Phase-contrast velocity mapping (other names include velocity-encoded cine, Q flow, or velocity mapping) are used for velocity measurements, and based on the accumulated phase of moving protons. In this sequence, bipolar gradients oriented in the expected direction of blood flow are applied to each frame of the imaging slice of interest to induce phase shifts. Phase refers to the angular position of an individual proton’s spin vector with respect to a frame of reference. Stationary objects within this slice have a net phase of zero, because all phase induced by the first lobe of the bipolar gradient is reversed by the second lobe. Moving objects (blood) gain a net phase depending on the direction of blood flow, and this net phase is proportional to the velocity of blood. This net phase can be displayed as a phase map with differences in signal intensity representing different velocities. Pixels depicting flow in the phase-encoding direction appear bright, and flow opposite to the phase encoding direction appears dark objects with a phase shift of zero (stationary) are grey or speckled, as can be seen in the lungs or chest wall.

Velocity mapping produces two sets of images: magnitude image and phase velocity image . The magnitude image is used for anatomic orientation of the imaging slice and to identify the boundaries of the vessel imaged Fig. 8.3. Blood has an increased signal, whereas turbulent flow is depicted with signal loss within the magnitude image. The phase image encodes the velocities within each pixel. Using both images, a region of interest can be traced on each time frame of the data set. The region of interest must be drawn for each frame of the cardiac cycle carefully because of movement and deformation of the vessel Fig. 8.4. Within each region of interest, the peak instantaneous velocity for each time frame can also be obtained with the simplified Bernoulli equation; the peak instantaneous gradient can be estimated by substituting in the peak instantaneous velocity. Mean pressure gradients are obtained by averaging all of the instantaneous velocities over systole [29].

Importantly, in clinical practice there are alternative methods for calculating TV regurgitant volume:

Recently developed 4D CMR flow resolves the problem of TV annulus motion, owing to retrospective valve tracking and velocity encoding in three orthogonal directions simultaneously during the cardiac cycle allowing the visualisation of complex flow patterns Fig. 8.5 [33]. 4D CMR Flow refers to phase-contrast CMR with flow-encoding in all three spatial directions that is resolved relative to all three dimensions of space and to the dimension of time along the cardiac cycle (3D + time = 4D).

4D CMR Flow visualizations offer more versatile and comprehensive depictions of flow fields than any other in-vivo imaging technique. Further, advanced 4D CMR Flow analysis parameters are currently used in the research setting but require testing for clinical utility. Future work explore the utility of this technique for TV lesions and other areas of clinical utility [34].

SSFP cine images assess the dynamic changes of cardiovascular geometry during the c ardiac cycle, allowing non-invasive assessment of global and regional cardiac function. [38].

In practice, a slice thickness of 6–10 mm in adults and 5–8 mm in children can be recommended. Slices do not necessarily need to be contiguous, and a small slice gap (e.g., 2–4 mm) is acceptable to reduce the measurement and post-processing time without influencing the accuracy of measurements. Accurate measurement of ventricular volumes, function and mass are vital for assessing the impact of valve lesions on the ventricles. RV volumes are particularly useful as these are difficult to achieve by other methods. CMR-derived ventricular stroke volumes can also be used to quantify mitral and tricuspid regurgitation by stroke volume difference calculation [39].

The basic protocol for ventricular function assessment is very simple. A series of SSFP sequences are acquired for qualitative and quantitative assessment of regional and global systolic function. From the localizers we can obtain the vertical long axis images, followed by the horizontal long axis and the short axis images as shown in the image above Fig. 8.6 [40].

RV volumes assessment can be also obtained from acquiring an axial stack. Which can make the identification of the basal slice borders much easier [41]. There are some standardized recommendations by the society of CMR that can help maintain the accuracy and reproducibility of CMR volumetric assessment, with special emphasis on the RV [42]; (1) RV end-diastolic volumes, RV end-systolic volume, RV ejection fraction, RV-SV, and cardiac output, are better indexed to body surface area, (2) The contiguous stack of short axis or axial cine images is evaluated with computer-aided analysis packages, (3) Endocardial borders are contoured at end- diastole and end-systole phases. The RV end-diastolic image should be chosen as the image with the largest RV blood volume. For its identification, the full image stack has to be evaluated and one phase has to be identified as end-diastole for all short axis/axial locations. All contours are included just up to the pulmonary valve and but not superior to this level. Trabeculations of the RV are ignored and a smooth endocardial border is drawn to improve reader reproducibility Fig. 8.7.

The procedure of late gadolinium enhancement (LGE) was described by Kim et al. in 2003. Injection of gadolinium chelate via an intravenous line in a bolus of 0.1–0.2 mmol/kg was described. After a 10–15 min delay the LGE sequence is acquired by a segmented T1 inversion recover gradient echo sequence [43]. An inversion time (TI) has to be properly selected to null the signal from normal myocardium, so that the contrast between scar tissue and normal myocardium is maximized Fig. 8.8 [43, 44]. The quality of LGE imaging depends on the effective nulling of signal from normal myocardium. This requires very precise selection of the appropriate inversion time.

This can also be achieved by performing a so-called TI-scout, which acquires images at multiple time delays after a single inversion pulse within the same acquisition. A sequence called TI scout is acquired with multiple inversion times to choose from before performing the actual IR-GRE sequences. The optimal TI is usually within the range of 200–250 ms [45].

Then the phase sensitive inversion recovery sequences (PSIR) was developed. It did not depend much on the choosing the accurate inversion time. Yet it showed a lower contrast to noise ratio compared to the regular inversion recovery sequences [46, 47]. 2D- and 3D-acquisition sequences are available. 3D acquisitions enable imaging of the entire heart in a single breath-hold, but are prone to image blurring.

Most studies with LGE have focused on the assessment of fibrosis in the LV. Desai and co-workers, as well as Amano et Kumazaki, suggested that the RV has a shorter optimal TI than LV. Others as Grosse-Wortmann et al. suggested that this was probably due to partial volume averaging caused by the thin wall of the RV. They suggested that if the spatial resolution was sufficient to visualize clearly the thickness of the RV myocardium, then the TIs for the RV and LV myocardium are most likely similar Fig. 8.9. In cases of TV disease, the presence or absence of myocardial fibrosis has not been proven to influence prognosis. It has been shown to be of more importance in cases of congenital anomalies of the TV [48].

The most common TV lesion is tricuspid regurgitation (TR). Trivial to mild TR is common (60–70%) and appears to be more common in patients more than 50 years old. [49] Although little is known about the significance of mild TR; moderate to severe TR has been associated with increased mortality [49, 50]. Causes of TR are either primary (i.e. intrinsic, organic, or structural) or secondary (i.e. functional TR with anatomically normal TV). The valve morphology can help differentiate the both groups.

It is a rare phenomenon and appears to be congenital (i.e. bicuspid, dysplastic) in most cases or, less likely, to be acquired due to endocarditis, rheumatic disease, or carcinoid [52–55].

Ebstein’s anomaly is a congenital abnormality that may present very early in neonatal life by severe cardiomegaly and heart failure, which can be seen on conventional radiography as the classic “box-shaped heart”. It is a rare congenital anomaly of the TV (less than 1% of all congenital heart disease) occurring in about 1–5 per 200,000 live births [62].

The main diagnostic criteria of Ebstein’s anomaly are; tethering of the TV leaflets (mainly the septal leaflet) to the underlying myocardium (failure of delamination); apical displacement of the functional annulus; Dilatation of the “atrialized” portion of the RV, with varying degrees of thinning of the RV wall; Redundancy of the anterior leaflet which becomes elongated “sail-like”; and dilatation of the right atrioventricular junction (true tricuspid annulus). The most typical feature is apical displacement of the hinge point of the valve from the atrioventricular ring of more than 8 mm/m² body surface area (Fig. 8.11) [63]. The anatomic severity of Ebstein’s anomaly was classified based on echocardiographic appearance as mild, moderate or severe; primarily based on the amount of displacement of the leaflets, the degree of tethering of the anterior leaflet and the degree of RV dilatation [64].

In 1988, Carpentier et al. [65] proposed the following classification of Ebstein’s anomaly; Type A: the volume of the true RV is adequate, Type B: a large atrialized component of the RV exists, but the anterior leaflet of the TV moves freely, Type C: the anterior leaflet is severely restricted in its movement and may cause significant obstruction of the right ventricular outflow tract, and Type D: almost complete atrialization of the RV except for a small infundibular component. The goals of surgery are to improve functional status and reduce the risk of sudden death in patients with Ebstein’s anomaly.

The American College of Cardiology/American Heart Association (ACC/AHA) 2008 guidelines for surgical intervention included other criteria, as symptoms or deteriorating exercise capacity; cyanosis (O₂ saturation less than 90%); paradoxical embolism; progressive cardiomegaly on chest x-ray; and progressive RV dilation or reduction in RV systolic function. Nevertheless, the decision about whether to perform surgery in individual patients with Ebstein’s anomaly is often debated because of unpredictable surgical outcomes [66].

Axial SSFP cine images used for visualizing the septal and anterior TV leaflets, coronal SSFP cine images used for assessing the atrialized RV, the RV, and the TV posterior leaflet and sagittal SSFP cine images show the infundibulum and the pattern of attachment of the TV anterior leaflet. Axial or short axis SSFP cine images are usually used for quantification of anatomical and functional RV in Ebstein’s anomaly. Usually an axial stack is preferred, as the basal images in such patients are very difficult to assess in terms of there the outlines of the functional ventricle are Figs. 8.12 and 8.13.

CMR limitations patients with Ebstein’s anomaly would be mainly the visualization of small atrial septal defects or patent foramen ovale, as well as sharp visualization of TV leaflet morphology which can be easily answered by echocardiography. Yet CMR offers quantifying of blood flow which allows reliable estimation of shunt volume. Old SGE sequences can replace SSFP sequences for better assessment of TV morphology and abnormal flow jets.

There are also emerging future CMR techniques such as T1-Mapping sequence and CMR Feature Tracking (CMR-FT) sequence that have been used in patients with Ebstein’s anomaly on research basis but not established yet on the clinical. T1-Mapping measures the depiction of diffuse myocardial fibrosis through measurement of myocardial T1 times using the modified look-locker inversion recovery (MOLLI) sequence with and without gadolinium-enhanced inversion recovery-prepared sequences. CMR-FT measures the intra- and inter- ventricular dyssynchrony within, and between, the cardiac chambers by quantitating the differences in time to peak strain duration within the LV and RV and between the two chambers respectively demonstrating RV intra-ventricular dyssynchrony [67].

Rheumatic heart disease remains a major origin of heart valve disease in the developing world [68, 69]. TV involvement is seen in 6.0–8.5% of cases, and TR develops in two-thirds of these patients. Imaging criteria include thickened leaflets with restriction in motion, diastolic doming (i.e. hemispheric shape of the leaflets due to adhesion), and encroachment of the leaflet tips on the ventricular inlet [69].

Infective endocarditis (IE) can involve a native TV or valve prosthesis (5–10%) [70]. TV IE is usually associated with the intravenous drug abuse. Associated findings include thickening, shortening, perforations, or complete destruction of the leaflets and intramural or para-valvular abscesses.

Infection-induced endothelial damage leads to cell death and surface deterioration [71]. Further damage may occur if endocarditis progresses into myocarditis, or if vegetation causes coronary artery embolization leading to ischemia, or if infection is spread causing destruction of the conductive tissues. Such effect of IE on the heart may be detected by CMR myocardial damage can be demonstrated non-invasively by detecting gadolinium contrast enhancement in the late phase [72]. These areas of LGE have been shown to be consistent with irreversible myocardial damage and fibrosis. Moreover, the recent CMR sequences T1 and T2 mapping help in tissue characterization [73].