View clinical trials related to SCAD.
Filter by:Rationale: The interaction between nonvitamin K oral anticoagulants (NOACs) and platelet aggregation is complex. The direct activated factor X inhibitors (factor Xa inhibitors) an NOAC antagonizes thrombin generation, one of most important platelet agonist, so that, factor Xa inhibitors has a potential effect in decreasing thrombin-mediated platelet aggregation. On the other hand, patients who experience ACS continue to have a hypercoagulable state for long periods after the index event. The COMPASS trial showed that, in patients with stable coronary artery disease (SCAD), Rivaroxaban (a direct anti-Xa inhibitor) in addition to antiplatelet agent, compared to antiplatelet therapy alone, reduced the composite endpoint of myocardial infarction, stroke and death. Objective: Analyze the role of edoxaban on platelet aggregation in SCAD patients. Methods and Results: This is a prospective, non-randomized, interventional study of SCAD patients taking low-dose acetylsalicylic acid (ASA). Subjects initially will receive in the following sequence: ASA 100 mg once daily (QD) plus edoxaban 60 mg QD, clopidogrel 75 mg QD alone, clopidogrel 75 mg QD plus edoxaban 60 mg QD, and edoxaban 60 mg QD alone. Platelet function will be assessed by standard of care technology, at baseline and after each intervention phase, by Multiplate-ADP® (primary endpoint), Multiplate-Aspi® and Multiplate-TRAP®. In addition to immature platelets fraction (% IPF) and count (IPC). Coagulability will be assessed, at baseline and after each intervention phase, by thromboelastogram (TEG) assessment. Specifically, after the phases in which edoxaban will be administered activated factor X (FXa) level and Plasminogen activator inhibitor-1 (PAI-1) will be evaluated in addition to previous. Finally, inflammatory markers will be, at same way, assessed at baseline and after intervention each phase: ultrasensitive C-reactive protein (us-PCR). Keywords: edoxaban, direct factor Xa inhibitor, stable coronary artery disease, aspirin, clopidogrel, platelet aggregation.
Within a CAD patient cohort there is a wide variability of clinical manifestation and severity of coronary disease. Distinct determinants that would explain the variety of CAD phenotypes with differing prognosis are yet undiscovered. Aim of this study is to find genetic variants, biomarkers, and clinical cardiovascular risk factors that relate to specific coronary artery disease phenotypes and related pathologies in a patient population.
Natural history multicenter, prospective, observational registry with 10-year follow-up
This case control study aims to determine whether spontaneous coronary artery dissection (SCAD) is associated with autoimmune diseases and to update the incidence of SCAD in a population-based cohort.
The primary goal of this project is to describe the clinical and physiologic characteristics of Spontaneous Coronary Artery Dissections (SCAD) in order to increase awareness, understanding, treatment and prevention of a potentially fatal cardiovascular event. This study will be a retrospective and prospective review of medical course and current health of men and women with SCAD.
The purpose of the research is to identify mutations (defects in the genetic blueprint) that cause spontaneous coronary artery dissection (SCAD), in other words, spontaneous tears in blood vessels that supply the heart. Some mutations may be inherited (passed on) from a parent without an apparent blood vessel problem while others may develop for the first time in the affected person.