Relationship Between Sleep Apnea Syndrome and Patent Foramen Ovale Among Victims of Cryptogenic Ischemic Stroke

Stroke Clinical Trial

Official title:

Assessment of the Relationship Between Sleep Apnea Syndrome and Patent Foramen Ovale Among Young Subjects Victims of Cryptogenic Ischemic Stroke

Clinical Trial Details — Status: Enrolling by invitation

Administrative data

• NCT number: NCT04846205
• Other study ID #: IRBN212021/CHUSTE
• Status: Enrolling by invitation
• Start date: March 24, 2021
• Est. completion date: October 1, 2021

Study information

• Verified date: April 2021
• Source: Centre Hospitalier Universitaire de Saint Etienne
• Contact: n/a
• Is FDA regulated: No
• Study type: Observational

Clinical Trial Summary

Obstructive sleep apnea syndrome (OSAS) and patent foramen ovale (FOP) are considered as risk factors for stroke. OSAS generates a pressure increase in the right cavity during inspiratory efforts, which increases the number of right-left shunt embolus and therefore the risk of stroke. OSA and FOP are often thought as two separate entities, however, due to their high frequencies, they sometimes coexist and can influence the pathophysiology of each other. More researches are needed in this area to confirm this complex association and its role in triggering stroke.

Description:

Obstructive sleep apnea syndrome (OSAS) and patent foramen ovale (PFO) are considered as risk factors for stroke. In most cases, the presence of FOP has no clinical impact. Certain hemodynamic conditions inducing a right-left pressure gradient can promote the reopening of a FOP and allow the passage of blood, presenting micro or macro-thrombi, from the venous system to the arterial system, explaining the mechanism of paradoxical embolism. OSAS generates a pressure increase in the right cavity during inspiratory efforts, which increases the number of right-left shunt embolus and therefore the risk of stroke. OSA and FOP are often thought as two separate entities, however, due to their high frequencies, they sometimes coexist and can influence the pathophysiology of each other. Evidence of a clinically significant interaction and causation in the genesis of stroke remains limited. More researches are needed in this area to confirm this complex association and its role in triggering stroke.

Recruitment information / eligibility

• Status: Enrolling by invitation
• Enrollment: 150
• Est. completion date: October 1, 2021
• Est. primary completion date: October 1, 2021
• Accepts healthy volunteers: No
• Gender: All
• Age group: 18 Years to 60 Years

Eligibility

Inclusion Criteria:

• Patients who have had a cerebral or retinal infarction confirmed by brain imaging or a defined transient ischemic attack without an identifiable cause after a detailed etiological assessment

Exclusion Criteria:

• Identification of a cause of ischemic stroke:
• Atheromatous stenosis > 50% (or atherosclerotic plaque < 50% threatening) of supra aortic trunk or intracranial arteries on echodoppler of the supra aortic trunk and transcranial or scanner angiography.
• Emboligenic heart disease : atrial fibrillation and atrial flutter, thrombus in left atrium, spontaneous contrast in left atrium, decreased atrial flow, left ventricular ejection fraction (LVEF) < 40%, LV aneurysma, left intraventricular thrombus, recent myocardial infarction, cardiomyopathy ventricular dilated left with LVEF < 35%, mitral stenosis, prosthetic mitral or aortic valve, infectious and non-infectious endocarditis, valve or mural tumor, complicated aortic arch atheroma (plaque > = 4 mm, ulcerated plaque, thrombus on plaque), aortic dissection
• Lacunar infarction symptomatic = < 1.5 cm on the CT scan, = < 2 cm on the diffusion MRI or the FLAIR.
• No atherosclerotic arteriopathy : dissection, primary and secondary angitis, spastic angiopathy, etc…
• Coagulopathy to come a long-term anticoagulant treatment (> 6 months) (anti-phospholipid syndrome, thrombophilia).
• Blood disorders and cancer
• Recent intravenous drug use (in the 6 months before the stroke).
• Other potential causes:
• Severe respiratory impairment or pulmonary arterial hypertension

Related Conditions & MeSH terms

• Apnea
• Apnea Syndrome
• Foramen Ovale, Patent
• Sleep Apnea Syndromes
• Stroke
• Syndrome

Intervention

Diagnostic Test:
• systematic etiological
Theses following tests are made as usual practice : Ventilator polygraphy, or polysomnography between 1 month and 1 year after cryptogenic ischemic stroke. Transoesophageal ultrasound

Locations

Country	Name	City	State
France	CHU de Saint-Etienne	Saint-Étienne

Sponsors (1)

Lead Sponsor	Collaborator
Centre Hospitalier Universitaire de Saint Etienne

Country where clinical trial is conducted

France, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Apnea hypopnea index	Apnea Hypopnea Index (AHI) > 15 / h on ventilator polygraphy (PV), or AHI >10/h on polysomnography (PSG) will be considered as a risk factor	1 year after the ischemic stoke
Secondary	Presence of foramen oval	Presence of a foramen oval on transoesophageal ultrasound during the etiological assessment of the stroke.	1 year after the ischemic stoke