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DOI: 10.1148/radiol.2352040340
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(Radiology 2005;235:617-622.)
© RSNA, 2005

Technical Developments

Human Peripheral Arteries: Feasibility of Transvenous Intravascular MR Imaging of the Arterial Wall1

Lawrence V. Hofmann, MD, Robert P. Liddell, MD, John Eng, MD, Bruce A. Wasserman, MD, Aravind Arepally, MD, David S. Lee, MD and David A. Bluemke, MD, PhD

1 From the Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins Hospital, Blalock 545, 600 N Wolfe St, Baltimore, MD 21287. Received February 20, 2004; revision requested April 29; revision received July 22; accepted August 19. Address correspondence to L.V.H. (e-mail: lhofmann@jhmi.edu).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 Materials and Methods
Results
 Discussion
 REFERENCES
 
Feasibility of in vivo transvenous intravascular magnetic resonance (MR) imaging of the human arterial wall was determined. All subjects provided written informed consent, and institutional review board approved the study. Six arteries in six patients were imaged with a guidewire placed in the iliac vein (n = 5) or left renal vein (n = 1). Pre- and postcontrast T1-weighted and T2-weighted transvenous MR imaging were performed. An atherosclerotic plaque with a fibrous cap was identified on 27 (42%) of 64 images of veins without stents; intimal hyperplasia in a renal artery with a stent was identified on 12 images. Contrast-to-noise ratios (CNRs) on arterial wall postcontrast T1-weighted images were superior to those on images obtained with other sequences (P < .001), and the postcontrast images demonstrated the greatest number of plaques with a low–signal intensity core and fibrous cap. Preliminary results show that transvenous MR imaging is feasible for high-spatial-resolution imaging of the arterial wall and atherosclerotic plaque. Postcontrast T1-weighted imaging affords greatest CNR for the arterial wall.

© RSNA, 2005


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
Materials and Methods
Results
 Discussion
 REFERENCES
 
A primary goal of atherosclerosis imaging research during the past 5–10 years has been to prospectively identify the unstable or vulnerable plaque, thereby providing better guidance for local or systemic treatment (1). The hypothesis about vulnerable plaque states that rupture of the thin fibrous cap of the plaque, with exposure of the thrombogenic lipid core, precipitates a cascade of platelet aggregation and arterial thrombosis and/or embolism and leads to acute myocardial infarction or stroke (2,3). Novel imaging methods have been developed to better visualize the fibrous cap, measure its thickness, and characterize the composition of the underlying plaque core. Magnetic resonance (MR) imaging, with its superior soft-tissue resolution, appears well suited for imaging atherosclerotic plaque. Investigators have successfully acquired high-spatial-resolution images of carotid artery plaque with surface coils because of the superficial location of the plaque (4–6).

Imaging of vessels within the abdomen and pelvis presents a marked challenge. The relatively large distance between the artery of interest and the surface coil, as well as increased motion artifact, make plaque characterization exceedingly difficult. Efforts to overcome these limitations have led to the development of intravascular MR imaging. Animal studies have been conducted with large (5–8-F) intraarterial MR receiver coils (7–10). Although these studies produced high-spatial-resolution images of the arterial wall, the large device size and the need to gain arterial access increased the risk of complications. One alternative is a transvenous approach to arterial wall imaging. Risks of arterial dissection, embolism, thrombosis, and hematoma formation are markedly reduced with venous access.

We hypothesized that in certain areas of the body, the close proximity of the vein to the artery would be sufficient to obtain high-spatial-resolution images of the arterial wall. This technique, which we term transvenous MR imaging, should substantially reduce the risk of complications and pulsatile motion artifacts associated with intraarterial placement of an intravascular MR receiver guidewire. Transvenous MR imaging recently has been demonstrated in vivo in a large animal model (11). To date, however, there are no MEDLINE-referenced reports of in vivo intravascular MR imaging in humans. Thus, the primary goal of this study was to determine the feasibility of in vivo transvenous MR imaging of the arterial wall in humans.


   Materials and Methods
TOP
 ABSTRACT
 INTRODUCTION
 Materials and Methods
Results
 Discussion
 REFERENCES
 
Study Population
This study was funded by Surgi-Vision (Gaithersburg, Md), but the authors had control of the data and the information submitted for publication. One author (D.A.B.) was serving as a consultant for the company at the time of the study, but the other authors had control of the data, as well as of the information submitted for publication. After institutional review board approval, subjects were recruited from those scheduled for interventional angiography in the radiology department. Six consecutive patients who met the inclusion criteria during the period from October 2001 to March 2002 (five men, one woman; mean age, 65 years ± 11.2 [standard deviation]) participated in the study (Table 1). All subjects gave written informed consent. They had been previously scheduled for clinically indicated angiography (aortography and bilateral lower extremity angiography for claudication [n = 3], aortography and pelvic angiography for aortic stent-graft evaluation [n = 1], lower extremity angiography for an arteriovenous malformation [n = 1], or renal artery angiography for possible in-stent restenosis [n = 1]). Patients were excluded from the study if they were younger than 18 years old, had severe claustrophobia, or had a known contraindication to MR imaging.


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  		TABLE 1. Patient Demographics

 
Guidewire Characteristics
The guidewire (MicroClear Intravascular Guidewire; Surgi-Vision) used in our study has been previously described (9), was approved by the U.S. Food and Drug Administration, and was commercially available at the time of the study. Briefly, the device is a 75-cm-long 0.030-inch-diameter loopless antenna that consists of a soft conducting wire that has an inner conductor made from a 50-{Omega} 0.6-mm coaxial cable with a polyester jacket. The proximal end of the coaxial cable was connected through a matching tuning-decoupling circuit to the MR imaging unit.

Guidewire Placement
With ultrasonographic guidance, a micropuncture kit (Micropuncture Introducer Set; Cook, Bloomington, Ind) was used to place a 5-F sheath (Avanti; Cordis, Miami, Fla) in the common femoral vein. With fluoroscopic guidance, the guidewire was positioned within the vein (common iliac vein [n = 5] or left renal vein [n = 1]) closest to the artery of interest with a 5-F reversed-curve catheter (Sos3; Angiodynamics, Queensbury, NY). Then the catheter and guidewire were secured to the patient’s leg with a clear plastic adhesive (OpSite; Smith & Nephew, Kingston upon Hull, England). One author (L.V.H.) was responsible for the sheath and the guidewire placement in all subjects. Conscious sedation was induced with midazolam (Versed; Roche Pharmaceuticals, Nutley, NJ) and fentanyl citrate (Fentanyl; Baxter Healthcare, Round Lake, Ill), and vital signs were monitored throughout the procedure according to institutional protocol. The patient was then transported to the MR imaging suite.

MR Imaging
Electrocardiographically gated double inversion-recovery fast spin-echo black-blood MR images were obtained with a 1.5-T MR imaging system (CV/i; GE Medical Systems, Waukesha, Wis) by using the guidewire with and without coupling to a cardiac phased-array coil (GE Medical Systems) with two anterior and two posterior elements. One of the four elements was electrically disconnected, and the guidewire was used as the fourth channel of the array. With the body coil, an initial fast multiplanar spoiled gradient-echo sequence with a 40-cm field of view was performed to obtain a scout image. Then, transverse and coronal gradient-echo sequences were performed with the internal and surface coils to determine the course of the artery of interest. Four to five transverse vessel locations (images obtained perpendicular to the long axis of the vessel) per patient were interrogated by using transvenous MR imaging with fat-suppressed chemical shift double inversion-recovery fast spin-echo T1-weighted (repetition time, one R-R interval; echo time, 12 msec; echo train length, 16–24; field of view, 8–10 cm; number of signals acquired, six; matrix, 256 x 160; and section thickness, 3 mm) and T2-weighted (repetition time, two R-R intervals; echo time, 50 msec; echo train length, 16–24; field of view, 8–10 cm; number of signals acquired, six; matrix, 256 x 160; and section thickness, 3 mm) pulse sequences. Gadodiamide (Omniscan; Amersham, Princeton, NJ) was then intravenously administered (0.2 mmol/kg). After a 5-minute delay, T1-weighted MR imaging was repeated. Inversion times (median inversion time, 125 msec; range, 100–150 msec) were adjusted visually to suppress signal from the vessel lumen. Imaging time was 50–60 seconds for each image. After MR imaging, the guidewire was removed, and the patient was transported back to the fluoroscopy suite for conventional angiography and venous sheath removal. There were no procedure-related complications.

Image Analysis
Digital Imaging and Communications in Medicine images were transferred to a personal computer (Dimension; Dell, Austin, Tex) equipped with software (eFilm Workstation, version 1.5.3; eFilm Medical, Toronto, Ontario, Canada). Cross-sectional images were matched according to location for the three pulse sequences.

For each cross-sectional image, the signal intensity and the standard deviation, as computed with the software for the given region of interest, of the arterial wall were measured at four corresponding locations. (This was performed by one author [R.P.L.], who had 1 year of vascular MR imaging experience after intensive instruction and training with another author [L.V.H.], who had 5 years of vascular MR imaging experience.) No signal intensity correction algorithms were used. Locations were determined by drawing a line from the guidewire through the artery of interest so that the artery was bisected. A second line was then drawn through the artery perpendicular to the first, so that the artery was divided into quarters. As a result, four points were produced where the lines intersected the arterial wall. These points were labeled similar to the positions on a clock face, with the 12-o’clock position being the point closest to the guidewire and the 6-o’clock position being the point farthest from the guidewire. The 3-o’clock and 9-o’clock positions were also labeled (Fig 1). Regions of interest (approximately 0.025 cm2) were drawn within the arterial wall at these four points. The background noise was measured in the adjacent periarterial tissue. The distance from the guidewire to each signal intensity point was measured and recorded. The contrast-to-noise ratio (CNR) was determined for each point location within the vessel wall with the following equation: CNR = (SIaw – SIadj)/SDbn, where SIaw is signal intensity of the arterial wall at a specific point (ie, 12-o’clock position), SIadj is signal intensity of adjacent perivascular tissue, and SDbn is the standard deviation of the background noise.



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  		Figure 1. Patient 2. Transverse double inversion-recovery fast spin-echo T2-weighted MR image (1600/50) of left common iliac artery and vein in 63-year-old black man shows signal intensity measurement of arterial wall with transvenous MR imaging at four consistent locations, similar to points on the face of a clock, and demonstrates diffuse arterial wall thickening. To determine locations, a line was drawn to connect the following three points: a point at the guidewire (arrowhead), a point on the arterial wall closest (12) to the guidewire, and a point on the arterial wall farthest (6) from the guidewire. A second line was drawn perpendicular to the first line; the two points where it intersected the arterial wall are labeled 3 and 9. Signal intensity and standard deviations were measured at each numbered location.

 
Two independent observers (L.V.H. and D.A.B., who had 5 and 10 years of vascular MR imaging experience, respectively) prospectively identified atherosclerotic plaques with a low–signal intensity core (American Heart Association [AHA] type IV, V, VI, VII, and VIII lesions) (3,12,13). If there was disagreement about findings on an image, a third observer (B.A.W., who had 8 years of vascular MR imaging experience) adjudicated. Briefly, the AHA classification of atherosclerotic plaque was modified for MR imaging classification. AHA type IV and V plaques have similar appearances at MR imaging and were defined as plaques with a lipid or necrotic core, surrounded by fibrous tissue with possible calcification; AHA type VI plaques were defined as complex plaques with a possible surface defect, hemorrhage, or thrombus; AHA type VII plaques were defined as calcified plaques; and AHA type VIII plaques were defined as fibrotic plaques without a lipid core and with possible small calcifications.

We did not attempt to substratify plaque appearance, but rather we grouped all plaque with a low–signal intensity core into a single category. To determine the CNR of the fibrous cap, signal intensity was measured by one author (R.P.L.) who drew regions of interest (approximately 0.0125 cm2) within the midpoint of the fibrous cap, the adjacent low–signal intensity core, and the adjacent lumen. The distance from the guidewire to each point was recorded. CNR between the fibrous cap and lipid core, as well as between the fibrous cap and lumen, was calculated with the following equation: CNR = (SIfc – SIadj)/SDbn, where SIfc is signal intensity of the fibrous cap, SIadj is signal intensity of either the lipid core or lumen, and SDbn is the standard deviation of the background noise.

To compare results among patients, absolute values for signal intensity were normalized by using the radial distance from the guidewire (9) with the following equation: SIcorr = dr · SIobs, where SIcorr is the corrected signal intensity, dr is the radial distance from the guidewire to the region of interest, as the signal decays at 1/dr, and SIobs is the observed signal intensity.

Statistical Analysis
Because we found that the data were not normally distributed, we employed nonparametric statistical analysis, with medians rather than means as the summary statistic. Medians were calculated for each pulse sequence, both with and without correction for distance. The medians were reported with an exact 95% confidence interval that was based on the binomial distribution (14). At each imaging location, the CNRs were compared between each pair of pulse sequences with the sign test (15). The sign test is used to evaluate the equality of matched pairs of observations. With this test, the null hypothesis is that the median of the differences is zero; no other assumptions were made about the distribution of the observations. Interobserver variability for determination of the presence or absence of a fibrous cap was measured with the {kappa} statistic. All statistical calculations were performed with software (Stata, version 7; Stata, College Station, Tex) by one author (J.E.).


   Results
TOP
 ABSTRACT
 INTRODUCTION
 Materials and Methods
Results
Discussion
 REFERENCES
 
In six patients, six vessels (five native atherosclerotic iliac arteries, one left renal artery with intimal hyperplasia with a stent) were imaged with the transvenous MR imaging technique. Three hundred four arterial wall CNR calculations were obtained from 76 images at 26 section locations (mean, 4.3 section locations per patient; range, 4–5). T2-weighted MR images were unavailable at two of the section locations (Table 2). The mean distances from the guidewire to the location of the signal intensity measurements were 1.5 cm ± 0.7 for the arterial wall and 1.0 cm ± 0.3 for the fibrous cap.


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  		TABLE 2. Median CNR of Arterial Wall and Fibrous Cap for Pulse Sequences with and without Distance Correction

 
T1-weighted images of the arterial wall obtained after contrast agent administration demonstrated superior CNR between the wall and adjacent perivascular tissue when they were compared with both T1-weighted images obtained before contrast agent administration (P < .001) and T2-weighted images (P < .001), with and without distance correction. The arterial wall CNRs obtained with T2-weighted and precontrast T1-weighted MR images without distance correction were not significantly different (P > .05). The T2-weighted images, however, were found to have a superior CNR when they were compared with precontrast T1-weighted images (P < .02) with distance correction (Table 2).

Excluding the 12 images of in-stent restenosis in patient 6, an atherosclerotic plaque with a fibrous cap and a low–signal intensity core was identified on 27 (42%) of 64 images without stents (Fig 2). CNR values for the fibrous cap and plaque core obtained from these 27 images demonstrated no significant difference among the three MR imaging sequences, with and without distance correction (P > .05) (Table 2). The {kappa} statistic for interobserver variability was 0.91 (excellent).



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  		Figure 2a. Patient 4. Transverse MR images of right common iliac artery with guidewire (black arrowhead) in right common iliac vein in 56-year-old white man. The guidewire is the only receiver coil used in transvenous MR images. Changes in lumen (white arrow) were observed on each image. (a) Precontrast transvenous fat-saturated double inversion-recovery fast spin-echo T1-weighted MR image (800/12) shows diffuse thickening of arterial wall (black arrow) and only minimal decrease in lumen diameter. (b) Transvenous double inversion-recovery fast spin-echo T2-weighted MR image (1600/50) demonstrates a focal plaque on anterior wall with low-signal- intensity core (white arrowhead, also in c) and thin fibrous cap (black arrow, also in c). With this pulse sequence, the lumen was more narrowed than was observed on precontrast T1-weighted MR image in a. (c) Postcontrast transvenous fat-saturated double inversion-recovery fast spin-echo T1-weighted MR image (800/12) demonstrates circumferential wall enhancement. A focal plaque on the anterior wall with low-signal-intensity core and thin enhancing fibrous cap were seen. Moderate narrowing of lumen is similar to that on T2-weighted image in b. (d) Summation image of all three images obtained with surface coil and same imaging parameters was acquired at same time as c. Common iliac arterial wall was not well visualized, and a faint outline of the arterial lumen was observed. Circumferential wall enhancement of common iliac vein was observed.

 


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  		Figure 2b. Patient 4. Transverse MR images of right common iliac artery with guidewire (black arrowhead) in right common iliac vein in 56-year-old white man. The guidewire is the only receiver coil used in transvenous MR images. Changes in lumen (white arrow) were observed on each image. (a) Precontrast transvenous fat-saturated double inversion-recovery fast spin-echo T1-weighted MR image (800/12) shows diffuse thickening of arterial wall (black arrow) and only minimal decrease in lumen diameter. (b) Transvenous double inversion-recovery fast spin-echo T2-weighted MR image (1600/50) demonstrates a focal plaque on anterior wall with low-signal- intensity core (white arrowhead, also in c) and thin fibrous cap (black arrow, also in c). With this pulse sequence, the lumen was more narrowed than was observed on precontrast T1-weighted MR image in a. (c) Postcontrast transvenous fat-saturated double inversion-recovery fast spin-echo T1-weighted MR image (800/12) demonstrates circumferential wall enhancement. A focal plaque on the anterior wall with low-signal-intensity core and thin enhancing fibrous cap were seen. Moderate narrowing of lumen is similar to that on T2-weighted image in b. (d) Summation image of all three images obtained with surface coil and same imaging parameters was acquired at same time as c. Common iliac arterial wall was not well visualized, and a faint outline of the arterial lumen was observed. Circumferential wall enhancement of common iliac vein was observed.

 


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  		Figure 2c. Patient 4. Transverse MR images of right common iliac artery with guidewire (black arrowhead) in right common iliac vein in 56-year-old white man. The guidewire is the only receiver coil used in transvenous MR images. Changes in lumen (white arrow) were observed on each image. (a) Precontrast transvenous fat-saturated double inversion-recovery fast spin-echo T1-weighted MR image (800/12) shows diffuse thickening of arterial wall (black arrow) and only minimal decrease in lumen diameter. (b) Transvenous double inversion-recovery fast spin-echo T2-weighted MR image (1600/50) demonstrates a focal plaque on anterior wall with low-signal- intensity core (white arrowhead, also in c) and thin fibrous cap (black arrow, also in c). With this pulse sequence, the lumen was more narrowed than was observed on precontrast T1-weighted MR image in a. (c) Postcontrast transvenous fat-saturated double inversion-recovery fast spin-echo T1-weighted MR image (800/12) demonstrates circumferential wall enhancement. A focal plaque on the anterior wall with low-signal-intensity core and thin enhancing fibrous cap were seen. Moderate narrowing of lumen is similar to that on T2-weighted image in b. (d) Summation image of all three images obtained with surface coil and same imaging parameters was acquired at same time as c. Common iliac arterial wall was not well visualized, and a faint outline of the arterial lumen was observed. Circumferential wall enhancement of common iliac vein was observed.

 


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  		Figure 2d. Patient 4. Transverse MR images of right common iliac artery with guidewire (black arrowhead) in right common iliac vein in 56-year-old white man. The guidewire is the only receiver coil used in transvenous MR images. Changes in lumen (white arrow) were observed on each image. (a) Precontrast transvenous fat-saturated double inversion-recovery fast spin-echo T1-weighted MR image (800/12) shows diffuse thickening of arterial wall (black arrow) and only minimal decrease in lumen diameter. (b) Transvenous double inversion-recovery fast spin-echo T2-weighted MR image (1600/50) demonstrates a focal plaque on anterior wall with low-signal- intensity core (white arrowhead, also in c) and thin fibrous cap (black arrow, also in c). With this pulse sequence, the lumen was more narrowed than was observed on precontrast T1-weighted MR image in a. (c) Postcontrast transvenous fat-saturated double inversion-recovery fast spin-echo T1-weighted MR image (800/12) demonstrates circumferential wall enhancement. A focal plaque on the anterior wall with low-signal-intensity core and thin enhancing fibrous cap were seen. Moderate narrowing of lumen is similar to that on T2-weighted image in b. (d) Summation image of all three images obtained with surface coil and same imaging parameters was acquired at same time as c. Common iliac arterial wall was not well visualized, and a faint outline of the arterial lumen was observed. Circumferential wall enhancement of common iliac vein was observed.

 
All patients except patient 6 had diffuse homogeneous wall thickening (AHA type III plaque), which was defined as thickness of greater than 1 mm. The diffuse wall thickening observed on the transvenous MR images in patient 6 was caused by intimal hyperplasia from a platinum stent (Omniflex; Angiodynamics, Queensbury, NY) placed in the left renal artery 7 months previously (Fig 3). The presence of the stent did not affect the signal intensity of the arterial wall; only minimal susceptibility artifact was seen.



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  		Figure 3a. Patient 6. Right renal artery in-stent restenosis in 79-year-old white woman. (a) Posteroanterior spot radiograph of guidewire (thick arrow) placed through a reversed-curve catheter (arrowhead) is within left renal vein. Platinum stent (thin arrow) is in the left renal artery. (b) Posteroanterior selective digital angiogram of left renal artery shows narrowing (arrowheads) of vessel lumen within stent. (c) Precontrast transvenous transverse fat-saturated double inversion-recovery fast spin-echo T1-weighted MR image (800/12) of right renal artery (thick white arrow) demonstrates narrowing of vessel lumen from neointima (small arrowhead). Stent struts (thin white arrow) produce minimal susceptibility artifact. Guidewire (large arrowhead) is in left renal vein (black arrow). (d) Transverse transvenous double inversion-recovery fast spin-echo T2-weighted MR image (1600/50) of right renal artery depicts arterial wall (thick white arrow) and neointima (small arrowhead). Stent struts (thin white arrow) are not easily observed. Guidewire (large arrowhead) is within left renal vein (black arrow).

 


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  		Figure 3b. Patient 6. Right renal artery in-stent restenosis in 79-year-old white woman. (a) Posteroanterior spot radiograph of guidewire (thick arrow) placed through a reversed-curve catheter (arrowhead) is within left renal vein. Platinum stent (thin arrow) is in the left renal artery. (b) Posteroanterior selective digital angiogram of left renal artery shows narrowing (arrowheads) of vessel lumen within stent. (c) Precontrast transvenous transverse fat-saturated double inversion-recovery fast spin-echo T1-weighted MR image (800/12) of right renal artery (thick white arrow) demonstrates narrowing of vessel lumen from neointima (small arrowhead). Stent struts (thin white arrow) produce minimal susceptibility artifact. Guidewire (large arrowhead) is in left renal vein (black arrow). (d) Transverse transvenous double inversion-recovery fast spin-echo T2-weighted MR image (1600/50) of right renal artery depicts arterial wall (thick white arrow) and neointima (small arrowhead). Stent struts (thin white arrow) are not easily observed. Guidewire (large arrowhead) is within left renal vein (black arrow).

 


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  		Figure 3c. Patient 6. Right renal artery in-stent restenosis in 79-year-old white woman. (a) Posteroanterior spot radiograph of guidewire (thick arrow) placed through a reversed-curve catheter (arrowhead) is within left renal vein. Platinum stent (thin arrow) is in the left renal artery. (b) Posteroanterior selective digital angiogram of left renal artery shows narrowing (arrowheads) of vessel lumen within stent. (c) Precontrast transvenous transverse fat-saturated double inversion-recovery fast spin-echo T1-weighted MR image (800/12) of right renal artery (thick white arrow) demonstrates narrowing of vessel lumen from neointima (small arrowhead). Stent struts (thin white arrow) produce minimal susceptibility artifact. Guidewire (large arrowhead) is in left renal vein (black arrow). (d) Transverse transvenous double inversion-recovery fast spin-echo T2-weighted MR image (1600/50) of right renal artery depicts arterial wall (thick white arrow) and neointima (small arrowhead). Stent struts (thin white arrow) are not easily observed. Guidewire (large arrowhead) is within left renal vein (black arrow).

 


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  		Figure 3d. Patient 6. Right renal artery in-stent restenosis in 79-year-old white woman. (a) Posteroanterior spot radiograph of guidewire (thick arrow) placed through a reversed-curve catheter (arrowhead) is within left renal vein. Platinum stent (thin arrow) is in the left renal artery. (b) Posteroanterior selective digital angiogram of left renal artery shows narrowing (arrowheads) of vessel lumen within stent. (c) Precontrast transvenous transverse fat-saturated double inversion-recovery fast spin-echo T1-weighted MR image (800/12) of right renal artery (thick white arrow) demonstrates narrowing of vessel lumen from neointima (small arrowhead). Stent struts (thin white arrow) produce minimal susceptibility artifact. Guidewire (large arrowhead) is in left renal vein (black arrow). (d) Transverse transvenous double inversion-recovery fast spin-echo T2-weighted MR image (1600/50) of right renal artery depicts arterial wall (thick white arrow) and neointima (small arrowhead). Stent struts (thin white arrow) are not easily observed. Guidewire (large arrowhead) is within left renal vein (black arrow).

 
Images obtained with the surface coils alone did not produce sufficient arterial wall signal to allow regions of interest to be drawn. Therefore, the CNRs for these images were not calculated (Fig 2d).


   Discussion
TOP
 ABSTRACT
 INTRODUCTION
 Materials and Methods
Results
 Discussion
REFERENCES
 
In vivo transvenous MR imaging with a 0.030-inch guidewire is a feasible technique for imaging the arterial wall. In this preliminary study, this technique provided high-spatial-resolution imaging for a number of different arterial disease states: diffusely thickened wall (AHA type III plaque), plaques with a central core of low signal intensity and a fibrous cap (AHA types IV–VIII), and in-stent restenosis.

Consistent with the animal model of atherosclerosis (11), the human arterial wall CNR (AHA type III plaque) improved after intravenous gadolinium-based contrast agent administration because of circumferential wall enhancement. The cause of this enhancement is unknown, but it is believed to be associated with the degree of development of the vasa vasorum (16,17). The known role of neovascularization and inflammation in atherogenesis also may offer an explanation (18). Researchers have demonstrated increased plaque vascularity in patients with unstable angina, and inflammation-induced endothelial permeability may augment the movement of contrast material into the extravascular and extracellular compartments (4,19).

As with images with AHA type III plaque, the postcontrast T1-weighted MR images were superior for depiction of complex atherosclerotic plaques (AHA types IV–VIII). Median CNR of the fibrous cap was superior on the postcontrast T1-weighted MR images. Similarly, a greater number of complex plaques were identified by using this sequence. Wasserman et al (4) reported comparable findings in the carotid artery. They described preferential enhancement of fibrocellular tissue, relative to enhancement of other plaque components. The authors likened this observation to the enhancement demonstrated in fibrous tissue found in the myocardium, breast, and postoperative spine.

CNR measurements were sensitive to the guidewire-artery distance because of the inherent properties of the coil (9). After correction for distance, the postcontrast T1-weighted MR images continued to produce the greatest CNR. Distance-corrected T2-weighted images were superior to precontrast T1-weighted MR images. T2-weighted MR images have inherently lower signal than do T1-weighted images, but CNR often is superior with the T2-weighted technique. In practice, improved vessel wall signal after contrast material administration is particularly important for vessels that are farthest from the guidewire in order to have sufficient signal for imaging.

In-stent restenosis has not been effectively imaged with surface coils (20). With transvenous MR imaging of a platinum stent, we were able to directly visualize in-stent restenosis. The use of platinum stents in conjunction with MR imaging deserves further evaluation with both conventional and intravascular MR imaging methods.

The limitations of this study include the small sample size and the different vessels studied, as well as our inability to correlate the MR imaging data with histopathologic findings, as none of our patients required surgery. Investigators in numerous studies, however, have shown a strong correlation between MR imaging findings and histopathologic findings in atherosclerotic plaques (4,5,7,8,12,21–24). These results were used in our study to further modify the classification of plaque into two broad categories (presence or absence of a low–signal intensity core). In our small sample, 42% of iliac artery plaques (AHA types III–VIII) were complex. In comparison, 81% of carotid artery plaques were described as complex (12). Another limitation was that we were unable to adjust for the statistical correlation between observations made within the same patient, and therefore we were unable to employ parametric statistical analysis. This correlation means that each measurement is not completely independent of the others. As a result, our estimated P values may have been too low. We think that the intrapatient correlation, however, was unlikely to have caused underestimation of the P value by orders of magnitude, so that rejection of the null hypothesis could be justified in this study.

There are several limitations of the transvenous MR imaging technique. First, placement of the guidewire itself is invasive. Second, the guidewire must be within a vein in close proximity to the artery of interest because of signal decay (at 1/dr). Therefore, this approach would be feasible only in certain vessels, such as the abdominal aorta, renal artery, and iliac artery. Third, with the current guidewire design, image acquisition is slow, and a 50–60-second acquisition per image is required. Different views, such as coronal and sagittal, would be necessary to screen long vessel segments. Further advances in coil technology would allow shorter imaging times, potentially allowing intraarterial, as well as transvenous, studies to be performed safely.

Despite these limitations, future applications of an intravenous MR imaging technique can be envisioned. Intravascular MR imaging may have a role in guiding and, ultimately, in monitoring local catheter-based or systemic therapy. Yang et al (25) demonstrated the feasibility of using the guidewire to image the delivery of a mixture of a gene and gadopentetate dimeglumine into the vessel wall in experimental animals. By coupling this mixture with a reporter gene, it may be possible to monitor gene expression in the arterial wall (26,27). In addition, efforts to establish the nature of the vulnerable plaque may be aided by intravascular MR imaging technology, particularly in conjunction with surface coils, which would allow both large and small fields of view to be electronically selected.

In conclusion, transvenous MR imaging is feasible and can be used to obtain high-spatial-resolution images of atherosclerotic vessels within the abdomen and pelvis. In this preliminary study, postcontrast T1-weighted MR images produced the best CNR of the arterial wall and plaque components.


   FOOTNOTES
 
Abbreviations: AHA = American Heart Association, CNR = contrast-to-noise ratio

See Materials and Methods for pertinent disclosures.

Author contributions: Guarantors of integrity of entire study, L.V.H., D.A.B.; study concepts, L.V.H., B.A.W., A.A., D.A.B.; study design, L.V.H., J.E., B.A.W., A.A., D.A.B.; literature research, L.V.H., R.P.L., A.A., D.S.L.; clinical studies, L.V.H., D.A.B.; data acquisition, L.V.H., R.P.L., D.S.L., D.A.B.; data analysis/interpretation, all authors; statistical analysis, J.E., A.A.; manuscript preparation, L.V.H., R.P.L., B.A.W., A.A., D.S.L.; manuscript definition of intellectual content, L.V.H., A.A., D.A.B.; manuscript editing, L.V.H., R.P.L., B.A.W., A.A., D.S.L.; manuscript revision/review and final version approval, all authors


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 Materials and Methods
Results
 Discussion
 REFERENCES
 

  1. Dzau VJ, Braun-Dullaeus RC, Sedding DG. Vascular proliferation and atherosclerosis: new perspectives and therapeutic strategies. Nat Med 2002; 8:1249-1256.[CrossRef][Medline]
  2. Falk E. Coronary thrombosis: pathogenesis and clinical manifestations. Am J Cardiol 1991; 68:28B-35B.[CrossRef][Medline]
  3. Stary HC, Chandler AB, Dinsmore RE, et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis: a report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation 1995; 92:1355-1374.[Abstract/Free Full Text]
  4. Wasserman BA, Smith WI, Trout HH, 3rd, Cannon RO, 3rd, Balaban RS, Arai AE. Carotid artery atherosclerosis: in vivo morphologic characterization with gadolinium-enhanced double-oblique MR imaging—initial results. Radiology 2002; 223:566-573.[Abstract/Free Full Text]
  5. Hatsukami TS, Ross R, Polissar NL, Yuan C. Visualization of fibrous cap thickness and rupture in human atherosclerotic carotid plaque in vivo with high-resolution magnetic resonance imaging. Circulation 2000; 102:959-964.[Abstract/Free Full Text]
  6. Hayes CE, Mathis CM, Yuan C. Surface coil phased arrays for high-resolution imaging of the carotid arteries. J Magn Reson Imaging 1996; 6:109-112.[Medline]
  7. Rogers WJ, Prichard JW, Hu YL, et al. Characterization of signal properties in atherosclerotic plaque components by intravascular MRI. Arterioscler Thromb Vasc Biol 2000; 20:1824-1830.[Abstract/Free Full Text]
  8. Zimmermann-Paul GG, Quick HH, Vogt P, von Schulthess GK, Kling D, Debatin JF. High-resolution intravascular magnetic resonance imaging: monitoring of plaque formation in heritable hyperlipidemic rabbits. Circulation 1999; 99:1054-1061.[Abstract/Free Full Text]
  9. Ocali O, Atalar E. Intravascular magnetic resonance imaging using a loopless catheter antenna. Magn Reson Med 1997; 37:112-118.[Medline]
  10. Martin AJ, Henkelman RM. Intravascular MR imaging in a porcine animal model. Magn Reson Med 1994; 32:224-229.[Medline]
  11. Hofmann LV, Liddell RP, Arepally A, Montague B, Yang X, Bluemke DA. In vivo intravascular MR imaging: transvenous technique for arterial wall imaging. J Vasc Interv Radiol 2003; 14:1317-1327.[Medline]
  12. Cai JM, Hatsukami TS, Ferguson MS, Small R, Polissar NL, Yuan C. Classification of human carotid atherosclerotic lesions with in vivo multicontrast magnetic resonance imaging. Circulation 2002; 106:1368-1373.[Abstract/Free Full Text]
  13. Yuan C, Mitsumori LM, Ferguson MS, et al. In vivo accuracy of multispectral magnetic resonance imaging for identifying lipid-rich necrotic cores and intraplaque hemorrhage in advanced human carotid plaques. Circulation 2001; 104:2051-2056.[Abstract/Free Full Text]
  14. Conover W. Practical nonparametric statistics New York, NY: Wiley, 1999.
  15. Snedecor G, Cochran W. Statistical methods Ames, Iowa: Iowa State University Press, 1989.
  16. Sharma S, Taneja K, Gupta AK, Rajani M. Morphologic mural changes in the aorta revealed by CT in patients with nonspecific aortoarteritis (Takayasu’s arteritis). AJR Am J Roentgenol 1996; 167:1321-1325.[Abstract/Free Full Text]
  17. Aoki S, Shirouzu I, Sasaki Y, et al. Enhancement of the intracranial arterial wall at MR imaging: relationship to cerebral atherosclerosis. Radiology 1995; 194:477-481.[Abstract/Free Full Text]
  18. Buffon A, Biasucci LM, Liuzzo G, D’Onofrio G, Crea F, Maseri A. Widespread coronary inflammation in unstable angina. N Engl J Med 2002; 347:5-12.[Abstract/Free Full Text]
  19. Tenaglia AN, Peters KG, Sketch MH, Jr, Annex BH. Neovascularization in atherectomy specimens from patients with unstable angina: implications for pathogenesis of unstable angina. Am Heart J 1998; 135:10-14.[CrossRef][Medline]
  20. Tello R, Thomson KR, Witte D, Becker GJ, Tress BM. Dynamic gadolinium DTPA-enhanced magnetic resonance of intravascular stents. Invest Radiol 1998; 33:411-414.[CrossRef][Medline]
  21. Serfaty JM, Chaabane L, Tabib A, Chevallier JM, Briguet A, Douek PC. Atherosclerotic plaques: classification and characterization with T2-weighted high-spatial-resolution MR imaging—an in vitro study. Radiology 2001; 219:403-410.[Abstract/Free Full Text]
  22. Worthley SG, Helft G, Fuster V, et al. High resolution ex vivo magnetic resonance imaging of in situ coronary and aortic atherosclerotic plaque in a porcine model. Atherosclerosis 2000; 150:321-329.[CrossRef][Medline]
  23. von Ingersleben G, Schmiedl UP, Hatsukami TS, et al. Characterization of atherosclerotic plaques at the carotid bifurcation: correlation of high-resolution MR imaging with histologic analysis—preliminary study. RadioGraphics 1997; 17:1417-1423.[Abstract]
  24. Correia LC, Atalar E, Kelemen MD, et al. Intravascular magnetic resonance imaging of aortic atherosclerotic plaque composition. Arterioscler Thromb Vasc Biol 1997; 17:3626-3632.[Abstract/Free Full Text]
  25. Yang X, Bolster BD, Jr, Kraitchman DL, Atalar E. Intravascular MR-monitored balloon angioplasty: an in vivo feasibility study. J Vasc Interv Radiol 1998; 9:953-959.[Medline]
  26. Weissleder R, Moore A, Mahmood U, et al. In vivo magnetic resonance imaging of transgene expression. Nat Med 2000; 6:351-355.[CrossRef][Medline]
  27. Bogdanov A, Weissleder R. In vivo imaging of gene delivery and expression. Trends Biotechnol 2002; 20:S11-S18.[CrossRef]



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Circulation, November 8, 2005; 112(19): 3009 - 3017.
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