Carotid artery dissection

A major cause of cerebral infarction in the young.

Carotid artery dissection causes 2.5% of all strokes, and has a higher frequency among patients younger than the age of 40 years.

Often occurs in otherwise healthy individuals without known risk factors for stroke and frequently develops spontaneously without relevant trauma.

The main symptoms associated with carotid ornery dissection or headache, facial, orbital, or cervical palsy ipsilateral to the dissection and a partial Horner syndrome.
Ipsilateral amaurosis fugax of the eye is frequent.
Cranial nerve palsy or tinnitus are rare manifestations.
Patients may be asymptomatic or experienced a stroke.
Diagnosis is established by MRA, CT angiography, or angiography of the neck vessels.

Ultrasound imaging of the carotid artery can be helpful in monitoring the dissection.

Carotid artery endarterectomy usually not used to treat carotid artery dissections.

Incidence of spontaneous internal carotid artery dissection is 1.72 to 100,000 patients per year.

Predisposing factors are injuries in the head and neck and genetic factors-Ehlers-Danlos Sx, and Marfan syndrome.
Dissections are divided into traumatic and spontaneous ones.
Pathologically with a dissection a hematoma occurs inside the wall of the artery which causes significant blood vessel stenosis and blood flow disturbance that can lead to stroke or other ischemic events.
In addition rupture to the lumen of the vessel creating a thrombogenic surface occurs with the high possibility of a thromboembolic stroke.
Carotid artery dissection can extend intracranially with a rupture of the vessel wall that can cause a subarachnoid hemorrhage.

Initial symptoms usually involves pain that affects one side of the neck, face, or head.

Pain may start abruptly but usually is of gradual onset.

Pulsatile tinnitus or bruits are present in about 25% of patients.

Early neurologic findings involve the sympathetic plexus and a Horner’s syndrome is present in about 50% of patients, other abnormalities include cranial nerve XII or cerebellar dysfunction.

Patients may eventually have a TIA or thrombotic stroke.

The mean time between onset of pain and neurologic symptoms is four days.

An important cause of stroke in young adults accounts for up to 25% of such cases.

Magnetic resonance angiography (MRA) with fat suppression is the gold standard test.

Alternative examinations include carotid duplex ultrasonography and CT angiogram.

Management includes anticoagulation with heparin, with maintenance and anticoagulation for three months.

While  revascularization is the cornerstone of atherosclerotic acute coronary syndrome management, SCAD is primarily managed medically in most clinically stable patients. Dissected vessels tend to heal over time, so the  natural history of SCAD appears to be spontaneous gradual healing of the vessel wall, with complete angiographic resolution of the lesion reported in most cases (73% to 97%) within 4 to 6 weeks.

Revascularization procedures are associated with high failure rates and poor outcomes in the setting of disrupted arterial wall integrity. 

Instrumentation of the damaged and friable coronary blood vessel vessel may worsen the disease and impair the healing process. 

A balloon dilation can lead to proximal or distal extension or migration of intramural hematoma, worsening the luminal diameter. 

The  healing of the vessel and changing architecture can result in stent mal-position and future complications of stent thrombosis over the long term

supports a conservative approach.

Percutaneous coronary intervention (PCI) in the setting of SCAD is associated with worse outcomes and high complication rates.

PCI procedural failure rate was 53% in those managed with PCI: false lumen, loss of flow after stent placement, and significant residual stenosis. 

PCI is  associated with a high risk for emergency coronary artery bypass grafting: 13% vs 2% in the medically managed group. 

Despite often poor outcomes, revascularization procedures may be appropriate in patients with the following high-risk features:

Left main coronary artery dissection

Ongoing ischemia

Hemodynamic instability

Refractory arrhythmia.

Neither PCI with intracoronary stenting nor CABG appears to be protective against recurrent dissection.

Medical therapy recommendations: 

Antiplatelet therapy consisting of aspirin and a P2Y12 inhibitor for 12 months.

No role for anticoagulants, thrombolysis

Beta-blockers-reduce shear stress on the vessel wall and minimizing risk of propagation, lower blood pressure, and modulate heart rate.

Its use is associated with reduced risk of recurrent SCAD.

There is no proven connection has been identified between cholesterol and risk of SCAD, therefore lipid-lowering therapy, we do not routinely prescribe statins in patients with SCAD.

Chronic management of SCAD includes, screening for fibro-muscular dysplasia, monitoring for chest pain and recurrence, and cardiac rehabilitation.

Fibromuscular dysplasia is an idiopathic arteriopathy not caused by underlying atherosclerosis or inflammation, with a predilection for medium-sized vessels. 

It is the condition most commonly associated with SCAD, with an estimated prevalence of 25% to 86%.

The hallmark imaging finding is the “string of beads,” which occurs where areas of fibrosis that cause narrowing, alternate with regions of dilation.

The renal, carotid, and vertebral arteries are most often affected, but nearly any site may be involved.

Patients with a family history or physical examination findings suggestive of known arteriopathies may benefit from a genetics evaluation. 

Coronary computed tomography angiography is preferred for imaging when possible, as it has higher spatial resolution than magnetic resonance angiography or ultrasonography. 

Patients are at risk of chronic angina, recurrent SCAD, and noncardiac chest pain.

Approximately 20% of patients with SCAD who are readmitted within 30 days of the index event, many develop chronic nitrate-responsive chest pain.

Chronic angina is suspected to be related to coronary microvascular dysfunction, which is common in this population. 

More than 70% had coronary microvascular dysfunction defined by a coronary flow reserve < 2.5 or an index of microcirculatory resistance > 25 units.

A long-acting nitrate or calcium channel blockers, or both, may be considered as needed for chronic microvascular dysfunction.

The recurrent SCAD rate is  10.4% over a median follow-up of 3.1 years.

Surgery is rarely required.

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