Circulation: In vivo 3T MRI may identify plaques prone to sudden disruption
In vivo 3T MRI can detect features of vulnerable plaques in an animal model of controlled atherothrombosis and MRI may be used as a noninvasive modality for the identification of plaques that are prone to disruption, according to a study published in the May issue of Circulation: Cardiovascular Imaging.
Lead author James A. Hamilton, PhD, professor of biophysics and physiology, and colleagues from Boston University School of Medicine explained that the ability to identify atherosclerotic plaques with a high risk for sudden disruption before stroke or myocardial infarction would be helpful to physicians. Their study sought to test whether in vivo MRI can distinguish between plaques that disrupt after pharmacological triggering (vulnerable) and those that do not (stable).
According to the researchers, two pharmacological triggerings of atherothrombosis were completed in the rabbits after the first round of MRI scanning, followed by a second round of MRI 48 hours post-triggering.
Atherosclerosis was identified by the pretriggered images in all rabbits, and thrombosis was identified in nine of 17, or 53 percent, of the rabbits by the post-trigger MRI results, said the authors.
Hamilton and his colleagues wrote that after the animals were euthanized, 95 plaques were analyzed. Twenty-eight of the rabbits presented with thrombi (vulnerable) and 67, or 70.5 percent, did not (stable). Pretriggered MRI revealed comparable stenosis in stable and vulnerable plaques, but vulnerable plaques where found to have a larger plaque area when compared with stable plaques.
In addition, vulnerable plaques exhibited positive remodeling 67.8 percent of the time, compared to the 22.3 percent in which the plaque is hidden within the vessel wall instead of occluding the lumen. Enhanced gadolinium uptake, associated with histological findings of inflammation, tissue necrosis and the proliferation of blood vessels in tissue not normally containing them was determined as having the ability to predict dangerous plaque.
Among several limitations of their research, the authors noted that the rabbit model is the absence of plaque calcification and intraplaque hemorrhage, and pharmacologically triggered plaque disruption in rabbits may not reflect spontaneous plaque rupture in humans.
While the study yielded “promising results for application to human disease,” Hamilton noted that clinical practice should not change based on one test for vulnerable plaque, whether it is with MRI or any other imaging modality. “Rather, a combination of tests should be used to provide greater confidence when choosing and/or monitoring therapy,” he said.
Lead author James A. Hamilton, PhD, professor of biophysics and physiology, and colleagues from Boston University School of Medicine explained that the ability to identify atherosclerotic plaques with a high risk for sudden disruption before stroke or myocardial infarction would be helpful to physicians. Their study sought to test whether in vivo MRI can distinguish between plaques that disrupt after pharmacological triggering (vulnerable) and those that do not (stable).
According to the researchers, two pharmacological triggerings of atherothrombosis were completed in the rabbits after the first round of MRI scanning, followed by a second round of MRI 48 hours post-triggering.
Atherosclerosis was identified by the pretriggered images in all rabbits, and thrombosis was identified in nine of 17, or 53 percent, of the rabbits by the post-trigger MRI results, said the authors.
Hamilton and his colleagues wrote that after the animals were euthanized, 95 plaques were analyzed. Twenty-eight of the rabbits presented with thrombi (vulnerable) and 67, or 70.5 percent, did not (stable). Pretriggered MRI revealed comparable stenosis in stable and vulnerable plaques, but vulnerable plaques where found to have a larger plaque area when compared with stable plaques.
In addition, vulnerable plaques exhibited positive remodeling 67.8 percent of the time, compared to the 22.3 percent in which the plaque is hidden within the vessel wall instead of occluding the lumen. Enhanced gadolinium uptake, associated with histological findings of inflammation, tissue necrosis and the proliferation of blood vessels in tissue not normally containing them was determined as having the ability to predict dangerous plaque.
Among several limitations of their research, the authors noted that the rabbit model is the absence of plaque calcification and intraplaque hemorrhage, and pharmacologically triggered plaque disruption in rabbits may not reflect spontaneous plaque rupture in humans.
While the study yielded “promising results for application to human disease,” Hamilton noted that clinical practice should not change based on one test for vulnerable plaque, whether it is with MRI or any other imaging modality. “Rather, a combination of tests should be used to provide greater confidence when choosing and/or monitoring therapy,” he said.