Radiation-induced vasculopathy

David Goldemund M.D.
Updated on 07/06/2024, published on 14/02/2022

Patients after head and neck radiotherapy should be regularly monitored with ultrasound to detect carotid steno-occlusive disease

  • radiation therapy (RT) plays an important role in managing both primary and metastatic tumors
  • structures such as the brain, cranial nerves, spinal cord, and brain and heart vessels may be adversely affected by RT
  • radiation-induced vasculopathy (angiopathy) is a heterogeneous and poorly defined complex of vascular injuries attributable to radiation exposure
    • both small and large vessels may be affected, manifesting as extracranial carotid stenosis, intracranial stenosis, and other vascular anomalies (e.g., cavernous malformations, aneurysms, moya-moya syndrome, etc.)
    • vasculopathy is not limited to cerebral arteries, premature coronary artery disease (CAD) usually involves the ostium or proximal coronary arteries
    • total dose, duration of exposure, and tissue type exposed are factors influencing the development and severity of vasculopathy
  • vasculopathy carries an increased risk of cardiovascular complications in the decades following the initial RT
    • occlusive vasculopathy may manifest years after initial RT (2-25 y) with an increased incidence due to improved oncological treatment and extended patient survival rates
    • early identification of radiation vasculopathy is critical for initiating early therapeutic interventions
  • radiation-induced vasculopathy is also associated with an increased risk of autonomous dysregulation (baroreceptor failure) (Sharabi, 2003)


Vascular injury

  • acute radiation exposure leads to impaired blood-brain barrier (BBB) integrity ⇒ vasogenic edema occurs
  • the late vascular complications are primarily attributed to endothelial damage within the vascular system, manifesting as:
    • telangiectasia
    • aneurysm formation
    • microangiopathy leading to impaired blood flow and tissue damage
    • atherosclerosis affecting medium to large vessels
  • significant carotid vasculopathy (as a late complication of radiotherapy) is predominantly observed following radiotherapy in the ear, nose, and throat (ENT) regions

Glial and white matter injury

  • oligodendrocytes are more susceptible to radiation-induced damage compared to relatively resistant neurons
  • MRI shows brain atrophy and extensive leukoencephalopathy


Classification of post-radiation CNS injuries
Acute (< 14 days after radiation therapy)
  • the acute injury involves increased capillary permeability and vasodilation, leading to vasogenic edema
  • clinical presentation:  headache, nausea, vomiting, fever, altered consciousness, or worsening of pre-existing focal symptoms
  • current protocols for administering corticosteroids to patients undergoing radiation therapy (RT)  aim to reduce acute injury
Early delayed (> 2 weeks to several months)
  • both vasogenic edema and demyelination
  • clinical presentation:  headache, nausea, vomiting, worsening of pre-existing focal symptoms
  • CT/MRI: edema in the irradiated area, hyperintense lesions on FLAIR/T2 sequences
Late (months to years)
  • late diffuse encephalopathy
    • demyelination, atrophy, and necrotizing leukoencephalopathy
    • cognitive dysfunction leading to progressive dementia, apraxia, and incontinence
    • MRI shows atrophy and diffuse white matter changes
  • focal necrosis
    • focal, usually progressive symptoms
    • contrast-enhanced lesions with surrounding edema on brain MRI
      • differentiating these changes from tumor recurrence or metastasis can be challenging- biopsy or PET may assist in diagnosis
  • stroke-like migraine attacks after radiation therapy (SMART) syndrome
  • cranial nerve injury, ototoxicity, and endocrinopathy
  • cerebrovascular disease (radiation-induced vasculopathy)
    • stenosis/occlusion of large and medium extra- and intracranial vessels due to accelerated atherosclerosis
      • typically after irradiation of tumors in the ENT region
      • asymptomatic x symptomatic (ischemic vascular events)
    • moya-moya syndrome [Bitzer, 1995]
      • in young patients and children when tissues near the siphon are irradiated (e.g., in craniopharyngioma treatment)
    • microangiopathy with subcortical ischemic lesions
    • aneurysms

Diagnostic evaluation

Imaging findings of radiation vasculopathy exhibit a predictable location and time course. Acute injury occurs within several weeks of treatment, early delayed injury within several weeks to months, and late injury emerges months to years post-treatment

CT/MRI of the brain

  • specific finding: extensive leukoencephalopathy
  • CT – white matter hypodensities, vasogenic edema
  • T2/FLAIR – often symmetric hyperintense lesions
Radiation-induced encephalopathy with extensive bifrontal lesions
Radiation-induced encephalopathy with extensive bifrontal lesions
Radiation-induced encephalopathy (FLAIR)


  • significant bilateral common carotid artery (CCA) involvement is common
    • especially after radiotherapy in the ENT region
  • radiation-induced stenoses tend to be severe and involve longer segments than the traditional atherosclerotic disease
  • non-calcified plaques with hypoechoic foci predominate in B-mode  [Lam, 2012]
Severe carotid stenosis in a patient after radiotherapy for laryngeal carcinoma

CT/MR angiography

  • vascular imaging studies identify  the above-stated vascular changes extra-/intracranially
    • pathognomic is the focal presence of stenoses predominantly in the irradiated area and the absence of pathology in other segments
  • MRA/CTA/DSA may help to identify radiation-induced aneurysms or moyamoya revascularization patterns
Radiation-induced vasculopathy on DSA


  • antiplatelet therapy
    • in case of cancer-related thrombosis, LWHMs or DOACs are prescribed
  • vascular risk factors modification
    • statins – play a role in reducing vascular inflammation and stabilizing plaques
    • blood pressure monitoring and aggressive treatment of hypertension
    • smoking cessation
  • follow-up is essential to detect premature carotid artery stenosis and CAD
    • consider CEA or CAS  if significant stenosis is identified
    • vascular anatomy, surgical risk factors, and the patient’s prognosis must be taken into account
    • both options share good short-term outcomes and similar perioperative complication rates; CEA probably offers more durable vessel patency
    • CABG can be challenging in the presence of heavily calcified or friable internal mammary arteries
  • both open and endovascular treatment of intracranial radiation-induced aneurysms have been reported
CAS in patient with radiation-induced vasculopathy

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Radiation-induced vasculopathy