Mechanistic Study of Bleeding Risk in Coronary Patients With Cerebrovascular Disease

Mechanisms Involved in the Bleeding Risk of Patients With Coronary Artery Diseased Previous Stroke or Transient Ischemic Attack in Use of Antiplatelet Therapy

Status

Completed

Phases

Unknown

Study type

Observational

Source

ClinicalTrials.gov

Registry ID

NCT02316119

Enrollment

140

Registered

2014-12-12

Start date

2013-01-31

Completion date

2016-04-30

Last updated

2016-04-26

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

Conditions

Cerebral Stroke, Coronary Artery Disease, TIA (Transient Ischemic Attack)

Keywords

bleeding risk, acute coronary syndrome, platelet agregation,

Brief summary

Background: About 5% of patients with acute coronary syndrome (ACS) have had previously ischemic stroke (IS) or transitory ischemic attack (TIA). This is a high-risk population, with a high incidence of ischemic events, and also of bleeding events. While the high ischemic risk in this population is attributed to a higher prevalence of cardiovascular risk factors, their predisposition to bleeding events is not well understood. Hypothesis: The increased bleeding risk in ACS patients with history of cerebrovascular event may be justified by a low platelet activity. Methods: Unicentric, prospective, case-control study, which included approximately 100 post-ACS patients with history of IS/TIA previously to the acute coronary event (Case Group) and 100 patients without IS/TIA (Control group). The groups were matched for gender, age, and ACS type and year of occurrence. All patients were taking aspirin, and the main exclusion criteria were use of dual antiplatelet therapy, previous hemorrhagic stroke, severe renal dysfunction, thrombocytopenia or coagulopathy. Main analysis: Platelet aggregation was evaluated by 6 methods: VerifyNow Aspirin®, VerifyNow P2Y12®, PFA 100®, thrombelastography (ReoRox®), light transmission aggregometry with ADP (LTA ADP) and epinephrine (LTA EPI) as agonists. Additional analysis: genetic, HDL transport and inflammatory evaliation

Interventions

None listed

Study design

Observational model

CASE_CONTROL

Time perspective

PROSPECTIVE

Eligibility

Sex/Gender

ALL

Age

18 Years to No maximum

Healthy volunteers

Inclusion criteria

* Post-ACS patients with history of IS/TIA previously to the acute coronary event and taking aspirin * Sign the consent form

Exclusion criteria

* Hemorrhagic stroke * Another antiplatelet drug than aspirin * Use of Anti inflammatory drug * Severe chronic kidney dysfunction * Liver disease * Coagulopathy * Platelet disfunction * Thrombocytopenia or thrombocytosis * Refuse to sign the consent form

Design outcomes

Primary

Measure	Time frame
Residual platelet activity by VerifyNow Aspirin (Aspirin reactivity units)	in the selection visit

Secondary

Measure	Time frame
Baseline platelet activity by VerifyNow P2Y12 (P2Y12 reactivity units)	in the selection visit

Other

Measure	Time frame
light transmission aggregometry with ADP (maximum amplitude)	in the selection visit
light transmission aggregometry with epinephrine (maximum amplitude)	in the selection visit
platelet acitivity by PFA 100® (seconds)	in the selection visit
kinetics of clot by thromboelastography usin Reorox ® (seconds, paschal/min, paschal)	in the selection visit

Countries

Brazil

Outcome results