Coronary Atherosclerosis T1-weighed Characterization with Integrated Anatomical Reference (CATCH): Comparison with High-risk Plaque Features on OCT

Yibin Xie¹, Young-Jin Kim², Jianing Pang¹, Qi Yang¹, Jung-Sun Kim³, Christopher T. Nguyen¹, Zixin Deng¹, Byoung Wook Choi², Zhaoyang Fan¹, Daniel S. Berman¹, Hyuk-Jae Chang³, and Debiao Li¹

¹Cedars-Sinai Medical Center, Los Angeles, CA, United States, ²Department of Radiology, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea, Republic of, ³Division of Cardiology, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea, Republic of

Synopsis

The aim of this work is to investigate the nature of pre-contrast and post-contrast T1w plaque hyper-intensity by comparing with coronary plaque morphology assessed by intracoronary optical coherence tomography (OCT). We scanned 13 healthy subjects and 30 stable angina patients using our recently developed whole-heart T1w coronary plaque characterization framework (CATCH). Compared with the classification based on OCT, we found that pre-contrast plaque to myocardial ratio (PMR) was significantly higher in the presence of large lipids, macrophages, and cholesterol crystals, whereas post-contrast PMR was significantly higher in the presence of macrophages and microvessels.

Purpose

Plaque rupture is recognized as the most important mechanism for acute coronary syndromes, accounting for approximately 70% of fatal acute myocardial infarctions and/or sudden coronary deaths¹. The detection of high-risk coronary atherosclerotic lesions is a “holy grail” in cardiovascular imaging. MR plaque characterization can potentially play an important clinical role as recent studies using T1-weighted (T1w) MRI with²or without³ contrast enhancement (CE) showed promising prognostic value⁴. However currently there is little direct validation of T1w plaque hyper-intensity from histopathology and/or invasive imaging methods, especially on delayed plaque enhancement. Recently we developed a MR imaging framework named CATCH for accelerated whole-heart T1w coronary plaque characterization with simultaneously acquired anatomical reference⁵. The aim of this work is to investigate the nature of T1w plaque hyper-intensity on pre-CE and post-CE CATCH by comparing with coronary plaque morphology assessed by invasive optical coherence tomography (OCT).

Methods

MRI protocol: CATCH consists of ECG-gated, inversion recovery (IR) prepared spoiled gradient echo sequence with golden angle 3D radial trajectory (Figure 1). T1w images and reference images were acquired in an interleaved fashion and a joint retrospective motion correction was performed (Figure 2). Healthy volunteers (n=13) and patients with stable angina pectoris (n=30) were scanned on clinical 3T scanners (Siemens Magnetom Trio or Verio) before and after CE. Scan parameters included: whole-heart 3D slab with FOV = 330³ mm³; spatial resolution = 1.1³ mm³; TR/TE = 4.6/2.3 ms; number of radial projections = 8500; scan time = ~10 minutes. CATCH images were analyzed and plaque to myocardial ratio (PMR) was calculated by two viewers who were blinded with respect to patient information and OCT results.

OCT protocol: After completing MRI, 26 eligible patients further underwent interventional X-ray angiography and intracoronary OCT with clinical OCT systems (LightLab Imaging M2 or C7-XR). OCT images were graded for 4 types of high-risk coronary plaque features (large lipids, macrophages, microvessels, and cholesterol crystals) by two experienced cardiologists without the knowledge of MR results. Each feature was scored based on a 5-point diagnostic scale.

Statistical analysis: In total 30 coronary segments that had both OCT and MR data were evaluated. A two-tailed two-sample heteroscedastic student’s t-test was performed between OCT-positive (score≥4) and OCT-negative (score≤3) segments for pre-contrast and post-contrast PMR.

Results

Based on PMR cutoff value of 1.4 as suggested by Noguchi et al⁴, no coronary hyper-intensive plaque (CHIP) was found in the healthy volunteers on either pre-CE or post-CE CATCH images. Four patients (13.3%) and 5 patients (19.2%) showed CHIPs on pre-CE CATCH and post-CE CATCH, respectively, among which two patients (7.7%) showed CHIPs on both. Figure 3 and Figure 4 are two representative patient cases that presented with a pre-CE CHIP and a post-CE CHIP, respectively. Corresponding imaging evidences shown included CT angiography, X-ray angiography and OCT. Figure 5 is the lesion-based statistics showing elevated PMR in the high-risk plaques as classified by OCT. Specifically pre-CE PMR was significantly higher in the presence of large lipids (+22.9%), macrophages (+19.2%), and cholesterol crystals (+26.2%), whereas post-CE PMR was significantly higher in the presence of macrophages (+21.3%) and microvessels (+33.7%).

Discussion

To the best of our knowledge this is the first study to demonstrate that pre-CE and post-CE T1w hyper-intensity on CATCH were both associated with high-risk plaque features assessed by OCT in patients with stable angina pectoris. Pre-CE hyper-intensity stemmed from endogenous source(s) with inherent short T1, possibly methemoglobin and large lipid pools. The association shown in this study between pre-CE hyper-intensity and macrophage accumulation was consistent with previous findings by Matsumoto et al⁶. More importantly we also found the association between pre-CE hyper-intensity and cholesterol crystals, as well as large lipids. Post-CE T1w hyper-intensity resulted from exogenous cause of T1 shortening, i.e., the residual gadolinium contrast media in the coronary vessel wall. Previous studies suggested that post-CE CHIPs may be associated with neovascularization, vascular inflammation and remodeling⁷. In this study our observation was in line with previous reports as we found the association between post-CE enhancement and macrophage clusters (inflammation) and microvessels (vessel remodeling) as detected on OCT. However the exact mechanism of delayed plaque enhancement is not fully clear and histological verification is warranted.

Conclusion

CATCH allowed accelerated whole-heart T1w coronary plaque characterization with simultaneously acquired anatomical reference. Coronary plaque hyper-intensity on pre-CE and post-CE CATCH was positively associated with high-risk plaque features detected by OCT.

Acknowledgements

Funding agencies: NIH/NHLBI (R01HL096119) and NSFC (81229001, 81322022)

References

1. Naghavi M, Libby P, Falk E et al. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I. Circulation 2003;108:1664-72.

2. Maintz D, Ozgun M, Hoffmeier A et al. Selective coronary artery plaque visualization and differentiation by contrast-enhanced inversion prepared MRI. European heart journal 2006;27:1732-6.

3. Kawasaki T, Koga S, Koga N et al. Characterization of hyperintense plaque with noncontrast T(1)-weighted cardiac magnetic resonance coronary plaque imaging: comparison with multislice computed tomography and intravascular ultrasound. JACC Cardiovascular imaging 2009;2:720-8.

4. Noguchi T, Kawasaki T, Tanaka A et al. High-Intensity Signals in Coronary Plaques on Non-contrast T1-Weighted Magnetic Resonance Imaging as a Novel Determinant of Coronary Events. J Am Coll Cardiol 2014;63:989-99.

5. Xie Y, Kim Y, Pang J et al. Time-efficient whole-heart coronary plaque characterization with simultaneously acquired MRA. In Proceedings of the 23th Annual Meeting of ISMRM, Toronto,Canada, 2015;a0557.

6. Matsumoto K, Ehara S, Hasegawa T et al. Localization of Coronary High-Intensity Signals on T1-Weighted MR Imaging: Relation to Plaque Morphology and Clinical Severity of Angina Pectoris. JACC Cardiovascular imaging 2015;8:1143-52.

7. Yeon SB, Sabir A, Clouse M et al. Delayed-enhancement cardiovascular magnetic resonance coronary artery wall imaging: comparison with multislice computed tomography and quantitative coronary angiography. Journal of the American College of Cardiology 2007;50:441-7.

Figures

Figure 1: Sequence diagram of CATCH. It is based on IR-prepared spoiled gradient echo with 3D radial trajectory. T1w (blood-nulled) images and anatomical reference were acquired in an interleaved fashion allowing inherent co-registration.

Figure 2: Schematic flow chart of the joint image reconstruction processes of CATCH for interleaved acquisition. Motion compensation and parallel imaging (SENSE) were integrated in the joint image reconstruction utilizing the higher SNR of the anatomical reference MR data.

Figure 3: A representative CHIP on pre-CE CATCH. A: Pre-CE CATCH images showing hyper-intensity at proximal RCA. B: CT angiography. C: X-ray angiography. D: OCT image at the corresponding plaque location, showing OCT image showed large signal-poor area suggestive of lipids and possible hemorrhage.

Figure 4: A representative CHIP on post-CE CATCH. A: Post-CE CATCH images showing delayed enhancement hyper-intensity at proximal RCA. B: CT angiography. C: X-ray angiography. D: OCT cross-sectional image at the corresponding location showing strong multi-focal back reflections and signal heterogeneity within the overlying tissue suggestive of superficial macrophage clusters.

Figure 5: Coronary plaques with high-risk features as classified by OCT were associated with elevated PMR on T1w CATCH images. Star signs (*) denote statistical significance (p<0.05). Positive sign (+) and negative sign (-) denote lesion groups with corresponding OCT classification for each high-risk plaque feature.

Proc. Intl. Soc. Mag. Reson. Med. 24 (2016)

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