International Stroke Conference
February 6–8, 2019

Richard Jackson, MD

I’m writing to you from ISC reporting on an extremely well-planned lecture series on symptomatic carotid artery identification by imaging. I’ve always thought this topic extremely vague as the imaging technology progressed, the medical treatment progressed, but the evaluation and treatment remained surgical with guidelines from the 1990s and most of the research spread across multiple sub-specialties. This same sentiment was echoed today in each mini-series lecture. There’s no easy way to summarize each mini lecture except to keep it in its original format and hit the relevant highlights, which are numerous to say the least.

First Lecture: “Ultrasound Imaging of Carotid Wall and Plaque” by J David Spence
His focus is clearly the identification of vulnerable plaques by ultrasound, and he was a proponent of upcoming volumetric plaque morphology assessment. He quotes the prevalence of asymptomatic carotid stenosis in the >60 year old population at 10% and identifies vulnerable plaques using TCD with emboli detection and plaque characteristics as echo-lucency, hemorrhage, and plaque ulcerations. Of interest was a paper he showed in which TMAO and lecithins produced by intestinal flora worsened carotid stenosis. As GFR decreased, including with age, the metabolites increased, possibly explaining the age relationship to carotid stenosis. Also of interest were the timelines in which carotid stenosis responded to medication. He presented his own carotid plaque and showed a transition from hypoechoic to hyperechoic in 3 months with atorvastatin, and then presented a paper in which ezetimibe doubled the effectiveness of statin therapy.

Second Lecture: “CT and MR Imaging of Carotid Wall and Plaque” by Kevin DeMarco
On CTA, soft plaques have focal hypodensity compared to the adjacent SCM muscle density.
MRI is the preferred modality of choice. On MRA, the necrotic core is dark on T1 and T2, dark on MPRAGE, and bright on TOF. Hemorrhage and the fibrous cap can also be evaluated.
A Large lipid rich core has an HR of 3 for stroke.
A thin ruptured cap has an HR of 6.

Third Lecture: “Imaging of Plaque Inflammation and Neovascularization” by Eline Kooi
Inflammation induces wall thickening and can be imaged by FDG-PET.
A subset of cryptogenic stroke patients were found to have plaque inflammation in non-stenotic lesions on PET.
Statin treatment decreased plaque neovascularization on PET.
Microvasculature and neovascularization can be visualized by contrast ultrasound.

Fourth Lecture: “Low Stenosis and High Risk / High Stenosis and Low Risk” by Ye Qiao
Luminal narrowing starts at a plaque burden around 60%. Remodeling of the carotid wall can be seen on MRI. Even in Low Stenosis high risk morphology such as fibrous cap and hemorrhagic are risk factors for stroke in low grade stenosis.
Calcification is a feature of low risk high grade stenosis unless it is in the fibrous cap, which indicates a high risk morphology as opposed to a deeper location.

Fifth Lecture: “Imaging of Plaque Regression and Progression: Impact of Drug Therapies” by Kevin DeMarco
In a 2016 Atherosclerosis paper, plaque regression was 15% at 12 months on statin therapy.
In a JACC Cardiovascular Imaging paper from 2011, statin depletes the lipid core first and then the volume decreases over the following 3 years.