Possibilities of transesophageal MRI for assessment of aortic disease: a review.

The thoracic aortic wall is a common site of atherosclerotic plaque in humans. Tools for serial, non-invasive assessment of these plaques are of value for addressing gaps in our basic understanding of the biology of plaque rupture and its relationship to atherosclerotic disease progression as well as for monitoring response to anti-atherosclerotic interventions in therapeutic clinical trials. Common approaches to assessment of the wall of the thoracic aorta in vivo are limited. Here we discuss some of the challenges and limitations encountered by conventional techniques and review a novel approach, transesophageal MRI (TEMRI). Initial experiences in applying the TEMRI approach to assessment of aortic morphology and pathology are discussed.

Transesophageal magnetic resonance imaging of the aortic arch and descending thoracic aorta in patients with aortic atherosclerosis.

OBJECTIVES: We sought to determine the feasibility and potential of transesophageal magnetic resonance imaging (TEMRI) for quantifying atherosclerotic plaque burden in the aortic arch and descending thoracic aorta in comparison with transesophageal echocardiography (TEE). BACKGROUND: Improved morphologic assessment of atherosclerotic plaque features in vivo is of interest because of the potential for improved understanding of the pathophysiology of plaque vulnerability to rupture and progression to clinical events. Magnetic resonance imaging (MRI) is well suited for atherosclerotic plaque imaging. Performing MRI using a radio frequency (RF) receiver probe placed near the region of interest improves the signal-to-noise ratio (SNR). METHODS: High-resolution images of the thoracic aortic wall were obtained by TEMRI in 22 subjects (8 normals, 14 with aortic atherosclerosis). In nine subjects, we compared aortic wall thickness and circumferential extent of atherosclerotic plaque measured by TEMRI versus TEE using a Bland-Altman analysis. Additional studies were performed in a human cadaver with pathology as an independent gold standard for assessment of atherosclerosis. RESULTS: In clinical and experimental studies, we found similar measurements for aortic plaque thickness but a relative underestimation of circumferential extent of atherosclerosis by TEE (p = 0.001), due in large part to the lower SNR in the near field. CONCLUSIONS: Using TEMRI allows for quantitative assessment of thoracic aortic atherosclerotic plaque burden. This technique provides good SNR in the near field, which makes it a promising approach for detailed characterization of aortic plaque burden.

Real-time projection MR angiography: feasibility study.

Intraarterial injections of small doses of gadopentetate dimeglumine were combined with a fast spoiled-gradient-echo magnetic resonance (MR) sequence to obtain real-time projection angiographic images of the rabbit aorta and canine coronary arteries. Arterial filling and washout, as well as venous and perfusion phases, were clearly displayed, demonstrating that arterial fluoroscopy in which an MR technique is used is feasible.

Transesophageal magnetic resonance imaging.

The purpose of this study was to develop a non-invasive method of imaging the thoracic aorta that would provide both morphological detail within the aortic wall and information about regional aortic wall motion. An esophageal probe is described that allows transesophageal MR imaging (TEMRI) of the thoracic aorta and has several potential advantages over the competing non-vasculoinvasive techniques of transesophageal echocardiography (TEE) or standard MRI. The probe consists of a loopless antenna housed inside a modified Levin gastric tube, with external matching and tuning circuitry. Using this probe, the thoracic aorta has been imaged in longitudinal and cross-sectional views. Details of the aortic wall were readily seen. Tissue tagging for measurement of focal stress/strain relationships was demonstrated to be feasible. TEMRI avoids the risks inherent in intravascular MRI yet provides comparable image quality. Potential applications of the device are discussed.

Enhanced uptake and impaired intracellular metabolism of low density lipoprotein complexed with anti-low density lipoprotein antibodies.

We have previously shown that incubation of human macrophages with antigen-antibody complexes prepared with native human low density lipoprotein (LDL) and rabbit anti-LDL antibodies (LDL-ICs) results in an increased intracellular accumulation of cholesteryl esters (CEs) and induces a marked increase in the number of LDL receptors. To determine whether the increased CE accumulation in these cells occurred during incubation of the cells with LDL-ICs or whether it was secondary to the uptake of LDL by overexpressed LDL receptors, we incubated human macrophages with LDL-ICs for 22 hours, followed by incubation with native LDL for another 20 hours. We found that about 90% of the accumulated CEs could be accounted for by the first incubation with LDL-ICs. We then proceeded to show that the CEs accumulated during incubation of cells with LDL-ICs was secondary to enhanced uptake and impaired degradation of the LDL complexed with immunoglobulin G (IgG) (LDL-IC), which led to a marked intracellular accumulation of undergraded LDL (levels 199-fold higher than those obtained when the cells were incubated with the same concentration of native LDL not complexed with IgG). We have also shown that not all CEs accumulated in these cells were derived from accumulation of undegraded LDL and that some of them were derived from the reesterification of free cholesterol released during hydrolysis of LDL. LDL-ICs promoted increased CE accumulation and foam cell formation at concentrations as low as 25 micrograms/ml. To determine which receptors were involved in the uptake of LDL-ICs, we performed experiments in which the uptake of LDL-ICs was competitively inhibited with heat-aggregated gamma globulin, native LDL, beta-very low density lipoprotein, or acetylated LDL. Our results demonstrated that LDL-IC uptake was most effectively inhibited by heat-aggregated gamma globulin, partially inhibited by native LDL or by a monoclonal antibody to the LDL receptor, and not inhibited by acetylated LDL or beta-very low density lipoprotein. Thus, we conclude that the majority of LDL-ICs are taken up through Fc gamma receptors. Finally, we investigated whether the increase in LDL receptor expression was dependent on the receptor pathway used by the LDL-ICs, and we were able to demonstrate that when macrophages were incubated with LDL-ICs prepared with F(ab')2 fragments of the anti-LDL antibody, LDL receptor expression was not enhanced. Therefore, we postulate that the uptake of LDL-ICs through Fc gamma receptors results in an uncoupling of the normal regulation of the LDL receptor expression.