In this paper we evaluated the utility of a high-resolution (80-μm) receive-only intravascular loopless CMR detector as a possible guidewire for identifying imaging and measuring the fibrous cap thickness of atherosclerotic plaques in a widely-available clinical 3T MR system. In a 1-cm region (r ≤ 5 mm), potentially relevant to most cases of coronary and carotid vessel imaging, the detector retains over 17% of the peak sensitivity at its junction. Moreover its extended spatial sensitivity along a lead length of about double the whip length (Figures 1, 2, 6), permits angiographic imaging using relatively low-resolution coronal CMR to identify suspected atherosclerotic lesions, and supports a guidewire function under CMR alone that does not require X-ray fluoroscopy. This strategy differs from the CMR endoscopy approach [36, 37] where the detector's intrinsic sensitivity is limited to a thin sensitive disk by design, and the CMR's frame-of-reference is locked to the probe-head to provide a "probe's-eye view". Here we have shown that, after detection by low-resolution angiographic-type CMR, suspect lesions can subsequently be targeted for high-resolution CMR that visualizes calcifications as signal voids (Figure 3) and permits accurate characterization of FCT (Figures 5, 6), a key predictor of plaque vulnerability to rupture.
Although the FCT measurements were only performed on human specimens in an electrically bio-analogous saline phantom, the feasibility of the approach was demonstrated with a 0.76 mm maximum diameter biocompatible nitinol loopless antenna guidewire in vivo in the rabbit aorta (Figures 7, 8). In these studies, artifacts from respiratory and cardiac motion were relatively minor, perhaps reflecting the limited spatial extent of high-resolution imaging. At least motion did not seem to affect the accuracy of measurements of aortic wall thickness or plaque size in T2 or T1-weighted CMR, which agreed with histological measurements to within 2% and 10%, respectively. The scan time for 3D cardiac-gated in vivo 80 μm high-resolution CMR with the 3T loopless detector was 7-10 min (Figures 7, 8), which is within a range that is potentially tolerable for clinical research studies.
The improved performance of the 3T intra-vascular loopless detector compared to prior 1.5T devices derives from an approximately quadratic SNR performance with MR field-strength . Here, the SNR gain was exchanged for a high-resolution intravascular imaging capability, and a higher-speed lower-resolution angiographic-type CMR that permitted device tracking. In addition, the extended CMR-sensitivity of the guidewire about the cable/whip junction obviated the need for precise device positioning or repeated tracking-scans, enabling high-resolution imaging anywhere within the detector's sensitive region. At 80 μm resolution, the 3T loopless detector provided exceptional views of the vessel wall and pathology (Figures. 3, 4, 7, 8), with FCT measurements accurate to within 13 ± 9% on average compared to histology, with which they were strongly correlated (Figure 5). This was also true of plaques with a mean FCT of less than the 650 μm threshold for discriminating symptomatic from asymptomatic carotid artery stenoses, as identified by IVUS . The implication is that interventional 3T CMR with a loopless guidewire detector could potentially do the same.
Degrading the CMR spatial resolution negatively affected the accuracy of FCT measurements. Increasing the voxel size from 80 μm to 140 μm resulted in an over-estimate of 360 μm being recorded for a plaque with a 186 μm FCT measured by histology, possible distortions introduced during histological preparation notwithstanding. That an 180 μm cap is even observable with a 140 μm voxel size attests to the high contrast sensitivity of CMR, and again supports its potential for plaque detection at a coarser but more time-efficient spatial resolution, followed by high-resolution CMR for plaque characterization. Note also that the averaging of many measurements of FCT from high-resolution CMR can result in reasonably accurate estimates of FCT right down to the native resolution of the scans (Figure 5).
Nevertheless, the 80 μm resolution employed here is higher than the 65 μm FCT proposed for classifying fibrous caps in coronary plaques as vulnerable [7–10]. In the context of other intravascular imaging modalities, the CMR resolution achieved here is comparable to the best achieved by IVUS at around 100 μm [9, 11–13]. However, as shown in prior studies comparing CMR with IVUS [14, 29], CMR has better soft-tissue contrast and is not limited by the presence of calcifications [14, 29], which were common in our sample cohort (eg, Figure 3). We could not match OCT's resolution of 10-20 μm [9, 10], but CMR's FOV or penetration depth was a good order-of-magnitude larger than in OCT. Also, unlike either of these modalities, intravascular CMR did not require X-ray fluoroscopic guidance. Our scan-times for high-resolution CMR in the aorta were exacerbated by the use of cardiac-gated acquisition. Intravascular CMR of vessels further from the heart might benefit from more-efficient steady-state sequences if gating could be omitted. Also, the promise of a quadratically increasing SNR afforded by even higher B0 human MR scanners  offers further hope for 65 μm FCT measurements and/or much shorter scan-times.