Symposium - New Technologies and Their Application to Carotid Occlusive DJsease Saturday, March 8, 1997 12:00-5:30 pm 12:00 pm
Carotid Artery Disease and Stroke: Natural History and Medical Therapy Thomas Brott, MD 12:20 pm
Diagnosis of Carotid Artery Disease D. Eugene Strandness, ]r, MD Learning objectives: (1) To understand the effect of clinical trials; (2) to understand the impact of clinical trials on diagnostic testing; (3) to appreciate the role of ultrasound as a screening test before operation; and (4) to understand the possible role of magnetic resonance angiography and ultrasound as the sole diagnostic studies before carotid endarterectomy. IMAGING and Doppler are the two major components of duplex ultrasound systems used to diagnose carotid artery disease. Imaging provides a view in real time of the arteries and how they are involved by the disease process, which is usually atherosclerosis. From a practical perspective, most of our attention is directed at the carotid bulb, which is where the disease occurs most frequently and is recognized as a common cause of transient ischemic attacks and stroke. Doppler is used to detect the velocity patterns that occur as blood approaches and leaves the diseased site. The use of Doppler is predicated on the fact that there is a relation between the degree of narrowing of an artery and the blood velocity changes that occur at the site of greatest narrowing. This happens to be a favorable relation because the only predictor of clinical events is the degree of narrowing. The most important clinical event in the past several years has been the proof that carotid endarterectomy is an effective means to prevent stroke. This occurred with the publication of the results of four major trials-the North American Symptomatic Carotid Surgery Trial (NASCET), the European Carotid Surgery Trial (ECST), and the two trials of asymptomatic patients, the Veterans Asymptomatic Carotid Trial (VACT) and the National Institutes of Health-supported Asymptomatic Carotid Artery Surgery Trial (ACAS). Each of these trials showed a benefit of carotid endarterectomy, but there were some important differences that must be emphasized because they will affect the interpretation of cerebrovascular ultrasound. The benefits are listed here: 1. NASCET: a 70% diameter reduction. The distal internal carotid artery is the reference "normal" artery; 2. ECST: a 70% diameter reduction. All measurements
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from the bulb itself;
3. VACT: a 50% diameter reduction. The distal internal
carotid is the reference artery; 4. ACAS: a 60% diameter reduction. The distal internal carotid is the reference artery. It should be immediately obvious that something is surely wrong with these conclusions. How can a 50% or 60% lesion be dangerous in an asymptomatic patient but not in a symptomatic one? And how necessary is it to have end points for each of these degrees of narrowing? It would not be such an important point except that Dr. Henry Barnett of NASCET insists that a lesion must narrow the artery by 70%, not 69%, before surgery is considered. He also fails to mention that by ECST methods of measuring an arteriogram, a 50% diameter reduction is a 0% stenosis according to NASCET. When comparing these two studies, it is also possible to have a negative stenosis when NASCET methods are used! How do we accommodate these markedly different results when performing a radiologic study of the carotid circulation? In our research, we created a disease classification by categories of stenosis that, by definition, are rather broad but do have some clinical relevance. These are (a) normal, (b) 10/0-15%, (c) 160/0-49%, (d) 500/0-79%, (e) 80°/0-99%, and (j) total occlusion. It is immediately evident that we do not have a category for the 60% of ACAS or the 70% of NASCET. Although I believe that such fine categorization is at times ridiculous for clinical purposes, we must use these end points until common sense is introduced to this entire debate. The major criteria that lend themselves to change in arriving at these values are the peak systolic velocity, the end-diastolic velocity, spectral broadening, and the ratios of the peak systolic velocity at the site of narrowing divided by that found in the common carotid artery proximal to the bulb itself. For our studies, we use the following guidelines: 1. for the normal bulb: no evident atheroma in the bulb and the appearance of boundary layer separation;
2. for 10/0-15% stenosis: disease in the bulb, no bound-
ary layer separation, and minimal spectral broadening; 3. for 160/0-49% stenosis: spectral broadening with a peak systolic velocity less than 125 cm/second;
4. for 500/0-79% stenosis: peak systolic velocity more than 125 cm/second; 5. for 800/0-99% stenosis: end-diastolic velocity more than 145 em/second;
6. for occlusion: flow to zero at end-diastole in the common carotid, and no flow from the internal carotid artery. For the 60% and 70% diameter reduction, we chose the ratio of the peak systolic velocity at the site of narrowing to that from the common carotid artery. This does not require any change in how the studies are done. For the 60% stenosis, this ratio is 3.2. For the 70% stenosis, the ratio is 4.0. For reporting purposes, we cal-