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Coagulation Activity and Thrombogenesis in Patients With Atrial Fibrillation

NCT02451254 · Status: COMPLETED · Phase: NA · Type: INTERVENTIONAL · Enrollment: 60

Last updated 2019-05-24

No results posted yet for this study

Summary

Atrial fibrillation confers up to 5-fold increased risk of stroke in the absence of valvular heart disease. Although epidemiological studies have linked various clinical and echocardiographic risk factors to stroke, the exact mechanism of increased risk of stroke in AF remains poorly understood. Previous reports have suggested that loss of effective atrial contraction because of AF is associated with thrombogenesis. Microthrombi are most likely to form in the left atrial appendage. In contrast, intravascular thrombotic events in patients without AF are generally associated with abnormalities of vascular endothelial function and/or the coagulation system. On the assumption that more than 90% of all cardiac thrombi in patients with AF form in the LA appendage, and the fact that thrombi have been identified in 15-20% of patients with AF who have clinical risk factors for ischemic stroke, it has been deemed to be "our most lethal attachment". Administration of anticoagulant therapy is generally thought to be necessary as a preventive measure for patients at high risk of thromboembolism, but data indicating inadequate implementation of this highly effective therapy\]. Several studies have found regional differences in platelet activation and hypercoagulability in the LA compared with systemic circulation in patients with valvular and nonvalvular AF, suggesting local contributing factors. Animal studies have demonstrated increased platelet activation and endothelial dysfunction with acute AF. The ability of antiplatelet agents to reduce the risk of cardioembolic events in AF suggests that platelets may contribute to the pathophysiology. Platelet activation occurs with AF and rapid atrial pacing, providing a possible mechanistic link. Other biomarkers that have proposed to improve the prediction of thromboembolotic events in this patient population include von Willebrand factor and D-dimer and cerebral imaging. A comprehensive understanding of the pathophysiological sequence leading to thrombus formation in the LAA of patients with AF could be helpful to characterize those at high risk for thromboembolic events, and subsequently to optimize the management of high risk patients.

Conditions

Interventions

PROCEDURE

circumferential ablation

circumferential ablation of the pulmonary veins

DEVICE

SVT ablation

SVT ablation

Sponsors & Collaborators

  • Tel-Aviv Sourasky Medical Center

    lead OTHER_GOV

Principal Investigators

  • Ehud Chorin, MD · Tel Aviv Medical Center

Study Design

Allocation
NON_RANDOMIZED
Purpose
TREATMENT
Masking
NONE
Model
SINGLE_GROUP

Eligibility

Min Age
18 Years
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2015-12-01
Primary Completion
2018-06-12
Completion
2019-05-22

Countries

  • Israel

Study Locations

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Entities

Diseases

Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT02451254 on ClinicalTrials.gov