Guidelines for Cardiovascular Magnetic Resonance Imaging from the Korean Society of Cardiovascular Imaging-Part 3: Perfusion, Delayed Enhancement, and T1- and T2 Mapping

Abstract

This document is the third part of the guidelines for the protocol, the interpretation and post-processing of cardiac magnetic resonance (CMR) studies. These consensus recommendations have been developed by the Consensus Committee of the Korean Society of Cardiovascular Imaging to standardize the requirements for image interpretation and post-processing of CMR. This third part of the recommendations describes tissue characterization modules, including perfusion, late gadolinium enhancement, and T1- and T2 mapping. Additionally, this document provides guidance for visual and quantitative assessment consisting of "What-to-See," "How-To," and common pitfalls for the analysis of each module. The Consensus Committee hopes that this document will contribute to the standardization of image interpretation and post-processing of CMR studies.

Keywords: Cardiac magnetic resonance; Interpretation; Post processing.

Fig. 1. Dark banding artifact in 18-year-old man.

Defect (arrows) is approximately one pixel wide, prominent in phase-encoding direction (right-left in this case), and already appears before contrast reaches myocardium. Even though this defect is seen on both stress and rest perfusion images, there is no delayed enhancement in corresponding region on LGE image. LGE = late gadolinium enhancement

Fig. 2. Three-vessel disease in 70-year-old man.

Ring-like subendocardial perfusion defect (arrowheads) is seen on stress, and disappears on rest images (upper row). Differentiation from microvascular disease may be challenging. Patient had multifocal severe stenosis (arrowheads) at left anterior descending and left circumflex coronary arteries. Right coronary artery angiogram (on right lower) shows total occlusion (arrow) at proximal segment, and distal segment (arrow) reconstituted via big septal branch is seen on left coronary angiogram (on left lower) (Courtesy of Sung-A Chang, Samsung Medical Center).

Fig. 3. Microvascular disease in 73-year-old man with 20-year history of diabetes mellitus.

Patient complains of chest pain. Invasive coronary angiography shows insignificant findings. Note global subendocardial perfusion defect (arrowheads), which is more than one pixel wide on stress perfusion images.

Fig. 4. Inducible ischemia in 52-year-old woman with septal-type HCM.

Inducible, global, subendocardial perfusion defects (arrows) are present in mid to apical segments, and extent of defects is greater in hypertrophied septum of left ventricle on stress images. Compared to LGE images, fibrosis (arrowheads) exists within area of ischemia and is smaller than perfusion defects. HCM = hypertrophic cardiomyopathy

Fig. 5. Inducible ischemia and delayed perfusion in 50-year-old man who underwent coronary bypass graft surgery.

Delayed perfusion (arrow) due to long bypass graft is transmural and appears on both stress and rest images, while inducible perfusion defect (arrowhead) is subendocardial, lasts longer, and appears only on stress perfusion image. Invasive coronary angiography shows long, saphenous venous Y graft (arrow) to posterior descending coronary artery (Adapted from Kim et al. Korean J Radiol 2014;15:188-194 (8)).

Fig. 6. Simple diagram exhibiting semi-quantitative perfusion parameters.

AIF = arterial input function, SI = signal intensity

Fig. 7. Example of semi-quantitative perfusion analysis using dedicated software.

Regional maximal up-slope values are demonstrated based on 17-segment model on time–SI profile. Blue dot in anterior junction of right ventricular insertion point indicates reference point in left ventricular myocardium for segmentation.

Fig. 8. Role of TI in LGE imaging.

Left image (A) shows wrong nulling of normal myocardium that is shown to be darkest at border with higher SI centrally. These findings signify that degree of LGE may be underestimated if TI is too short. Right image (B) shows optimal nulling of myocardium with repeated image taken at longer TI and demonstrates larger LGE area in inferior wall (arrows). TI = inversion time

Fig. 9. Pattern assessment in LGE image in patient with coronary artery disease.

Most important finding of ischemic pattern is that LGE lesion follows coronary artery distribution. This patient shows delayed enhancement (arrows) at mid inferolateral wall of left ventricular myocardium, indicating left circumflex artery territory. Lesion of ischemic pattern starts at endocardium extending toward epicardium, according to concept of wave front phenomenon of myocardial death.

Fig. 10. Short-axis MR images demonstrate LGE pattern in various types of non-ischemic cardiomyopathy.

There is mid-wall enhancement in basal, interventricular, septal wall of myocardium in patient with DCM (black arrows), epicardial enhancement in patient with sarcoidosis (white arrows), patchy enhancement at junction of both ventricles in patient with HCM (white arrows), and global subendocardial enhancement in patient with amyloidosis (white arrows). DCM = dilated cardiomyopathy

Fig. 11. Short-axis LGE image in 49-year-old man with exertional chest pain performed 5 days after primary percutaneous coronary intervention to left anterior descending artery.

Full-thickness infarct within anterior and anteroseptal left ventricular mid-wall with microvascular obstruction (arrows) is shown as central hypo-enhanced region within avidly hyper-enhanced region of infarcted myocardium on LGE image.

Fig. 12. “n”-SD technique for quantifying LGE extent.

LGE image in 57-year-old man with chest pain shows subendocardial infarction at basal inferior wall of myocardium (arrows). Endocardial and epicardial borders are outlined and region of interest within remote dark myocardium as reference is drawn. According to threshold between enhanced and unenhanced myocardium selected, extent of LGE varies significantly as shown in these color maps. SD = standard deviation

Fig. 13. T1 mapping images of 60-year-old woman with HCM.

After obtaining native T1 and post-contrast T1 values in myocardium and blood, values and HCT are inserted into ECV formula. HCM is usually characterized by high T1 value and high ECV. This patient also had high T1 value of 1419 ms and high ECV value of 32.7%. ECV = extracellular volume, HCT = hematocrit

Fig. 14. T1 mapping images of 43-year-old male with Fabry disease.

After drawing endocardial contour and epicardial contour in native T1- and post T1 mapping images, T1 value and ECV are calculated. Fabry disease has special characteristics of low T1 value and normal ECV. This patient also had low T1 value of 1089.3 ms and normal ECV value of 23%.

Fig. 15. Acute myocardial infarction in 51-year-old man with chest pain.

Area of increased SI on T2WI was correlated with area of delayed enhancement on LGE image. T2WI = T2-weighted image

Fig. 16. Acute myocarditis in 40-year-old man with fever.

Increased SI observed in global myocardium on T2WI, and SI ratio of myocardium to serratus anterior muscle was increased to 2.0.

Fig. 17. Beta-thalassemia in 35-year-old man.

signal loss occurred at TE of 8.3 ms, and measured T2^* value was 3.8 ms. TE = echo time

Fig. 18. Images for HCM sample report.

Fig. 19. Images for ischemic cardiomyopathy sample report.