Imaging of high-risk carotid artery plaques: current status and future directions

Abstract

<jats:p>In this paper, the authors review the definition of high-risk plaque as developed by experienced researchers in atherosclerosis, including pathologists, clinicians, molecular biologists, and imaging scientists. Current concepts of vulnerable plaque are based on histological studies of coronary and carotid artery plaque as well as natural history studies and include the presence of a lipid-rich necrotic core with an overlying thin fibrous cap, plaque inflammation, fissured plaque, and intraplaque hemorrhage. The extension of these histologically identified high-risk carotid plaque features to human in vivo MRI is reviewed as well. The authors also assess the ability of in vivo MRI to depict these vulnerable carotid plaque features. Next, the ability of these MRI-demonstrated high-risk carotid plaque features to predict the risk of ipsilateral carotid thromboembolic events is reviewed and compared with the risk assessment provided by simple carotid artery stenosis measurements. Lastly, future directions of high-risk carotid plaque MRI are discussed, including the potential for increased clinical availability and more automated analysis of carotid plaque MRI. The ultimate goal of high-risk plaque imaging is to design and run future multicenter trials using carotid plaque MRI to guide individual patient selection and decisions about optimal atherosclerotic treatment strategies.</jats:p>

Intraplaque Hemorrhage and the Plaque Surface in Carotid Atherosclerosis: The Plaque At RISK Study (PARISK)

“…As stated previously, the common viewpoint is that these small leaky neovessels are responsible for the occurrence of intraplaque hemorrhage and subsequently the development of an unstable rupture-prone plaque. 5,[9][10][11][12]32 Our results-if confirmed in serial studies-can support the pathophysiologic relation between intraplaque hemorrhage and disrupted plaque surface. An alternative viewpoint to explain this relationship is that repeated fissuring of the plaque and associated formation of nonocclusive luminal thrombus incorporated in the plaque could be the cause of intraplaque hemorrhage.…”

Nonstenotic carotid plaque on CT angiography in patients with cryptogenic stroke

“…17 High-resolution carotid plaque MRI 18,19 is a technique that enables more detailed characterization of plaque composition than CTA, with identification of vulnerable plaque features such as intraplaque hemorrhage, lipid-rich necrotic core, and thinned or disrupted fibrous cap. [20][21][22] A study 23 using high-resolution MRI to examine nonstenotic carotid plaque in a smaller series of patients with cryptogenic stroke found high-risk imaging features indicative of type VI plaque (American Heart Association 24 ) in 38% (12/32) of carotid arteries ipsilateral to ischemic stroke, and no type VI plaque on the contralateral side. The absence of high-risk plaque on the contralateral side differs from our study, which found bilateral plaque $3 mm in 15% of patients with ESUS, and bilateral plaque $4 mm in 5% of patients.…”

“…However, the difference could also reflect the larger sample size of our study. Despite the evidence that high-resolution plaque MRI features predict recurrent stroke, 18,22 widespread clinical adoption has been slow. This partly reflects a lack of randomized controlled trials that incorporate plaque imaging, and partly reflects the need for specialized hardware (carotid surface coil), pulse sequences, and interpretive expertise that are not yet widely available, although improving with time.…”

Movable Thrombi Diagnosed Using Ultrasonography in Non-Significant Carotid Stenosis

“…4 HRMRI showed an intraplaque hemorrhage with a surface ulcer, which supported the identification of the mobile lesion as a ruptured plaque. 5 The term ESUS was first used to define those who potentially have a cryptogenic cause of the cardioembolic source and benefit from anticoagulation. Recently, new oral anticoagulant (NOAC) trials in ESUS patients have failed due to the heterogeneity of ESUS, 6 especially in atherothrombotic infarction ESUS patients who may benefit from antiplatelet agents, which may have led to the failure of NOAC trials.…”