Carotid Atherosclerosis: Etiology, Pathophysiology, Diagnosis, Treatment

Carotid Atherosclerosis Epidemiology

Carotid atherosclerosis is a chronic condition in which the inner wall of the carotid arteries develops atherosclerotic plaques that progressively occlude the vascular lumen and eventually decrease blood flow to the brain. These factors make the disease one of the leading causes of stroke worldwide. Carotid atherosclerosis prevalence varies significantly depending on a patient’s geographical location, lifestyle, and ethnic background.

Geographical Differences:

• Carotid atherosclerosis is highly prevalent in North America and Europe. Studies indicate that this condition affects up to 10 % of the elderly population in these regions. This may be attributed to a high incidence of comorbidities such as hypertension and diabetes. An indirect contributing factor is a high standard of living, often accompanied by reduced physical activity and unhealthy dietary habits.
• Asian countries are also experiencing a rise in carotid atherosclerosis, which correlates with urbanization and lifestyle changes. In Japan and China, rapid industrial development and a shift toward a more Western-style diet have contributed to an increase in atherosclerosis cases.
• Low- and middle-income countries often exhibit a lower prevalence of carotid atherosclerosis, likely due to a younger population and higher levels of physical activity. However, urban sprawl and malnutrition in these regions are contributing to a growing number of atherosclerosis cases.

Prevalence Factors:

• Urbanization rates and lifestyle changes among the population;
• Access to quality medical services, which enable early detection and treatment of conditions that induce atherosclerosis.
• National anti-smoking programs, education levels, and economic development, all of which directly influence public health.

Thus, carotid atherosclerosis is a multifactorial disease influenced by numerous socio-economic and cultural factors, all of which must be considered when developing prevention and treatment strategies at national and international levels.

Carotid Atherosclerosis Etiology

Hypertension, diabetes, smoking, hyperlipidemia, and genetic predisposition are primary risk factors for carotid atherosclerosis. Each of these factors contributes to endothelial damage in blood vessels, triggering the formation of atherosclerotic plaques. Special attention should be given to age and gender, as advancing age poses a greater risk of atherosclerosis, and males are more susceptible to this disease.

Carotid Atherosclerosis Pathophysiology

Carotid atherosclerosis is a chronic arterial disease. Its major symptoms include impaired lipid and protein metabolism, inflammation, and the formation of atherosclerotic plaques, which may trigger stenosis and vascular occlusion. Atherosclerosis develops in several stages:

• Endothelial damage: The first stage of the disease involves injury to the inner layer of the arterial wall, known as the endothelium, which is considered the primary event in the development of atherosclerosis. Endothelial damage may be linked to a variety of factors, including hypertension, smoking, hyperglycemia, and oxidative stress. Once compromised, the endothelium loses its barrier function, allowing low-density lipoproteins (LDL) to more easily penetrate the arterial wall.
• LDL oxidation: Oxidation converts LDL into oxidized LDL (ox-LDL). The substance exerts direct cytotoxicity and contributes to atherosclerosis. These modified lipoproteins activate the endothelium and recruit monocytes to the damaged site, further promoting the development of atherosclerotic plaques.
• Inflammation and foam cells: Monocytes that infiltrate the arterial wall differentiate into macrophages, which then engulf ox-LDL and transform into foam cells. As foam cells accumulate, they form a fatty streak — an early morphological indicator of atherosclerosis.
• Smooth muscle cell proliferation and fibrous capsule: In response to inflammation and vascular wall damage, smooth muscle cells migrate from the media into the intima. There, they proliferate and produce collagen along with other extracellular matrix components. Eventually, the intima becomes thicker, and an atherosclerotic plaque develops, encapsulated by a fibrous layer.
• Atherosclerotic plaque complications: Over time, an atherosclerotic plaque may become unstable and rupture, forming a blood clot and leading to acute vessel occlusion. The condition may trigger severe clinical consequences, including cerebrovascular accidents.

Clinical Manifestations

Early carotid atherosclerosis may be asymptomatic. As the disease progresses and significant stenosis develops, patients may experience transient ischemic attacks or even cerebral ischemic stroke.

Carotid Atherosclerosis Symptoms:

• Sudden numbness or muscle weakness in the face, arm, or leg (typically one-sided);
• Speech difficulties, visual impairment, or uncoordinated movements.

Diagnosis

Carotid atherosclerosis is diagnosed based on a range of investigations and laboratory tests. The results help identify the plaques, determine the severity of vascular damage, and assess the risk of complications.

Investigations

• Doppler ultrasound:
  Indications: Suspected carotid atherosclerosis; symptoms of transient ischemic attack or stroke; risk factors (hypertension, diabetes, hyperlipidemia).
  Signs: Atherosclerotic plaques detected; narrowing of the arterial lumen; altered blood flow at the stenosis site.
• Magnetic resonance angiography:
  Indications: Used for high-precision imaging of the arteries; assessment of stenosis severity and vascular bed anatomy in complex or uncertain cases.
  Signs: Detailed plaque structure; determination of severity and location of stenosis.
• Computed tomography (CT angiography):
  Indications: Suspected calcified plaques; assessment of surgical feasibility.
  Signs: Detailed data about plaques composition (including calcification); precise assessment of stenosis severity.

Laboratory Tests

• Lipid panel:
  Components: Total cholesterol, HDL, LDL, and triglycerides; atherosclerosis risk is linked to high LDL, low HDL, and, in certain cases, elevated triglycerides.
• Inflammatory markers (C-reactive protein): This test is instrumental in evaluating systemic inflammation that may contribute to atherosclerosis. Elevated CRP may also indicate a higher risk of cardiovascular events.
• Homocysteine: A blood test to determine homocysteine levels is primarily indicated with a family history of early atherosclerosis or thrombosis.
  Elevated homocysteine levels may be responsible for endothelial damage and increase the atherosclerosis risk.

These diagnostic modalities aid in identifying carotid atherosclerosis and evaluating the risk of severe complications, such as stroke. The results provide essential data for selecting appropriate treatment strategies and preventive measures.

Carotid Atherosclerosis Treatment

Understanding the underlying mechanisms of atherosclerosis is essential for developing targeted therapies. While certain factors, such as genetic predisposition, cannot be modified, most atherosclerosis risk factors can be managed through lifestyle changes and medical treatment.

Initial management focuses on conservative measures, including statins, antiplatelet agents, and antihypertensive medications. Significant stenosis or symptomatic disease require invasive techniques, such as carotid angioplasty or stenting. More severe cases may necessitate carotid endarterectomy.

Carotid Angioplasty and Stenting

Procedure: A catheter is inserted through the femoral or radial artery and guided to the stenosis site in the carotid artery. A balloon is then passed through the catheter. When it reaches the narrowed part of the artery and inflated at the narrowed section of the artery to widen the lumen. Following balloon inflation, a stent may be placed in the affected area to help maintain arterial patency and prevent restenosis.

• Indications: Symptomatic carotid artery stenosis (≥ 50 %) in patients with high surgical risks or anatomical complications. Asymptomatic stenosis (≥ 60–70 %) in cases of high surgical risks or limited access to the artery.
• Contraindications: Severely calcified arterial walls; Acute infections; Poor blood coagulation.
• Outcomes: The procedure is as effective as traditional surgery in lowering stroke risks. However, it is associated with a higher long-term risk of restenosis.

Hybrid Endovascular and Direct Surgical Approach

• Procedure: This is a combination of open surgery and endovascular stenting. First, a surgeon gains direct access to the carotid artery. Then, an endovascular surgeon performs stenting to restore proper blood flow.
• Indications: Severe carotid artery stenosis or occlusion, especially when other large vessels of the head and neck are affected; cases where conventional stenting or surgery are not feasible due to high surgical risks or complex anatomical features of a patient.
• Contraindications: Refer to Contraindications listed for Carotid Angioplasty and Stenting.
• Outcomes: The procedure allows for a more precise control of vascular lumen restoration and reduces the risk of complications compared to other approaches.

Carotid Endarterectomy

Procedure: A surgeon makes an incision in the neck over the affected carotid artery, opens the vessel, and removes an atherosclerotic plaque along with the intima. Then, the artery is sutured.

• Indications: Symptomatic stenosis (≥ 50 % according to NASCET criteria or ≥ 70 % according to ECST criteria). Asymptomatic stenosis (≥ 60 %) if life expectancy exceeds 5 years and surgical risks are low.
• Contraindications: No marked symptoms in mild stenosis; severe comorbidities.
• Outcomes: Stroke risks decrease by 50 % or more compared to medical therapy.

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Eversion Carotid Endarterectomy

• Procedure: Preferred treatment option in cases where standard carotid endarterectomy is complicated by anatomical factors Essential for minimizing tissue damage The eversion technique involves cutting and turning the arterial intima inside out, starting at the branching point An atherosclerotic plaque may be removed along with the arterial intima as a whole. The method is less traumatizing and eliminates the need for vascular repair.
• Indications and Contraindications: Refer to Indications and Contraindications listed for Carotid Endarterectomy. Note that the eversion option is preferable in cases of high surgical risks due to anatomical or physiological features of a patient.
• Outcomes: The procedure achieves results comparable to standard carotid endarterectomy but with a lower risk of postoperative complications and improved recovery rates.

General Contraindications

• Absolute contraindications: Current or recent stroke accompanied by significant neurologic deficits. Unstable medical conditions, such as acute cardiac failure or uncontrolled hypertension.
• Relative contraindications: Serious comorbidities that significantly reduce a patient’s life expectancy. Diffuse vascular conditions that complicate surgical access or increase procedural risks.

For more information on indications and contraindications in carotid atherosclerosis patients, please refer to acknowledged medical organizations such as American Heart Association or European Society for Vascular Surgery. A deeper understanding of the disease helps mitigate ischemic risks and optimize clinical outcomes.