Carotid atherosclerosis is a chronic disease in which atherosclerotic plaques form on the inner wall of the carotid arteries, narrowing the vessel lumen and impairing blood flow to the brain. The disease represents one of the leading causes of strokes worldwide. The prevalence of carotid atherosclerosis varies considerably according to geographic location, lifestyle, and ethnicity of the population.

Geographic differences:

North America and Europe show a high prevalence of carotid atherosclerosis. Studies show that up to 10% of the elderly population in these regions suffer from this disease. This may be due to high rates of comorbidities such as hypertension and diabetes, as well as a high standard of living that is often accompanied by less physical activity and an unhealthy diet;
Asian countries are also experiencing an increase in the incidence of carotid atherosclerosis, which correlates with urbanization and lifestyle changes. In Japan and China, for example, rapid industrial development and a more Westernized diet have led to an increase in the incidence of atherosclerosis;
Low- and middle-income countries often show a lower prevalence of carotid atherosclerosis, which may be related to the younger age of the population and higher physical activity. However, there is a tendency for cases to increase in these regions due to urbanization and nutritional deterioration.

Factors affecting prevalence:

Degree of urbanization and changes in the lifestyle of the population;
Accessibility and quality of health care, which affect the possibility of early detection and treatment of diseases that provoke atherosclerosis;
National smoking cessation programs, education levels, and economic development that directly affect the health of the population.

Thus, carotid atherosclerosis is a multifactorial disease dependent on a multitude of socioeconomic and cultural factors that need to be taken into account when developing prevention and treatment measures at the national and international levels.

Etiology of atherosclerosis

The main risk factors for atherosclerosis are hypertension, diabetes, smoking, hyperlipidemia and familial predisposition. Each of these factors contributes to vascular endothelial damage, which initiates the formation of atherosclerotic plaques. Age and gender also play a significant role, with the risk increasing with age, men are more susceptible to the disease.

Pathophysiology of atherosclerosis

3D animation – the development of atherosclerosis

Atherosclerosis is a chronic disease of the arteries characterized by impaired lipid and protein metabolism, inflammation and subsequent formation of atherosclerotic plaques that can lead to stenosis and vessel occlusion. The development of atherosclerosis can be divided into several key stages:

Endothelial dysfunction: the primary event in the development of atherosclerosis is damage to the endothelium, the inner layer of the arterial wall. Endothelial dysfunction can be caused by multiple factors including hypertension, smoking, hyperglycemia, and oxidative stress. Damaged endothelium loses its barrier function, which increases permeability to low-density lipoproteins (LDL);
LDL oxidation: under the influence of oxidative processes, LDL are converted into oxidized LDL (ox-LDL), which have direct cytotoxicity and contribute to the progression of atherogenesis. These modified lipoproteins activate the endothelium and attract monocytes;
Inflammation and foam cell formation: monocytes infiltrating the arterial wall differentiate into macrophages, which capture oxidized LDL and become foam cells. The accumulation of foam cells leads to the formation of a fatty patch, which is an early morphologic manifestation of atherosclerosis;
Smooth muscle cell proliferation and fibrous capsule formation: in response to inflammation and damage to the vascular wall, smooth muscle cells migrate from the medial sheath to the intima, where they proliferate and produce collagen and other extracellular matrix components. This leads to thickening of the intima and formation of a fibrous capsule of atherosclerotic plaque;
Complications of atherosclerotic plaque: Over time, an atherosclerotic plaque can become unstable and rupture, leading to thrombus formation and acute vessel occlusion. This can cause acute clinical manifestations such as acute cerebral circulatory collapse.

Clinical manifestations

In the early stages, carotid atherosclerosis may be asymptomatic. With disease progression and development of significant stenosis, transient ischemic attacks or ischemic stroke occur.

Symptoms of carotid atherosclerosis include:

Sudden numbness or weakness of the face, arm, or leg, (especially on one side of the body);
Difficulty with speech, vision, or coordination.

Diagnosis

Diagnosis of carotid atherosclerosis includes a number of instrumental and laboratory methods that help not only to detect the presence of plaques, but also to assess the degree of vascular damage and the risk of complications.

Instrumental diagnostic methods

Ultrasound with Doppler ultrasound:
Indications: suspected carotid atherosclerosis, presence of symptoms of transient ischemic attack or stroke, and presence of risk factors (hypertension, diabetes, hyperlipidemia).
Signs: the presence of atherosclerotic plaques, narrowing of the arterial lumen, changes in blood flow velocity in the area of stenosis.
Magnetic resonance angiography:
Indications: the need for high-precision arterial imaging to assess the degree of stenosis and vascular anatomy, especially in difficult or doubtful cases.
Signs: images can show the exact structure of the plaque, the extent and distribution of stenosis.
Computed tomography (CT angiography):
Indications: Suspicion of calcified plaques, need to evaluate the possibility of surgical intervention.
Indications: CT is capable of evaluating calcinates within the plaque, accurately assessing the degree of stenosis.

Laboratory diagnostic methods

Lipid profile:
Indicators: total cholesterol, HDL, LDL and triglycerides.
High LDL levels and low HDL levels increase the risk of atherosclerosis. High triglycerides are also associated with increased risk.
Inflammatory markers (C-reactive protein): assessment of the degree of systemic inflammation that may contribute to the progression of atherosclerosis.
Elevated CRP is associated with an increased risk of cardiovascular events.
Homocysteine: investigation of homocysteine levels in the blood, especially if there is a family history of early atherosclerosis or thrombosis.
High homocysteine levels may contribute to endothelial dysfunction and increase the risk of atherosclerosis.

These diagnostic methods allow not only to accurately determine the presence of carotid atherosclerosis, but also to assess the risk of developing serious complications, such as stroke, which is key to determining the tactics of treatment and prevention of the disease.

Treatment of carotid atherosclerosis

Understanding the mechanisms of atherosclerosis is key to developing targeted therapeutic strategies. It is important to note that although some factors, such as genetic predisposition, are not modifiable, many aspects of the etiology of atherosclerosis can be controlled through lifestyle modifications and drug intervention.

Treatment begins with lifestyle adjustments and drug therapy including statins, antiaggregants and antihypertensives. If the stenosis is significant or symptomatic, interventional techniques such as carotid angioplasty and stenting are used. In more severe cases, carotid endarterectomy may be required.

Carotid angioplasty and stenting

3D-animation – carotid artery stenting

How it is performed: The procedure involves inserting a catheter through the femoral or radial artery to the site of carotid artery stenosis. A balloon is then inserted through a catheter and inflated to widen the narrowed portion of the artery, after which a stent is placed at that site to maintain the lumen of the artery.

Indications: symptomatic carotid stenosis ≥ 50% if surgical risks are elevated or there are anatomic complications. Asymptomatic stenosis ≥ 60-70%, at high risk of surgical complications or limited arterial access.
Contraindications: pronounced calcifications of the arterial wall, acute infectious diseases, poor blood coagulation.
Results: efficacy is comparable to surgery in reducing the risk of stroke, but there is a risk of restenosis in the long term.

Direct endovascular hybrid surgery

How it is performed: a combination of open surgery and stenting. First, the surgeon performs direct access to the carotid artery, and then the endovascular surgeon performs stenting.
Indications: severe stenosis or occlusion of the carotid arteries, especially if accompanied by stenosis of other major vessels of the head and neck. Patients in whom traditional stenting or surgery is inappropriate due to high risk or anatomic features.
Contraindications: similar to contraindications for standard stenting.
Results: allows more precise control of the process of vascular lumen restoration, reduces the risk of complications.

Standard carotid endarterectomy

3D animation – carotid endarterectomy

How it is performed: The surgeon makes an incision in the neck in the area of the affected carotid artery, opens the artery and removes the atherosclerotic plaque along with the inner lining of the artery. After the plaque is removed, the artery is sutured.

Indications: symptomatic stenosis ≥50% by NASCET criteria or ≥70% by ECST criteria. Asymptomatic stenosis ≥ 60% with a life expectancy of more than 5 years and low surgical risk.
Contraindications: absence of pronounced symptomatology with small stenosis, severe comorbidities.
Results: a 50% or greater reduction in stroke risk compared with drug treatment.

Eversion carotid endarterectomy

How it is performed: may be the method of choice or when standard carotid endarterectomy is difficult due to anatomical features or when tissue trauma needs to be minimized. In the eversion technique, the surgeon “everses” the inner sheath of the artery, starting at the branching point. This allows removal of the atherosclerotic plaque along with the inner lining of the artery in its entirety, minimizing traumatization and the need for additional prosthetics of the vessel.
Indications and contraindications: similar to standard carotid endarterectomy, but is preferred when the risk of traditional surgery is high due to anatomic or physiologic features.
Results: it allows to achieve similar results to classical surgery, while reducing the risk of surgical complications and speeding up the patient’s recovery.

General contraindications

Absolute contraindications: current or recent stroke with massive neurologic deficit. Unstable medical conditions such as acute heart failure or uncontrolled hypertension.
Relative contraindications: serious comorbidities that significantly reduce life expectancy. Diffuse vascular disease that complicates surgical access or increases the risk of procedural complications.

For a more detailed study of the indications and contraindications for this disease in order to reduce the risk of ischemic events and optimize clinical outcomes for patients with carotid atherosclerosis, we recommend referring to the recommendations of internationally recognized medical organizations. For example, these include: American Heart Association and European Society for Vascular Surgery.

FAQ

1. What is the difference between non-stenotic and stenotic carotid atherosclerosis?

Nonstenotic atherosclerosis – narrowing of the artery less than 50%. There are plaques, but they don’t critically impair blood flow. Often discovered incidentally during ultrasound.
Stenosing atherosclerosis – narrowing exceeds 50%, which can cause symptoms (TIA, stroke). Requires active treatment: medications (statins, antiaggregants) or surgery (endarterectomy, stenting).

2. What does atherosclerosis of the carotid arteries 30 percent mean?

Carotid atherosclerosis of 30 percent means that the lumen of the carotid artery is narrowed by 30 percent due to the deposition of atherosclerotic plaques on the inner wall of the vessel. This condition is called carotid stenosis and is measured in percentages – how much the diameter of the vessel is reduced compared to normal.

3. What diameter and condition is considered normal for carotid arteries?

Normally, the carotid arteries have a free lumen with no evidence of narrowing or turbulence. The diameter of the internal carotid artery is usually 4 to 6 mm, blood flow velocity is within 125 cm/s and below, with no areas of acceleration or plaques. The vessel wall is smooth, elastic, and blood flow is laminar.

4. When does carotid stenosis become dangerous?

Narrowing of the artery up to 50% most often does not pose a serious threat and is asymptomatic. A stenosis of 70% or more is considered dangerous, which significantly impairs blood flow to the brain and increases the risk of ischemic stroke. With 50 to 69% narrowing, the risk is already moderate, especially if there are complaints such as transient weakness, speech or vision impairment.

5. When does carotid artery stenosis require surgery?

Surgical intervention is recommended for severe stenosis of 70% or more, even in the absence of symptoms. For moderate stenosis of 50% or more, surgery is considered if signs of cerebral ischemia are present. The decision to intervene is made taking into account the general condition of the patient, comorbidities and the results of duplex scanning.
Treatment: Carotid endarterectomy is preferred. Stenting – at high surgical risk.

6. Which doctor treats atherosclerosis of the carotid arteries?

Carotid atherosclerosis is treated by a vascular surgeon or angiosurgeon, especially if it is a significant stenosis requiring surgical intervention.
In the early stages and at asymptomatic course of patients are managed by a neurologist or therapist, who prescribes examination, control risk factors (hypertension, cholesterol, sugar), and if necessary refer to specialized specialists.
A cardiologist may also be involved in treatment, especially if atherosclerosis is systemic and accompanied by coronary heart disease.

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