The progression of the lesions of atherosclerosis and changes of their structure can stay clinically silent for decades. Magnetic resonance imaging (MRI) of atherosclerotic lesions has been performed to develop noninvasive method to monitor progression of the disease. Skinner et al. showed MRI could detect changes of the rabbit atherosclerotic lesions, such as necrotic core and fibrous cap in the aorta
in vivo. Yuan et al. used fat suppression technique to show the outer boundary of the aorta in the same rabbit model and Rhim et al. reported the MR features of normal artery layers and atherosclerotic lesions of human autopsy cases
in vitro. In this study, the usefulness of MRI for monitoring changes after angioplasty of pre-existing lesions was tested in rabbits with basal lesions similar to those observed in humans.
A combination of Fogarty balloon injury (at 1 week) and a mildly hypercholesterolemic diet (0.2% cholesterol, 5% peanut oil) was used in 16 New Zealand white rabbits to promote the rapid formation of atherosclerotic lesions. After 5 months on the diet, balloon angioplasty was performed on these lesions with a Gruntzig catheter in the iliac artery and abdominal aorta. MRI was used to monitor the initial lesion formation after 3 and 5 months on the diet, and 2 days, 2 weeks, and 1 and 2 months after angioplasty. The MRI images were compared to angiograms just before the angioplasty and histology sections after sacrifice and perfusion fixation of the rabbits.
The combination of early Fogarty injury and mildly hypercholesterolemic diet induced fibroproliferative lesions similar to type Vb lesions of atherosclerosis seen in humans. Angioplasty induced deep dissections in the majority of the animals at the shoulders of lesions. These dissections often extended into the media. The cellular, proliferative response postangioplasty was localized and limited to sites of dissection. Correlation between angiographic and MRI measurements of lumen diameter was good (
r=0.924). A significant increase in arterial wall area was observed postangioplasty at sites of dissection without any loss of lumen. In contrast, proximal and distal to the sites of injury, there was no change in wall area but a transient reduction in lumen area. MRI and MR angiogram could visualize major dissections after angioplasty. MRI could visualize even small linear dissections, which could hardly be detected by MR angiogram.
Comparison of MRI results with histology confirmed that changes in the wall and lumen postangioplasty, including small linear dissections in the lesions and arterial remodeling, are detectable by MRI.
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