Carotid atherostenosis is a cause of acute ischemic stroke through flow failure from local occlusion or activated plaque resulting in arterial to arterial embolism. Treatment of symptomatic stenotic plaques by surgical or endovascular means has been shown to provide benefit.¹,² However, atherosclerotic plaque precedes stenosis by many decades. Carotid ultrasonography has been shown to identify carotid stenosis and also provide information about nonstenotic plaque.³

Advances in B-mode imaging permit assessment of the carotid arterial wall. Routine studies show the three components of the arterial wall (Figure 19.1) in the far wall of the common, internal and external carotid arteries. Such measurements of the intima and media thickness have been used in multiple studies for future vascular risk stratification.⁴,⁵ Although initially the distal 2 cm of the common carotid artery was measured, currently a different approach is utilized.

It made little sense to measure a single segment of the common carotid artery when plaque was visible at the carotid bifurcation where it is more prevalent. From a biologic perspective, the use of B-mode imaging to identify plaque prior to stenosis might provide earlier identification of risk and permit programs of risk reduction.

The utility of carotid plaque identification was shown in the Framingham Off-Spring study. When plaque was defined as an intima-media thickness of 1.5 mm or greater, there was improvement in risk stratification beyond the Framingham Risk Score improving net reclassification.⁶ Plus, measuring for plaque was technically easier than measuring the distance (height) of the blood intimal interface to the media-adventitia interface of the distal 2 cm of the common carotid artery.

However, the use of a “cut point” for plaque may not make biologic sense because lipid accumulation is time dependent.
A subject with a measure of 1.49 mm must surely be reclassified as having plaque when measured again after a year or so. If so, then subject went from no-plaque to plaque during the period of observation. Biologically, it makes better sense to consider the measure as an individual number, ie, quantitatively rather than categorically.

In more recent studies such as the Bioimage trial,⁷ plaque was identified as a localized increase in intima-media thickness that is 50% larger than the surrounding 1 cm, a 0.5 mm encroachment into the lumen, or 1.5 mm or greater in thickness. The underlying presumption was that plaque was a localized collection of lipid in the subendothelial space rather than a specific number.

The Bioimage study compared plaque at any location in the common, internal or external carotid arteries against coronary artery calcium scores (CAC) and had clinical vascular events as the primary endpoint (MACE). Both baseline measures of CAC and plaque showed a relationship to future vascular risk. As either measure increased at baseline, then there was an increased risk of a vascular outcome during study time (Figure 19.2). Ultrasound measures were helpful in the 32% of the population with 0 CAC scores. The utility of identification of carotid plaque and its amount was proven to have benefit in predicting coronary endpoints as well as stroke.