Assessment of Thrombogenicity in Acute Coronary Syndrome
The purpose of this study is to assess platelet dependent thrombogenicity in patients after acute coronary syndrome using an ex vivo arterial injury model.
Type 2 Diabetes Mellitus
Acute Coronary Syndrome
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
|Official Title:||Assessment of Platelet-dependent Thrombosis in Patients With Acute Coronary Syndromes Using an ex Vivo Arterial Injury Model|
- Thrombus area [ Time Frame: Within 10 days after acute coronary syndrome ] [ Designated as safety issue: No ]
- Factors affecting thrombus area [ Time Frame: Within ten days after acute coronary syndrome ] [ Designated as safety issue: No ]
|Study Start Date:||October 2008|
|Study Completion Date:||May 2011|
|Primary Completion Date:||January 2011 (Final data collection date for primary outcome measure)|
Type 2 diabetes mellitus
We aim to determine the effects of dual antiplatelet therapy with aspirin 75mg once a day and clopidogrel 75mg once a day on platelet dependent thrombogenicity in patients with type 2 diabetes mellitus and acute coronary syndrome. Eighty patients (40 with type 2 diabetes and 40 without) have been studied one week after Non ST-elevation acute coronary syndrome. All patients were on secondary prevention therapy as recommended by international guidelines.
Abnormal platelet activity seen in patients with Type2 Diabetes Mellitus (T2DM) may be an important contributor to their enhanced cardiovascular risk and higher rates of cardiovascular events following acute coronary syndrome, despite dual antiplatelet therapy with aspirin and clopidogrel. We have earlier demonstrated high thrombogenicity in individuals with T2DM and CAD in the absence of acute ischaemic events, despite therapeutic doses of aspirin.We hypothesise that patients with T2DM will have increased thrombogenicity after acute coronary syndrome despite optimal secondary prevention medication.Measuring ex vivo thrombus area using an arterial injury model simulates plaque rupture and reflects the summative effect of all haemostatic abnormalities. The thrombus area of patients with ACS and T2DM will be compared to the controls without T2DM.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00728286
|Royal Victoria Hospital, Newcastle upon Tyne Hospitals NHS Trust|
|Newcastle upon Tyne, Tyne and Wear, United Kingdom, NE1 4LP|
|Principal Investigator:||Azfar G Zaman, MD FRCP||Freeman Hospital, Newcastle upon Tyne NHS Trust, Newcastle upon Tyne. NE7 7DN|