Excerpt
This article is the first of 2 parts.
Ischemic stroke is one of the leading causes of death and long-term disability around the world. Extracranial atherosclerotic disease is implicated in 15% to 20% of all ischemic strokes. Carotid artery stenosis causes roughly 300,000 to 400,000 ischemic strokes a year in the United States. Thus, early detection and aggressive treatment of this extracranial vascular disease are an urgent priority in combating and preventing cerebral ischemic disease.
The common carotid artery bifurcation in the neck is one of the most common sites for development of atherosclerotic plaques. Atherosclerosis is a bland arterial collection of cholesterol, complicated by smooth muscle cell accumulation. Endothelial denuding injury leads to platelet aggregation and release of platelet factors, which will trigger the proliferation of smooth muscle cells in the arterial intima.
Atheromas start to develop by age 20, and their progression is related to specific traits, conditions, or habits that may raise the chance of developing atherosclerosis. Such conditions are known as risk factors, and their presence and aggravation will increase the chances of developing atherosclerosis. Most risk factors can be controlled, thus atherosclerosis can be prevented or delayed. Those that can be controlled include a high level of low-density lipoprotein in the blood, a low level of high-density lipoprotein in the blood, hypertension, exposure to tobacco smoke, diabetes mellitus, obesity, and an inactive lifestyle. However, age and a family history of heart disease are risk factors that cannot be controlled.
Plaque formation starts in the posterior wall of the common carotid artery, close to the carotid bulbus, and it progressively involves the external and internal carotid arteries leading to ulcers, calcifications, or intraplaque hematomas. Cervical carotid artery atheromas are categorized as either asymptomatic or symptomatic.
Asymptomatic atheromas are discovered incidentally during routine clinical examination, mainly in patients with murmurs in the neck region. These patients have no history of brain ischemia, and imaging examinations reveal the presence of an atheroma in the cervical carotid artery.
When the patient presents with ischemic events, and those events lie ipsilateral to carotid stenosis, there is greater urgency for surgical intervention. The risk of stroke in untreated carotid artery stenosis for symptomatic and asymptomatic patients differs markedly (26% vs 6.2% over 3 years, respectively).
Carotid endarterectomy (CEA) has been performed since the early 1950s, but it was not until the North American Symptomatic Carotid Endarterectomy Trial (NASCET, 1991) that the overwhelming superiority of surgical therapy for carotid artery stenosis was accepted. NASCET was the first randomized controlled trial to define the place of CEA in clinical practice. Until 1991, the best strategies for management of carotid stenosis were unproven by class 1 evidence.
Carotid artery surgery is an element of neurosurgery with which the young neurosurgeon should be comfortable, both with the topic and with identifying and stratifying patients with carotid stenosis. This will enable the neurosurgeon to offer patients the best available treatment for stroke prevention. This article will assist neurosurgeons to recognize the most important risk factors related to carotid atherosclerotic plaques, explain how to make a treatment plan for patients with cervical carotid stenosis, and discuss the merits of CEA and stenting.