Clinical trial NCT05149261: Coagulopathy in Acute Aortic Syndrome
Official title: Coagulopathy in Acute Aortic Syndrome
Study type: OBSERVATIONAL
Overall status: UNKNOWN
Conditions: Coagulopathy
Keywords: Coagulopathy
Acute aortic dissection
Blood transfusion
Lead sponsor: European Georges Pompidou Hospital
Sponsor class: OTHER
First posted: 2021-12-08
Enrollment: 500
Sex: ALL
Minimum age (years): 18
Standard ages: ADULT
OLDER_ADULT
Observational model: COHORT
Time perspective: PROSPECTIVE
Sampling method: NON_PROBABILITY_SAMPLE
Study population: The EGPH offers, since 2009, a multidisciplinary network called "SOS Aorta" to centralize clinico-radiological suspicions of acute aortic syndrome in Ile de France and provide responsive and accessible medico-surgical care permanently. We included prospectively and analysed retrospectively (descripive study) all patient aged more than 18y who were admitted at EGPH for AAS suspicion via SOS Aorta Network.

Brief summary: The existence of AAS coagulopathy has been reported, related to blood contact with the walls of the non-endothelialized false lumens. It is likely that endothelial dysfunction generated by vascular lesions may largely contribute to the development of coagulopathy, such as described in trauma-induced coagulopathy. This endotheliopathy of the AAS has never been evaluated. The coagulopathy of AAS and more specifically the endotheliopathy are poorly described and therefore have no standardized treatment.

The main objective of this study is to describe the coagulopathy

Detailed description: Acute aortic syndromes (AAS) result from an organic lesion of the aortic wall. The various symptoms of AAS, mainly the acute chest pain, leads to a breakdown of the intima or the media of the aorta. This syndrome is made of three entities : aortic dissection (DA), intra-mural hematoma (HIM) and penetrating atherosclerotic ulcer (PAU). Surgery is a complex emergency treatment of choice. Patients suffering from these pathologies die mainly from hemorrhagic shock due to haemostasis disorders, which requires massive transfusion. The existence of AAS coagulopathy has been reported, related to blood contact with the walls of the non-endothelialized false lumens. It is likely that endothelial dysfunction generated by vascular lesions may largely contribute to the development of coagulopathy, such as described in trauma-induced coagulopathy. This endotheliopathy of the AAS has never been evaluated. The coagulopathy of AAS and more specifically the endotheliopathy are poorly described and therefore have no standardized treatment.

The main objective of this study is to describe the coagulopathy and more specifically the endotheliopathy of AAS, in particular assessing coagulation disorders, hyperactivation of fibrinolysis, quantitative or functional platelets disorder and endotheliopathy. The secondary objective is to determine the factors associated with this coagulopathy. This includes 1 / assessment of potential risk factors for coagulopathy, 2 / the prognosis of coagulopathy by assessing the relationship between coagulopathy and transfusion requirements and mortality.

Eligibility criteria: Inclusion Criteria:

* admitted to hospital via the "SOS Aorta" network for acute aortic syndrome (AAS) suspicion

Exclusion Criteria:

* aged \< 18y
* pregnant women
* no social security

Primary outcomes:
measure: total transfusion requirements
timeFrame: Day 2
measure: death from AAS
timeFrame: Day 30
measure: coagulopathy rTQ > 1.2 incidence
timeFrame: baseline
Secondary outcomes:
measure: total transfusion requirements
timeFrame: Day 1
measure: total transfusion requirements
timeFrame: Day 2
measure: total transfusion requirements
timeFrame: Day 3
measure: total transfusion requirements
timeFrame: Day 7
measure: biological AAS coagulopathy : coagulation factors consumption
timeFrame: Day 1, Day 2, Day 3, Day 7
measure: biological AAS coagulopathy : coagulation factors consumption
timeFrame: Day 2
measure: biological AAS coagulopathy : coagulation factors consumption
timeFrame: Day 3
measure: biological AAS coagulopathy : coagulation factors consumption
timeFrame: Day 7
measure: biological AAS coagulopathy : fibrinolysis D-dimers
timeFrame: Day 1
measure: biological AAS coagulopathy : fibrinolysis D-dimers
timeFrame: Day 2
measure: biological AAS coagulopathy : fibrinolysis D-dimers
timeFrame: Day 3
measure: biological AAS coagulopathy : fibrinolysis D-dimers
timeFrame: Day 7
measure: hospitalisation duration
timeFrame: hospital discharge
measure: impact of misdiagnosis and misdiagnosis-induced treatments
timeFrame: Day 2
measure: impact of misdiagnosis and misdiagnosis-induced treatments
timeFrame: Day 7
measure: platelets dysfunction
timeFrame: day 1
measure: platelets dysfunction
timeFrame: day 2
measure: platelets dysfunction
timeFrame: day 3
measure: platelets dysfunction
timeFrame: day 7
measure: platelets dysfunction
timeFrame: baseline
measure: endotheliopathy
timeFrame: baseline
measure: endotheliopathy
timeFrame: baseline
measure: endotheliopathy
timeFrame: baseline
measure: endotheliopathy
timeFrame: baseline
measure: endotheliopathy
timeFrame: baseline
measure: endotheliopathy
timeFrame: baseline
measure: endotheliopathy
timeFrame: baseline
measure: endotheliopathy
timeFrame: baseline
measure: symptoms-surgery delay
timeFrame: baseline
measure: clinical severity shock
timeFrame: baseline
measure: clinical severity shock
timeFrame: baseline
measure: clinical severity shock
timeFrame: baseline
Other outcomes:
Locations:
city: Paris
country: France
facility: Université de Paris
Study officials:
affiliation: European Georges Pompidou Hospital
name: Diane Zlotnik, MD
role: PRINCIPAL_INVESTIGATOR
affiliation: European Georges Pompidou Hospital
name: Anne Godier, MD-PhD
role: STUDY_CHAIR
References: