INTRODUCTION:

MECHANISM OF ATHEROSCLEROSIS:

The mechanism of atherosclerosis in carotid artery is similar to the atherosclerosis in other arterial locations. Reactive oxygen species (ROS) have been implicated in the initiation and progression of atherosclerosis. vascular cell adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion molecule on endothelial cells (ELAMs) Monocyte adherence to endothelial cells is mediated through adhesion molecules.

Low-density lipoprotein cholesterol (LDL-C) is mildly oxidized to minimally modified LDL (MM-LDL) which stimulates endothelial and smooth muscle cells to produce chemoattractant proten-1 (MCP-10) MM-LDL is further oxidized to fully oxidized LDL (OX-LDL). MCP-1 and OX-LDL accelerate migration of monocytes to subendothelial area.

Monocyte macrophages express the LDL receptor, but the rate of uptake of native LDL is insufficient to produce foam cells. OX-LDL is a ligand for the scavenger receptor expressed in monocyte differentiated into tissue macrophage. This monocyte/macrophage differentiation is facilitated by release of monocyte colony stimulating factor (MCSF) from endothelial cells under the influence of MM-LDL. The differentiated macrophage develops receptor for OX-LDL which is taken up by receptors to produce foam cells. The production of foam cells is the early stage of atherosclerosis. Foam cells also generate ROS. Smooth muscle cell proliferation and migration, synthesis of connective tissue and matrix, migration of monocytes and formation of foam cells results in the development and progression of atherosclerosis.

DEFINITION:

Carotid artery stenosis is a narrowing or constriction of any part of the carotid arteries, usually caused by atherosclerosis

TERMINOLOGY:

Transcient ischemic attack, mini stroke.

INCIDENCE:

Approximately 80 to 85% strokes are ischemic due to carotid artery stenosis (CAS). The prevalence of significant CAS is 7% in women and 9% in men. Severe asymptomatic CAS varies from 0 to 3.1%. Prevalence of symptomatic CAS is high in patients with peripheral arterial disease.

The thrombotic plaques are more frequently detected in patients with stroke (66.9%) than with TIA (36.1%) and asymptomatic patients (26.8%). They also reported that out of 45 carotid plaques removed during carotid endarterectomy 39.6% were thrombotic plaques, 15.8% were vulnerable plaques, and 44.6% were stable plaques

CAUSES AND RISK FACTORS:

CAS is due to atherosclerosis, the major risk factors for which include dyslipidemia, age. smoking, hypertension, diabetes, obesity, cigarette smoking, family history of atherosclerosis, advanced glycation end products (AGEs) and its receptors (RAGE, soluble RAGE [sRAGE]), lack of exercise and C-reactive protein (CRP)

SIGNS AND SYMPTOMS:

The plaque can be stable and asymptomatic, or it can be a source of embolization. Emboli break off from the plaque and travel through the circulation to blood vessels in the brain. As the vessels get smaller, an embolus can lodge in the vessel wall and restrict the blood flow to parts of the brain. This ischemia can either be temporary, yielding a transient ischemic attack, or permanent resulting in a thromboembolic stroke.

Transient ischemic attacks (TIAs) are a warning sign, and may be followed by severe permanent strokes, particularly within the first two days. TIAs by definition last less than 24 hours and frequently take the form of a weakness or loss of sensation of a limb or the trunk on one side of the body, or the loss of sight (amaurosisfugax) in one eye. Less common symptoms are artery sounds (bruits), or ringing in the ears (tinnitus).

PATHOPHYSIOLOGY:

CAS is a progressive narrowing of the carotid artery due to development of atherosclerosis, characterized by local thickening of the interior arterial wall. Pathogenesis of atherosclerosis has been reviewed early by Prasad. Classical types of lesion are fatty streaks, fibrous cap, and complicated lesion, based on the progression of atherosclerosis.

Carotid plaques consist of lipid core with infiltration of inflammatory cells covered with a fibrous cap. A typical fibrous cap consists of the following:

(1) Fibrous cap composed of smooth muscle cells, few leukocytes, dense connective tissue that contains elastin, collagen fibrils, proteoglycans, and a basement membrane;

(2) A cellular area beneath that consists of a mixture of macrophages, smooth muscle cells, and T lymphocytes;

(3) A deeper necrotic core that contains cellular debris, lipids, cholesterol crystals, and calcium deposit. With time the plaque can become large and produce narrowing in the carotid artery.

DIAGNOSIS:

Carotid artery stenosis sometimes causes an abnormal sound, or bruit in the artery that can be heard with a stethoscope. Imaging tests to diagnose, localize and measure stenosis include:

Carotid ultra sound (including Doppler ultrasound):

This test uses sound waves to create real-time pictures of the arteries and locate blockages. Doppler is a special ultrasound technique that can detect areas of restricted blood flow in the artery.

Computed tomography angiography (CTA):

CTA uses a CT scanner to produce detailed views of the arteries anywhere in the body – in this case, in the neck. The test is particularly useful for patients with pacemakers or stents.

Magnetic resonance angiography (MRA):

This non-invasive test gives information similar to that of CTA without using ionizing radiation.

Cerebral angiography:

Also known as intra-arterial digital subtraction angiography (IADSA), cerebral angiography is a minimally invasive test in which a catheter is guided through an artery to the area of interest. Contrast material is injected through the tube and images are captured with x-rays.

70 percent stenosis of the right internal carotid artery as seen by ultrasound. Arrow marks the lumen of the artery.

CT image of a 70 percent stenosis of the right internal carotid artery

Screening:

Screening is recommended for people, who have vascular disease elsewhere in the body, including:

· Peripheral artery disease (PAD)

· Coronary artery disease (CAD)

· Atherosclerotic aortic aneurysm (AAA)

· Medications alone (an antiplatelet drug (or drugs) and control of risk factors for atherosclerosis).

· Medical management plus carotid endarterectomy or carotid stenting, which is preferred in patients at high surgical risk and in younger patients.

· Control of smoking, high blood pressure, and high levels of lipids in the blood.

MEDICAL MANAGEMENT:

The treatment of asymptomatic patients with CAS includes lifestyle changes and use of pharmacological agents.

Lifestyle changes:

Cessation of smoking and use of tobacco products, Use of foods low in saturated fats, cholesterol, and sodium. Control of body weight, Daily physical exercise, Reduction of dietary calories intake. Limitation of alcohol use.

Pharmacological agents:

Asymptomatic patients with low-grade CAS (less than 50%) should receive intensive medical treatment. Medical treatment is targeted at risk factors of CAS and includes: lipid lowering agents, anticoagulant agents, AGE-lowering agents, agents that increase the levels of sRAGE, and CRP-lowering agents.

Surgery and stenting:

The largest clinical trial performed, CREST (The Carotid Revascularization Endarterectomy versus Stenting Trial), randomized patients at risk for a stroke from carotid artery blockage to either open surgery (carotid endarterectomy) or carotid stent placement with embolic protection. This trial followed patients for 4 years and found no overall difference in the primary end point of both treatment arms (myocardial infarctions, any perioperative strokes or ipsilateral strokes within 4 years, or death during procedure.

REFERENCE:

1. Bartlett ES, Walters TD, Symons SP, Fox AJ (January 2006). "Quantification of carotid stenosis on CT angiography". AJNR. American Journal of Neuroradiology. 27 (1): 13–19.

2. Guideline on the Management of Patients with Extracranial Carotid and Vertebral Artery Disease" American Heart Association.264 – 268 "Carotid Artery Stenosis information. Internal carotis occlusion". Patient.info. Retrieved 2018-10-08. 304 - 308

3. Screening for Carotid Artery Stenosis. December 2007. U.S. Preventive Services Task Force. Agency for Healthcare Research and Quality, Rockville, MD. 820 –825.27 (1): 13–19.

Received on 16.09.2019 Modified on 28.09.2019

Int. J. of Advances in Nur. Management. 2020; 8(1): 100-102.

DOI: 10.5958/2454-2652.2020.00024.4