NCT05800821

Prediction of Cerebral Hyperperfusion Syndrome After Carotid Revascularization Using Deep Learning

Recruiting now Last updated 25 November 2025

What this trial tests

trial testing Carotid revascularization in Carotid Artery Diseases in 500 participants. Currently enrolling.

Timeline

3 May 2023

Primary endpoint
3 May 2028

3 May 2030

Quick facts

Lead sponsor	State Institution "Republican Scientific and Practical Center" Cardiology, Belarus
Status	Recruiting now
Study type	OBSERVATIONAL
Enrollment	500
Start date	3 May 2023
Primary completion	3 May 2028
Estimated completion	3 May 2030
Sites	1 location across Belarus

Drugs / interventions tested

• Carotid revascularization

Conditions studied

• Carotid Artery Diseases — all drugs for Carotid Artery Diseases →
• Carotid Atherosclerosis — all drugs for Carotid Atherosclerosis →
• Carotid Artery Stenosis — all drugs for Carotid Artery Stenosis →
• Cerebral Hyperperfusion Syndrome — all drugs for Cerebral Hyperperfusion Syndrome →

Sponsor

State Institution "Republican Scientific and Practical Center" Cardiology, Belarus — full company profile →

Who can join

Adults 30 to 80, any sex, with Carotid Artery Diseases or Carotid Atherosclerosis. Patients with the condition only — healthy volunteers not accepted.

Sponsor's own description

Cerebral hyperperfusion syndrome (CHS) was initially described as a clinical complication following carotid endarterectomy (CEA), but it may occur after both CEA and carotid artery stenting. It is characterised by throbbing ipsilateral frontotemporal or periorbital headache, and sometimes diffuse headache, eye and facial pain, vomiting, confusion, macular oedema, visual disturbances, focal motor seizures with frequent secondary generalisation, focal neurological deficits, and intracerebral or subarachnoid haemorrhage.

Knowledge of CHS among physicians remains limited. Most studies report an incidence of 1-3% after carotid endarterectomy. CHS is most common in patients with increases of more than 100% in cerebral perfusion compared with baseline after carotid revascularization, and is rare in patients with perfusion increases of less than 100% compared with baseline.

The pathophysiological mechanism of CHS is only partially understood. The chronic low-flow state induced by severe carotid disease results in compensatory dilation of cerebral vessels distal to the stenosis, as part of the normal autoregulatory response to maintain adequate cerebral blood flow (CBF). In this chronically dilated state, the vessels lose their ability to autoregulate vascular resistance in response to changes in blood pressure. Dysautoregulation has been shown to be proportional to the duration and severity of chronic hypoperfusion. After revascularization and reperfusion, impaired cerebral autoregulation may contribute to a cascade of intracranial microcirculatory changes, with an inability to respond adequately to the augmentation of CBF following carotid recanalization.

Although most patients present with mild symptoms and signs, progression to severe and life-threatening complications can occur if CHS is not recognised and treated promptly. Because CHS is diagnosed on the basis of several non-specific signs and symptoms, patients may be misdiagnosed as having one of the better-known causes of perioperative complications, such as thromboembolism.

Publications & conference data

No peer-reviewed publications indexed yet for this trial.