Carotid artery stenosis: causes, symptoms, diagnosis

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The main cause of cerebrovascular accidents is atherosclerosis of the carotid arteries. Atherosclerotic plaques cause narrowing of the carotid arteries, which is an obstacle to normal blood circulation in the brain. Gradually, a complete blockage of the carotid artery develops, which is called occlusion. Impaired patency of the carotid artery is the main cause of ischemic stroke in the modern world. The risk of developing a stroke if the carotid artery is narrowed symptomatically by 70% or more is about 15% per year.

Many people die or become disabled from stroke every year, although modern vascular surgery can prevent it in most patients. Only regular diagnosis and trust in doctors will significantly reduce the risk of stroke. It is much easier to treat atherosclerosis of the carotid artery than ischemic stroke and its consequences.

Causes and risk factors

The carotid arteries are paired large arterial vessels that supply blood to the brain in those sections where the centers of thinking, speech, personality, sensory and motor function are located. The carotid arteries run through the neck and enter the brain through openings in the skull.

When fatty substances and cholesterol accumulate, an atherosclerotic plaque is formed, which narrows the carotid arteries. This reduces blood flow to the brain and increases the risk of ischemic stroke. A stroke occurs when blood flow does not reach any part of the brain. During a stroke, some brain functions are suddenly lost. If the lack of blood flow lasts more than three to six hours, then these disorders become irreversible.

Why does a stroke develop when the carotid artery narrows?

• Significant narrowing of the carotid artery reduces blood circulation in the brain, and with a sudden drop in pressure (suddenly getting out of bed, flying, overheating in the sun or major surgery), the blood flow suddenly stops, which leads to the death of nerve cells.
• Tearing off a piece of atherosclerotic plaque with its transfer by the bloodstream into small arteries of the brain, which leads to their blockage.
• Acute thrombosis (formation of a blood clot) due to narrowing of the carotid artery with complete cessation of blood flow in certain areas of the brain.

Introduction

So, a dangerous triangle of the face. We can describe this zone in this way: the apex of the triangle is located in the glabella area, its legs enclose the nasolabial folds and reach the base, which is located under the lower lip [Fig. 1].

Rice. 1. Dangerous triangle of the face.

The area within this zone is often corrected with filler: just think about glabellar lines, nasal hump correction, nasolabial folds and lip remodeling. The anatomical feature, or originality of this zone, which makes it so “insidious”, lies in its blood supply and especially in the topography of the arteries.

Risk factors for carotid atherosclerosis

Risk factors for carotid artery disease are similar to those for other types of cardiovascular disease. They include:

• Age
• Smoking
• Hypertension (high blood pressure) is the most important risk factor for stroke
• High cholesterol
• Diabetes
• Obesity
• Sedentary lifestyle
• Family history of atherosclerosis

Men under 75 years of age have a greater risk of developing carotid artery stenosis than women in the same age group. In the group over 75 years of age, women have a greater risk of stroke. In patients suffering from coronary artery disease, narrowing of the carotid artery is often detected.

Therapeutic strategies to prevent and manage complications

It is obvious that it is necessary to use techniques that minimize the risk of developing these dangerous complications. The text of the atlas describes, area by area, all the precautions and manipulations that must be taken to reduce this risk: the use of a cannula, the depth of injection, the quantity and quality of filler injected, and so on. Pallor of the skin and patient complaints of sudden pain in the injection area are signs that blood flow has stopped in this area. We must be able to control this situation.

All measures are aimed at restoring blood flow: urgent dissolution of the filler (if hyaluronic acid was used), warm compresses, massage, etc. Then there are prescriptions that need to be followed at home: antibiotic therapy to prevent bacterial superinfection, antiplatelet agents, topical medications.

In the introduction to the atlas I placed the inscription

“Only non-practitioners do not make mistakes; only through practice does it become possible to reduce the risk of error.”

If all measures are carried out on time and correctly, the spread of the necrosis zone will be minimal, a large area of ​​skin will be preserved and, therefore, the chance of restitutio ad integrum will be higher.

Complaints and symptoms

Atherosclerosis of the carotid arteries can be asymptomatic or cause complaints associated with impaired cerebral blood flow. Most often, patients may complain of temporary impairment of brain function (transient ischemic attack) or persistent loss of brain function (ischemic stroke).

Transient ischemic attack (TIA)

A TIA occurs when blood flow to the brain is briefly interrupted. This is the initial phase of acute cerebrovascular accident, which is reversible. It has the same symptoms as a stroke, but these symptoms go away within minutes or hours.

A TIA requires emergency medical attention because it is impossible to predict whether it will progress to a stroke. Immediate treatment can save lives and increase the chances of a full recovery.

Modern research has shown that patients who have had a TIA are 10 times more likely to suffer a major stroke than a person who has not had a TIA.

Ischemic stroke has the following symptoms:

• Sudden loss of vision, blurred vision, difficulty in one or both eyes.
• Weakness, tingling, or numbness on one side of the face, one side of the body, or one arm or leg.
• Sudden difficulty walking, loss of balance, lack of coordination.
• Sudden dizziness.
• Difficulty speaking (aphasia).
• Sudden severe headache.
• Sudden memory problems
• Difficulty swallowing (dysphagia)

Ischemic stroke and transient ischemic attack begin in the same way, so any ischemic stroke can be called an ischemic attack if the symptoms completely resolve within 24 hours of the onset of the disease. The presence of a time interval between the onset of stroke symptoms and the death of parts of the brain allows for urgent surgery to restore cerebral blood flow.

Dissection of the internal carotid and vertebral arteries: clinical picture, diagnosis, treatment

In recent years, interest in the dissection of arteries supplying the brain, a relatively new and insufficiently studied problem of cerebrovascular diseases, has been steadily growing in the world. Its main clinical manifestation is ischemic stroke (IS), which often develops at a young age. The study and intravital diagnosis of cerebral artery dissection has become possible thanks to the widespread introduction of magnetic resonance imaging (MRI) into the clinic. MRI makes it safe for the patient to carry out repeated angiographic examination, which is important for diagnosing dissection, since it represents a dynamic pathology, and also, using the T1 mode with signal suppression from adipose tissue (T1 fs), to directly visualize intramural (intrawall) hematoma (IMH) - direct sign of dissection. The use of MRI has shown that dissection is a very common pathology, and not a rarity, as previously thought. In addition, it has become apparent that cerebral artery dissection is only fatal in a small number of cases, whereas it was originally considered a fatal disease.

In Russia, targeted studies of cerebral artery dissection began in the late 90s of the last century at the Scientific Center of Neurology of the Russian Academy of Medical Sciences (until 2007, the Scientific Research Institute of Neurology of the Russian Academy of Medical Sciences) almost simultaneously with research carried out abroad. But the first morphological descriptions of individual cases of cerebral dissection, clinically, however, unrecognized, were made in the 80s of the 20th century. in our country, D. E. Matsko, A. A. Nikonov and L. V. Shishkina et al. Currently, this problem is being studied at the Scientific Center of Neurology of the Russian Academy of Medical Sciences, where more than 200 patients with intravital verified dissection of the cerebral arteries were examined, more than half of whom were patients with dissection of the internal carotid (ICA) and vertebral arteries (VA).

Dissection of the cerebral arteries is the penetration of blood from the lumen of the artery into its wall through an intimal tear. The IMG formed in this case, separating the layers of the arterial wall, spreads along the length of the artery to different distances, most often towards the intima, leading to narrowing or even occlusion of the arterial lumen, which causes cerebral ischemia. Minor stenosis caused by IMH may be clinically asymptomatic. The spread of IMH towards the outer membrane (adventitia) leads to the development of a pseudoaneurysm, which can cause isolated cervical headache, or to a true dissecting aneurysm. Thrombi formed in a dissecting aneurysm are a source of arterio-arterial embolism and IS. Dissection develops both in the main arteries of the head (ICA and VA) and in their branches (middle, posterior, anterior cerebral arteries, basilar artery). However, most researchers believe that dissection occurs more often in the ICA and VA than in their branches. At the same time, it cannot be excluded that dissection in the branches of the ICA and VA is often underestimated due to the difficulty of visualizing IMG in them and is mistakenly regarded as thrombosis. Dissection can develop at any age - from infancy to the elderly, but in most cases (according to the Scientific Center of Neurology of the Russian Academy of Medical Sciences - 75%) it is observed in young people (up to 45 years). It is noted that with intracranial lesions, the age of patients is, as a rule, less than with extracranial lesions, and with the involvement of the VA - less than with lesions of the carotid arteries. The distribution of patients by gender also depends on the location of the dissection: the ICA is more often affected in men, and the VA – in women. Dissection usually develops in individuals who consider themselves healthy, do not suffer from atherosclerosis, thrombophilia, diabetes mellitus, and rarely have moderate arterial hypertension.

Dissection of the internal carotid artery.

The main provoking factors for ICA dissection are head or neck trauma, usually mild; physical activity with tension in the muscles of the shoulder girdle and neck; bending, throwing back, turning the head; drinking alcohol; current or previous infection; taking contraceptives or the postpartum period in women. In conditions of previous weakness of the arterial wall, these factors and conditions play a provoking, rather than causal role, leading to intimal rupture and the development of dissection, which in these cases is considered spontaneous.

Clinically, dissection of the ICA most often manifests as IS, and less often as transient cerebrovascular accident (TCI). More rare (less than 5%) manifestations include isolated neck/headache, localized in most cases on the dissection side; isolated unilateral damage to the cranial nerves due to their ischemia, when the arteries supplying the nerve arise from the dissected ICA; isolated Horner's syndrome, caused by the effect of IMG on the periarterial sympathetic plexus, when the hematoma mainly extends towards the adventitia and does not significantly narrow the lumen of the ICA. Small IMHs may be asymptomatic and incidentally detected on MRI. A characteristic sign of cervical cerebrovascular accident during ICA dissection is headache/neck pain. Pain, usually dull, pressing, less often pulsating, shooting, appears several hours or days before AI on the side of dissection. Its cause is irritation of the sensitive receptors of the vascular wall by the hematoma developing in it. In approximately a third of patients with IS, it is preceded by a transient SMC in the cerebral territory of the ICA or ophthalmic artery in the form of a short-term decrease in vision on the side of the dissection. NMC, as a rule, develops in the middle cerebral artery (MCA) and is manifested by motor, sensory and aphasic disorders, which in half of the cases are detected in the morning upon awakening, in the other half of the cases - during active wakefulness.

The prognosis for life in most cases is favorable; death occurs in approximately 5% of cases. It usually occurs with extensive cerebral infarctions caused by dissection of the intracranial part of the ICA with transition to the MCA and anterior cerebral artery. In the majority of patients, especially with damage to the extracranial part of the ICA, the prognosis for life is favorable and good recovery of impaired functions is observed. When the intracranial part of the ICA is involved and the dissection extends to the MCA or with embolism of the latter, the recovery of impaired functions is much worse.

Relapses of dissection occur infrequently and are usually noted in the 1st month after the onset of the disease. They can appear both in an intact and in an artery that has already been dissected.

The main mechanism for the development of IS is hemodynamic under conditions of an increasing stenotic-occlusive process in the ICA caused by IMH. Less commonly, cerebrovascular accident develops through the mechanism of arterioarterial embolism. Its source is thrombi formed in a dissecting aneurysm, thrombosed fragments of IMH entering the bloodstream during a secondary intimal breakthrough, or thrombotic layers at the site of an intimal rupture.

Vertebral artery dissection.

Dissection of the VA, according to most authors, is observed somewhat less frequently than dissection of the ICA. However, it cannot be excluded that the VA is involved more often than indicated in the literature, since many cases of VA dissection manifesting as isolated cervicocephalgia are not clinically recognized and are not statistically taken into account.

The main clinical signs of VA dissection are ischemic cerebrovascular accidents and isolated neck/headache. This pain occurs in about a third of cases. Rare manifestations include circulatory disorders in the cervical spinal cord, isolated radiculopathy, and hearing impairment. In more than a third of patients, dissection is found in both VAs, and dissection of one VA may be the cause of UCI, and the second VA may be the cause of isolated neck/headache, or be clinically asymptomatic and detected only by neuroimaging. A characteristic feature of NMC during VA dissection, as well as during ICA dissection, is its association with neck/headache on the side of the dissected VA. Typically, pain is localized along the back of the neck and in the back of the head, appearing several days or 2-3 weeks before focal neurological symptoms. Pain often occurs after repeated bending, turning the head, or keeping the head in an uncomfortable position for a long time, and less often after a head/neck injury, usually mild. The tension of the VA observed in this case with weakness of the vascular wall causes intimal rupture and initiates dissection. The causes of neck/headache during VA dissection are irritation of the pain receptors of the arterial wall by the hematoma forming in it, as well as ischemia of the neck muscles, the blood supply of which involves the branches of the VA. Another feature of NMC is that often (about 80%) it develops at the moment of turning or tilting the head. Focal neurological symptoms are ataxia, vestibular disorders, less often - sensory disorder, dysarthria, dysphagia, dysphonia, paresis.

The most common mechanism for the development of CVA during VA dissection is arterio-arterial embolism. This is indicated by clinical manifestations (acute development of symptoms of cerebral ischemia, usually during active wakefulness, often when turning/tilting the head) and angiography results (the presence in most patients of hemodynamically insignificant stenoses, which do not significantly impair cerebral hemodynamics and ensure distal movement of emboli) . Many researchers consider the source of embolism to be fragments of IMH entering the bloodstream during a secondary intimal breakthrough. According to other researchers, these are intravascular mural thrombi formed at the site of intimal rupture. Neuroimaging studies, primarily MRI angiography (MRA) and MRI T1 fs, which allow identifying IMH, are of decisive importance in verifying the dissection of the ICA and VA. The most common characteristic angiographic sign of ICA/PA dissection is uneven, less often - uniform prolonged stenosis (“rosary symptom”, or “strings of beads”, “string symptom”), pre-occlusive cone-shaped narrowing of the ICA lumen (“candle flame symptom”). Such characteristic angiographic signs of dissection as dissecting aneurysm and double lumen are much less common. Dissection is a dynamic pathology: ICA/VA stenoses caused by IMG are completely or partially resolved in all cases after 2–3 months. Recanalization of the original occlusion caused by dissection is observed in only half of the cases. Characteristic MRI signs of dissection are IMG, which is visualized on T1 fs for ≥2 months, and an increase in the outer diameter of the artery. It should be borne in mind that during the 1st week of the disease, IMH is not detected by MRI in the T1 fs mode, so computed tomography (CT) and MRI in the T2 fs mode acquire diagnostic value.

In most cases, over time there is a good or complete restoration of impaired functions. VA dissection may recur. After 4–15 months, relapse was observed in 10% of patients.

Morphological examination of the cerebral arteries during dissection plays a fundamental role in elucidating the causes of weakness of the arterial wall leading to dissection. It makes it possible to identify dissection, thinning, and sometimes the absence of the internal elastic membrane, areas of fibrosis in the intima, and incorrect orientation of myocytes in the media. It is assumed that changes in the vascular wall are caused by genetically determined weakness of connective tissue, primarily collagen pathology. However, no mutations in the collagen gene were found. For the first time in the world, employees of the Scientific Center for Neurology of the Russian Academy of Medical Sciences have suggested that the cause of weakness of the arterial wall is mitochondrial cytopathy. This was confirmed by a study of muscle and skin biopsies. Histological and histochemical examination of the muscles revealed red ragged fibers, a change in the reaction to succinate dehydrogenase and cytochrome oxidase, and a subsarcolemmal type of staining in fibers with an intact reaction. Electron microscopic examination of the skin arteries revealed changes in mitochondria, vacuolization, deposition of fat, lipofuscin and glycogen in cells with altered mitochondria, and calcium deposits in the extracellular matrix. The complex of identified changes characteristic of mitochondrial cytopathy allowed Russian researchers to propose the term “mitochondrial arteriopathy” to designate arterial pathology that predisposes to dissection.

The treatment of IS caused by dissection has not been definitively determined, since there are no randomized placebo-controlled studies involving a large number of patients. In this regard, there are no clearly established treatment methods in the acute period of stroke. Most often, the introduction of direct anticoagulants is recommended, followed by a transition to indirect anticoagulants, which are used for 3–6 months. The purpose of their administration is to prevent arterio-arterial embolism and maintain IMG in a liquefied state, which contributes to its resolution. It should be borne in mind that the prescription of large doses of anticoagulants can lead to an increase in IMH and a deterioration in the blood supply to the brain. As an alternative to these drugs in the acute period of stroke, the use of antiplatelet agents is recommended, and, according to preliminary data, there is no difference in stroke outcomes. In order to assess the safety of treatment with low molecular weight heparin and aspirin in the acute period of dissection, French researchers measured the volume and extent of IMH during the 1st week of treatment. A slight increase in these parameters was observed in a third of patients, but in no case was there an increase in the degree of stenosis or the development of re-dissection. The use of anticoagulants and antiplatelet agents is limited to 2–3 months, during which the development of IMH occurs. Further prophylactic use of these drugs is not advisable, since the cause of IS during dissection is not hypercoagulation, but weakness of the arterial wall. Since the main reason predisposing to the development of dissection is weakness of the arterial wall, therapeutic measures both in the acute and long-term periods of stroke should be aimed at strengthening it. If we take into account the data on mitochondrial cytopathy, leading to energy deficiency of the cells of the arterial wall and its dysplasia, which contributes to the occurrence of dissection, the use of drugs with “trophic” and energy-tropic effects can be considered justified. One of these drugs is Actovegin, which is used in both acute and long-term periods of stroke caused by dissection. It is a biologically active substance of natural origin - a deproteinized derivative of calf blood. The main effect of Actovegin is to activate cellular metabolism by facilitating the flow of oxygen and glucose into the cell, which provides an additional influx of energy substrates and increases by 18 times the production of ATP, the universal donor of energy necessary for the life and functioning of the cell. Other drugs with neurometabolic effects are also used to restore functions impaired due to stroke: Cerebrolysin, piracetam, gliatilin, ceraxon.

In the acute period of dissection, in addition to drug treatment, compliance with the following rules is of great importance: it is necessary to avoid sudden head movements, injuries, physical stress, straining, which can lead to an increase in dissection.

Dissection of the ICA and VA is a common cause of IS at a young age, and less often – a cause of isolated neck/headache.

Knowledge of the clinical and angiographic features of this type of vascular pathology of the brain allows for its correct treatment and secondary prevention.

Course of the disease

Once atherosclerotic plaques appear, they will no longer be able to resolve, but only gradually progress. The rate of growth of an athersclerotic plaque depends on many risk factors, including cholesterol levels. All people over 50 years of age are recommended to undergo an annual ultrasound of the carotid arteries in order to exclude the development of atherosclerotic plaques and the risk of ischemic stroke.

With the development of complications of atherosclerosis of the carotid arteries, discirculatory encephalopathy quickly progresses. Frequent TIAs, and even more so ischemic stroke, contribute to the death of part of the brain tissue and disruption of brain function. Patients with atherosclerosis of the carotid arteries often develop vascular dementia (dementia).

After restoration of the patency of the carotid artery, the phenomena of cerebrovascular insufficiency are stopped, and the likelihood of repeated cerebrovascular accidents is significantly reduced.

Preparing for a non-surgical procedure

Before elective stenting, your endovascular surgeon will review your medical history and perform a physical examination. Can be assigned:

• Ultrasound . To obtain images using sound waves of the narrowed artery and the speed of blood flow to the brain.
• Contrast-enhanced computed tomography (MSCT) or Magnetic resonance angiography (MRA) . This diagnostic produces highly detailed images of blood vessels using radiofrequency waves in a magnetic field or X-rays injected with a radiopaque contrast agent.

Food and medicine

You will receive instructions about what you can eat or drink before your angioplasty and ICA stenting. Preparation may be different if you are already in the hospital before the intervention.

The night before your endovascular surgery:

• Follow your doctor's instructions about adjustments to your current medications. Your doctor may tell you to stop taking certain medications before having angioplasty, especially if you take certain diabetes medications or blood thinners.
• Arrange transportation home in advance. Angioplasty usually requires a hospital stay, and you may not be able to go home the next day due to the lingering effects of the sedation.

Forecast

Carotid atherosclerosis carries a significant risk of ischemic stroke. With asymptomatic narrowing of the internal carotid artery of more than 70%, the risk of ischemic stroke exceeds 5% per year. If the patient has had episodes of cerebrovascular accidents, then this risk is already 25% per year.

The risk of ischemic stroke in asymptomatic atherosclerotic plaques with a narrowing of less than 70% does not exceed that in patients without atherosclerosis.

After adequate restoration of blood circulation in the carotid arteries, the risk of ischemic stroke is reduced by more than 3 times.

Recommendations

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