Report from NASCI: Coronary CTA moves field closer to individualized medicine

October 18, 2007

Researchers using coronary CT angiography have replicated ex vivo and intravascular ultrasound studies that have characterized plaque into its various components and shown a predisposition for plaque to form in low shear stress areas.

Researchers using coronary CT angiography have replicated ex vivo and intravascular ultrasound studies that have characterized plaque into its various components and shown a predisposition for plaque to form in low shear stress areas.

The hope is that coronary CTA may one day lend itself to individualized care, said coauthor Dr. Pal Suranyi, a first-year resident at the Medical University of South Carolina in Charleston.

"In the future, cardiac CT may assess total plaque burden, which includes calcified and noncalcified plaques. Those with a certain threshold of noncalcified plaque, which are more likely to rupture and cause acute coronary events, can be treated more aggressively," Suranyi said.

Understanding plaque composition and distribution is important because eccentric and long lesions are more likely to predict a worse outcome than concentric lesions. Additionally, plaque vulnerability seems to be related not to the presence of calcium itself, but rather to the presence of a lipid core and the thickness of the fibrous cap, according to Suranyi, who reported the study at the 2007 annual meeting of the North American Society for Cardiac Imaging.

"CTA is not simply a lumenogram. We can look at calcified plaques and also at the vessel wall, where, based on Hounsfield units, we can differentiate lipid-rich regions and fibrous regions and differentiate mixed, calcified, and noncalcified plaques," he said.

Led by Dr. Benedetta Enrico, a radiologist from Policlinico Universitario A. Gemelli in Rome, researchers at MUSC retrospectively analyzed the coronary CTA data sets of 73 patients.

Of the 382 plaques examined, the majority were either mixed (72%) or purely noncalcified (3%), while the purely calcified plaques were a minority (25%).

"If we only look at calcium, we are missing a huge part of the picture," Suranyi said.

The most common type of plaque was eccentric (80%), while a significant majority (55%) was located on the myocardial side, a place of low shear stress. Twenty-eight percent were epicardial, 17% lateral.

Nearly half of all noncalcified and mixed plaques (45%) were myocardial, whereas only 21% were epicardial, 14% lateral. The finding was significant. More than half (51%) of plaques involved bifurcations. The most frequent (40%) pattern was one that started before and extended beyond the bifurcation but spared the side branch.

Atherosclerosis is commonly thought of as a systemic disease, creating the false impression that plaque is evenly distributed throughout the coronary tree, Suranyi said. But there must be local factors at work that contribute to a majority of plaques being distributed to low shear stress areas of the arteries.

The clinical significance of this finding is unknown. Suranyi and colleagues are currently following up patients with phone calls and record reviews. When and if they find patients who have had chest pain or cardiac events, they will note their plaque burden. With enough data, they might be able to draw some conclusions as to which plaque location and composition is more likely to rupture and in what time frame it will burst.

In another study, investigators from the University of Washington, Seattle, examined 44 carotid endarterectomy specimens (600 segments) to better understand the distribution of surface disruptions, which have a primary role in the occurrence of transient ischemic attack or stroke.

To exclude processing artifacts, only disruptions with the associated features of inflammatory infiltrate, thrombus, calcifications, or exposed necrotic core were included, according to lead author Chun Yuan, Ph.D., a professor in the departments of radiology, electrical engineering, and bioengineering.

Of the 44 specimens, disruptions were present in 33 (75%). The prevalence of disruptions in the common carotid and internal carotid arteries was 58.5% (24 of 41) and 53.4% (23 of 43), respectively.

Disruptions in quadrant 1 occurred in 8.3% and 17.4% of disrupted common carotid artery and internal carotid artery lesions, respectively, while disruptions in each of the other quadrants occurred in more than 40% and 30%. Of the 506 sections proximal to the point of maximum stenosis, 31% were disrupted, in contrast to only 7.4% of the distal locations. Disruptions were more common in moderately stenotic sections.

"While carotid plaque surface disruptions are distributed evenly among the common and internal carotid arteries, locations proximal to the point of maximal stenosis and quadrants remote from the flow divider appear to have an increased vulnerability," Yuan said.

Again, this study confirms findings that plaque tends to develop in low shear stress areas. The distribution of plaque is not uniform throughout the vessel, which suggests that a localized hemodynamic factor must be contributing to the development of the plaque or its rupture at a certain point.

Yuan suggested that these specific arterial sites be targeted during high-risk plaque assessment with MRI.

For more from the Diagnostic Imaging archives:

Coronary CT angiography saves lives and money: 20,000-plus cases prove it

Vessel imagers focus on plaque characterization

Coronary CT angiography finally finds itself an affordable home

Heavily calcified carotid plaque reduces stroke risk