<p>Craig Walker, MD<br />
Clinical Editor<br />
Interventional Cardiologist <br />
Founder, President, and Medical Director<br />
Cardiovascular Institute of the South<br />
Clinical Professor of Medicine <br />
Tulane University School of Medicine<br />
Louisiana State University School of Medicine</p>
Welcome to the May edition of Vascular Disease Management. I have chosen to comment on Dr Kim and colleagues’ article on “Advances in Carotid Imaging: Beyond Luminal Stenosis.” I have chosen to discuss this report as it highlights anatomical findings of various modalities that may influence the ultimate clinical expression of the carotid disease process.
There is great debate raging about the treatment of carotid disease. Many would argue that asymptomatic carotid disease should be treated only with medical therapy, while others would argue in favor of carotid stenting or carotid endarterectomy based on the findings of the ACT 1 and ACAS trials, respectively. While most would agree that either stenting or endarterectomy should be performed in symptomatic carotid disease, debate rages over which of these modalities is superior based on the randomized CREST trial. At present, carotid stenting is only reimbursed by CMS if there is symptomatic carotid disease of 80% or greater in high surgical risk patients. Carotid endarterectomy remains compensated in most patients with 60% or greater lesions whether symptomatic or not.
Carotid disease is perplexing. Some patients develop dense hemiplegia or death with occlusion of a single carotid, while others may have no significant findings even with occlusion of both carotids and one vertebral artery when the circle of Willis remains intact. Treatment and its potential benefit is therefore difficult to assess on an individual basis as the calculation of risk/benefit on a single patient is impossible. Because of this limitation, treatment is based on the relative risk in large populations. Unfortunately, what is now considered ideal medical therapy was not employed in most of the historical studies; therefore, many would argue that the previously quoted risk may no longer be applicable. Furthermore, it is likely that what is now considered ideal medical therapy is likely to continue to evolve. Historically, the decision about whether or not any intervention should be performed was based on symptoms and the degree of stenosis. Dr Kim and colleagues focus on imaging beyond the degree of stenosis as possible indicators of inherent risk of events.
Carotid ultrasound is the most utilized tool in the initial assessment of carotid disease. The degree of carotid stenosis and the presence of ulceration have historically proven to have prognostic significance. These are usually reported in carotid ultrasound studies. The importance of plaque echolucency as a predictor of spontaneous events and poorer prognosis with carotid stenting is being reported in observational studies. The utilization of contrast sonography to identify neovascularization associated with higher plaque vulnerability is also discussed.
Magnetic resonance studies are being utilized more frequently in carotid artery assessment. Assessments of fibrous cap thickness and lipid-rich necrotic plaque core are shown to have significance as predictors of future clinical events. Black-blood magnetic resonance imaging demonstrating high signal intensity as compared with adjacent sternocleidomastoid muscle predicts higher risk of embolic stroke with carotid stenting.
While computed tomography angiography is commonly utilized to assess the degree of carotid stenosis and lesion morphology, the assessment of soft plaque with low Hounsfield units may be further predictive of inherent risk of clinical events.
The role of positron emission tomography in assessing inflammation as a possible predictor of future events is also discussed.
All of these modalities have studies that suggest that prognosis is related to factors beyond the degree of stenosis. None of these studies, however, can predict who will remain asymptomatic even with vascular occlusion or an embolic event.
Imaging beyond the degree of stenosis may be the key in determining how patients with carotid disease should be treated. There is no debate that all of these patients should have aggressive medical therapy. One must question how medical therapy may evolve. Will the combination of high-dose statins with the powerful PCSK9 inhibitors become standard of care with lipid-rich plaque as these agents have resulted in plaque regression in other vascular beds? Might pretreatment with these agents lessen the risk of embolic events with carotid stenting? Whether patients should have carotid stenting or endarterectomy is clearly not yet answered. Even if this question were answered based on the most recent studies, one must question whether newer stent designs with protective mesh would yield different results. One must question whether better proximal or distal protection or even flow reversal during intervention would alter outcomes. The target seems to keep moving, as it always does with new treatment modalities.
This is an important article that is pertinent to all vascular specialists. It provides insight into the carotid disease process beyond the degree of stenosis or presence of ulceration. Unfortunately, I’m certain that debate as to optimal therapy of carotid disease is far from over.