Carotid Stenosis


Carotid stenosis may be caused by atherosclerosis, intimal fibroplasia, vasculitis, adventitial cysts, or vascular tumors. However, atherosclerosis is the most common etiology.


  • Narrowing of the carotid artery lumen is typically due to atherosclerotic changes in the vessel wall. Atherosclerotic plaques are responsible for 90% of extracranial carotid lesions and up to 30% of all ischemic strokes.
  • A “hemodynamically significant” carotid stenosis produces an internal carotid artery peak systolic velocity (PSV) >125 cm/s on carotid duplex imaging.
  • Carotid lesions are classified by the following:
    • Symptom status
      • Asymptomatic: homogenous and stable
      • Symptomatic: heterogeneous and unstable; present with stroke or transient cerebral ischemic attack
    • Degree of stenosis
      • Total occlusion: No detectable patent lumen
      • Near occlusion: Markedly narrow lumen on color Doppler ultrasound (US)
      • High grade: PSV >230 cm/s; 70–99% stenosis
      • Moderate grade: PSV 125 to 230 cm/s; 50–69% stenosis
      • Low grade: PSV <125 cm/s with visible plaque or intimal thickening; <50% stenosis
      • Normal: PSV <125 cm/s and no visible plaque or intimal thickening


More common in men and with increasing age (see “Risk Factors”)

Unclear (Asymptomatic patients often go undiagnosed.)


  • Moderate stenosis
    • Age <50 years: men 0.2%, women 0%
    • Age >80 years: men 7.5%, women 5%
  • Severe stenosis
    • Age <50 years: men 0.1%, women 0%
    • Age >80 years: men 3.1%, women 0.9%

Etiology and Pathophysiology

  • Atherosclerosis at the carotid bifurcation begins during adolescence. The carotid bulb has unique blood flow dynamics. Hemodynamic disturbances cause endothelial injury and dysfunction. Plaque formation in vessel wall results and stenosis then ensues.
  • Initial cause is not well understood, but certain risk factors are frequently present (see “Risk Factors”). Tensile stress on the vessel wall, turbulence, and arterial wall shear stress seem to be involved.


  • Increased incidence among family members
  • Genetically linked factors
    • Diabetes mellitus (DM), race, hypertension (HTN), family history, obesity, hyperlipidemia
    • In a recent single nucleotide polymorphism study, the following genes were strongly associated with worse carotid plaque: TNFSF4, PPARA, TLR4, ITGA2, and HABP2.

Risk Factors

  • Nonmodifiable factors: advanced age (>65 years old), male sex, family history, coronary artery disease (CAD), peripheral artery disease, aortic aneurysmal disease, congenital arteriopathies
  • Modifiable factors: smoking, diet, dyslipidemia, physical inactivity, obesity, HTN, DM
  • Possible factors: Chlamydia pneumoniae and Cytomegalovirus

General Prevention

  • Antihypertensive treatment to maintain BP <140/90 mm Hg; see “Hypertension, Essential.”
  • Smoking cessation to reduce the risk of atherosclerosis progression and stroke
  • Lipid control: plaque stabilization and regression of carotid atherosclerotic lesions seen with statin therapy

Commonly Associated Conditions

  • Transient ischemic attack (TIA)/stroke
  • CAD/myocardial infarction (MI)
  • Peripheral vascular disease (PVD)

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