Carotid Artery Disease
Gregory K. Albaugh
Mark M. Levy
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Mr. Wilson was referred after his primary care physician detected a bruit in his left neck on routine physical examination. He is 64 years old and smoked 1 pack of cigarettes daily until 17 years ago, when he quit smoking. He occasionally drinks alcohol. He has hypertension and hypertriglyceridemia. He takes atenolol 50 mg once a day and a statin agent for his cholesterol.
What is a bruit and what causes it?
A bruit is an abnormal sound auscultated over a vessel; it is typically rumbling in character. The bruit represents noise generated from turbulent blood flow within the vessel. Normally, blood flows through a vessel in laminar fashion. When there are luminal irregularities in the vessel, the blood flow becomes turbulent, generating audible sound energy referred to as a bruit. If the turbulence becomes more severe, it generates a palpable mechanical disturbance referred to as a thrill.
What is the chance that this bruit is associated with a high-grade carotid artery stenosis?
The chance that a bruit reflects significant stenosis is not high. Even with cerebrovascular symptoms, a bruit alone is insufficient to predict high-grade stenosis (1). Transmitted heart sounds may be auscultated in the neck. Other turbulent flow heard in the neck may be from the external carotid artery or, more rarely, from the thyroid in some cases of hyperthyroidism. It remains important to listen for carotid bruits nevertheless, because they may be indicative of carotid stenosis and guide further diagnostic workup. Both the presence of a bruit and advancing age have been demonstrated to be predictive factors for eventual transient ischemic attacks (TIAs) and cerebrovascular accidents (CVAs). Bruits may be most predictive for TIA or CVA in older diabetic female patients (2).
What symptoms would you ask about to determine if Mr. Wilson is having symptoms associated with his carotid disease?
Classic symptoms of carotid disease are those associated with TIAs or CVAs, namely focal sided motor or sensory loss, or aphasia. In addition, amaurosis fugax, meaning temporary monocular blindness and frequently described as a windowshade drawing down over one eye, is a characteristic symptom associated with embolization from a carotid lesion to the ophthalmic artery. In contrast to these localizing symptoms, more global nonlateralizing symptoms such as headache, presyncope, and confusion are not characteristically associated with carotid disease.
What is a TIA?
TIA: a reversible neurologic deficit lasting fewer than 24 hours. TIAs are frequently the consequence of emboli from the extracranial carotid system or the heart.
Acute CVA: a neurologic deficit that lasts longer than 24 hours
RIND (reversible ischemic neurologic deficit): a syndrome lasting between 24 and 72 hours. This term has fallen out of favor due to evidence that, although the neurologic deficit improves, areas of infarction can be demonstrated.
Crescendo TIAs: a syndrome of serial TIAs occurring over days to weeks, representing an ominous prodrome to frank stroke
Which diagnostic test should be ordered to evaluate the bruit?
Duplex ultrasound (US) is the primary diagnostic modality used to evaluate carotid stenosis. The duplex scan is composed of two components.
The first component is the two-dimensional B-mode black and white image that represents a cross-sectional shadow of the body part examined. The B-mode image can show the vessel calcification and homogeneity compared with the heterogeneity of the carotid plaque. In addition, the B-mode can be used to offer a preliminary estimate of the degree of stenosis observed in the carotid bulb or proximal internal carotid artery.
The second component of the duplex examination is the Doppler evaluation of blood flow traversing through the carotid artery itself. According to the Doppler frequency shift principal, sound energy of a given emitted frequency is reflected off of moving red cells and then received back on an US probe. By measuring differences between emitted and received sound frequencies and taking into account angles of insonation, the speed of blood traversing through a particular carotid segment may be accurately estimated. These flow velocities then can be correlated to either normal vessel diameters or vessel stenosis; the latter is generally associated with remarkable increases in associated blood velocity.
What other tests are available to study the carotid arteries?
Magnetic resonance arteriography (MRA) is increasingly performed to demonstrate the arterial anatomy of the carotid system. As a noninvasive study, like duplex, it offers negligible risk to the patient. Unlike carotid duplex examinations, however, its visual window includes the innominate artery and intrathoracic carotid segments. It also visualizes the carotid artery cephalad to the midcervical segment most easily visualized by duplex examination. Magnetic resonance imaging may depict the intracranial arteries including the circle of Willis, and standard tomographic imaging can rule out aneurysm or another mass lesion. Although many vascular surgeons do not consider MRA to be accurate enough as the sole evaluation modality on which to base surgery, many use it together with duplex US, when these studies offer consistent results.
Although carotid duplex US may best demonstrate carotid arterial flow physiology, contrast angiography, an invasive procedure, remains the gold standard in characterizing the corresponding anatomy. Contrast arteriography provides thorough evaluation not only of the midcervical carotid artery (like the duplex examination provides) but also of the aortic arch, the innominate artery, the intrathoracic carotid artery, the intracranial carotid, and the cerebral circulation itself. Conventional contrast arteriography has an associated risk of stroke and femoral access complications; therefore, it is not always performed before endarterectomy, particularly in facilities where the noninvasive imaging has a documented accuracy.
Mr. Wilson has a history of smoking, hypertension, and hypertriglyceridemia. What medications would be potentially helpful in lowering his risk of stroke or myocardial infarction (MI)?
Among the primary risk factors for CVA, hypertension, cigarette smoking, diabetes, and hypercholesterolemia are four that can potentially be modified with lifestyle or medical management. Mr. Wilson, although no longer smoking, has hypertension and hyperlipidemia. The use of beta-blockers and diuretics to treat hypertension has been shown to decrease the risk of stroke and myocardial events (3). In addition to a beta-blocker, this patient is also appropriately treated with a statin agent. Patients treated with statin agents demonstrated a 46% reduction in CVA risk in a meta analysis (4).
Due to these factors, Mr. Wilson is at increased risk for CVA and MI. Antiplatelet therapy has been shown to decrease adverse outcomes such as CVA and MI (5,6). Antiplatelet therapy consists of many different medications. The most commonly used agent is aspirin. Lipid-lowering agents such as lovastatin have shown benefit in controlling progression of disease (7). Control with beta-blockers decreases cardiac work and blood pressure. Angiotensin-converting enzyme inhibitors have also shown reduction in CVA, MI, and major cerebrovascular events in these patients (8). Most survival benefits from medical therapy in these patients are related to the reduced risk of cardiac ischemic events and cerebrovascular events.
Because Mr. Wilson’s carotid stenosis is presently considered asymptomatic, what is an accepted threshold at which to intervene beyond best medical management?
If the duplex scan demonstrate 80% to 99% stenosis and the individual surgeon’s operative stroke and death rates are low, then the asymptomatic patient may be offered carotid endarterectomy (CEA). Patients who present with greater than 60% stenosis on contrast arteriography were shown to suffer fewer fatal and nonfatal strokes over a 5-year period if CEA was performed according to the Asymptomatic Carotid Atherosclerosis Study (ACAS) trial (9).
It is generally accepted that a lesion that, on duplex US, is shown to be 80% to 99% stenotic will be at least 60% stenotic on contrast angiography. Lesions that fall short of these guidelines are commonly treated more conservatively with serial follow-up duplex US and antiplatelet therapy. (See Algorithm 21.1)
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