to aspirin results in an increased risk of future thrombotic events is of great clinical significance, but is still unknown. The investigators hypothesize that patients with a reduced response to aspirin, determined by platelet aggregation using the apparatus Verify Now Aspirin and Multiplate, have a higher risk of thrombosis. The purpose of this study is to investigate whether a higher incidence of cardiovascular events is found in patients with coronary artery disease (CAD) having a reduced biochemical response to aspirin compared with CAD patients having a normal biochemical response to aspirin. In addition to CAD, all patients have at least one of the following risc factors: previous myocardial infarction, type 2 diabetes mellitus and/or renal insufficiency.

Interventions

None listed

Study design

Observational model

COHORT

Time perspective

PROSPECTIVE

Eligibility

Sex/Gender

ALL

Age

18 Years to No maximum

Healthy volunteers

Inclusion criteria

* Coronary artery disease verified by coronary angiogram * Treatment with aspirin 75 mg/d for at least the previous 7 days * Previous myocardial infarction more than one year ago (groups with previous myocardial infarction) * Type 2 diabetes mellitus treated with oral antidiabetics and/or insulin (groups with type 2 diabetes mellitus) * Renal insufficiency; glomerular filtration rate \<60 ml/min at the time of blood sampling (groups with renal insufficiency)

Exclusion criteria

* Treatment with NSAIDs, clopidogrel, ticlopidine, dipyridamole, warfarin or any other drugs known to affect platelet function * Ischemic vascular event within the previous 12 months * Revascularization (angioplasty or coronary by-pass graft surgery) within the previous 12 months * Platelet count \<120 x 10\^9/L or \>450 x 10\^9/L * For patients without diabetes: fast glucose \>7 mmol/L * Unable to give informed consent

Design outcomes

Primary

Measure	Time frame
Combined primary endpoint: Cardiovascular death, acute myocardial infarction, ischaemic stroke	Evaluation after 3 years

Secondary

Measure	Time frame
Combined secondary endpoint: Cardiovascular death, acute myocardial infarction, ischaemic stroke	Evaluation after 5 years
Single endpoints:cardiovascular death; acute myocardial infarction; ischemic stroke; stent thrombosis; all-cause death	Evaluation after 3 and 5 years

Other

Measure	Time frame	Description
Genotype according to pre-specified genetic single nucleotide polymorphisms (SNPs)	Baseline	At the day of blood sampling, plasma samples are retrieved for DNA extraction. DNA samples are used to evaluate if pre-specified genetic single nucleotide polymorphisms (SNPs) are associated with platelet aggregation levels.

Countries

Denmark

Outcome results