April 11, 2013 — Researchers from Boston University School of Medicine (BUSM) have shown that using magnetic resonance imaging (MRI) to measure blood flow over atherosclerotic plaques could help identify plaques at risk for thrombosis. The findings, which appear in the March issue of Circulation Cardiovascular Imaging, offer a non-invasive application in the diagnosis and treatment of patients with atherosclerosis.
Atherosclerosis is a chronic disease of the human vascular system associated with lipid accumulation and inflammation. It can remain silent and undetected for many years but can cause acute cardiovascular events such as stroke or heart attack. This often occurs when a high-risk, dangerous atherosclerotic plaque disrupts at the vessel surface facing the blood, followed by partial or complete blockage of blood flow through the lumen by a thrombus. An unmet challenge of diagnostic medicine is to find such plaques before disruption occurs in order to prevent these occurrences.
While most studies have focused on the plaque within the vessel wall, the flow of blood in the vessel (hemodynamics) also is known to be important in the progression and disruption of plaques.
In this study the researchers found that the measurement of endothelial sheer stress (ESS), which is the indirect stress from the friction of blood flow over the vascular endothelium surface, can identify plaques in the highest risk category. After performing a non-invasive MRI examination of the aorta in a preclinical model with both stable and unstable plaques, a pharmacological “trigger” was used to induce plaque disruption. Low ESS was associated with plaques that disrupted and had other “high-risk” features, such as positive remodeling, which is an outward expansion of the vessel wall that “hides” the plaque from detection by many conventional methods.
These results are consistent with previous studies that examined coronary arteries of other experimental models using invasive intravascular ultrasound method to measure features of vulnerability but without an endpoint of plaque disruption, which is the outcome of the highest risk plaques.
For more information: www.bumc.bu.edu