Principles of CMR

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Chapter 1 Principles of CMR

Basic physics

MRI is based on nuclear magnetic resonance, the phenomenon of the resonance of atomic nuclei in response to radiofrequency (RF) waves.

The hydrogen atom is the simplest and most abundant element in the body and consists of one proton nucleus orbited by one electron. The hydrogen nucleus can therefore also be termed a proton, and current clinical MRI techniques are based on receiving and processing RF signals from protons. Protons have a magnetic axis which is normally randomly orientated. When a magnetic field is applied, the protons align in synchrony and spin around an axis in line with the main magnetic field—this spinning is termed precession. The rate at which protons precess is measured by the precession frequency, which changes linearly with increasing magnetic field strengths. When protons precess in synchrony they are said to be in-phase. There is loss of synchrony with time, and this is also termed out-of-phase.

At equilibrium within a magnetic field, overall proton alignment is in the direction of the main magnetic field and they have net longitudinal magnetization. This equilibrium can be disturbed by transmission of RF energy at the precession frequency of the proton which is 63 megaHertz (MHz) for water protons at 1.5 Tesla (T)—the strength of most commercially used magnets (Figure 1.1).

The degree of proton excitation is proportional to the amplitude and duration of the RF pulse. After excitation, proton relaxation occurs as the energy is dissipated and this process is defined by two parameters known as T1 and T2. T1 relaxation times measure the time after excitation to recover the longitudinal magnetization found in the equilibrium state. Transverse magnetization decays at a rate measured by T2, which is faster than the rate of T1 recovery. T1 and T2 relaxation vary according to the environment of the hydrogen atom within tissues and imaging sequences can be designed with different preference (or weighting) to one of these relaxation parameters for tissue characterization, known as T1-weighted (T1W) and T2-weighted (T2W) acquisitions. The values for T2 are always below that of T1, and T1 represents the upper limit of T2. T1 and T2 values tend to parallel each other when proton motion is relatively random, for example in adipose tissue, which has a short T1 and T2, and free water, which has a long T1 and T2. Tissues with a more organized structure contain abundant bound water. In this case proton motion is not random, there is increased transverse decay from the exchange of energy between protons, and T2 values become shorter than those of T1.

Localization of anatomical position within a selected imaging slice or volume is done with the application of frequency- and phase-encoding gradients. The corresponding direction of application of these gradients is known as the frequency encode or phase encode direction. With modifications of the phase-encoding gradients flowing blood can be differentiated from stationary anatomy via alterations in the phase of the MR signal. The velocity of material is proportional to the phase change or phase shift caused by its movement during gradient application.

Transmission and reception of RF energy is via special aerials known as coils with subsequent conversion of these raw data into images using ultrafast computers and a process known as Fourier transformation.

Main sequences

There are two fundamental types of sequence commonly used in CMR: gradient echo (GE) and spin echo (SE). As a general rule, with GE sequences both blood and fat appear white and so this technique is also known as white-blood imaging (Figure 1.2a). By contrast, in SE sequences blood is usually black but fat is white, giving rise to the term black-blood imaging (Figure 1.2b). SE sequences are more useful for anatomical imaging as opposed to the functional imaging performed with GE sequences. Variations of GE sequences are fast low-angle shot (FLASH), fast imaging with steady-state free precession (SSFP), and velocity mapping. GE imaging also forms the basis of the inversion recovery technique.

Areas of focal myocardial dysfunction and abnormal flow patterns are readily visualized with the technique of cine imaging using SSFP (or cines). Cines are obtained by rapid repetition of a variant of the basic GE sequence to obtain a series of cardiac images at progressively advancing points of the cardiac cycle which when put together form a cine loop. The weighting of SSFP sequences depends on the ratio of T2/T1, therefore most fluids and fat have a high signal and appear white. However, muscle and many other solid tissues have a long value for T1 and a short value for T2. This means that their signal intensity is reduced to shades of grey (Figure 1.2a). In addition to cines, the SSFP sequence can also be applied as a two-dimensional (2D) single-shot technique, as a real-time technique (not requiring breath holding or electrocardiogram (ECG) triggering), and as a three-dimensional (3D) volume scan.

Velocity mapping (or flow velocity mapping) techniques can determine the average velocity within a single imaging voxel, typically 1 ×1 ×10 mm3. The operator selects the required plane and sets a maximal encoding velocity (Venc; Figure 1.3). The initial Venc used is an approximation of the velocity expected based on factors such as clinical history, the type of valve or conduit lesion, and images already acquired. The Venc represents the practical upper limit of velocities that can be depicted unambiguously and should ideally be set to a numerical value just greater than the true velocity. Problems occur if it is set much higher or lower than this value—with the former leading to less sensitivity and the latter causing misrepresentation via the phenomenon of aliasing. Velocity aliasing is when the flow appears to be in the opposite direction and is characterized by a sudden transition of white-toblack or vice versa within the chosen flow region (Figure 1.3d). To eliminate or reduce aliasing a higher Venc must be set and the velocity mapping sequence repeated (Figure 1.3e). The maximal velocity of jets under interrogation should only be determined from the Venc-optimized images. Aliasing is also noted with 2D Doppler echocardiography and the technique of velocity mapping gives similar information. Subjects are asked to suspend their breathing for measurement of peak velocities using this method, which takes approximately 20 seconds to perform. An example of its use is for the quantification of peak velocity in valvular stenosis. Velocity mapping sequences are also used to calculate overall flow in a major vessel through the cardiac cycle and so can be used for quantification of regurgitation in valvular incompetence. For calculation of peak velocity and transvalvular flow, the plane used must be through plane—a plane perpendicular and mjust distal to the area of interest. Velocity mapping CMR is also used to confirm abnormal chamber communication and the ratio of pulmonary to systemic flow in shunts such as septal defects.

Compared to GE sequences, SE pulse sequences are usually more robust to system imperfections, such as magnetic field inhomogeneities. In SE imaging, structures need to be stationary for the delivery of two RF pulses. The T2 value of stationary fluid is long and gives high signal. Examples are fluid-filled structures such as cysts, which therefore appear white with SE sequences. However, flowing blood moves out of the selected slice before receiving the second pulse and so gives no signal and appears black (Figure 1.2b). Slower flowing blood can give persistent signal of varying signal intensity. Important variations of SE sequences are fast (or turbo) spin echo (FSE or TSE). FSE allows faster imaging than standard SE by acquiring more lines of data for every RF pulse delivered and allows acquisition of an entire image in a single heartbeat.

The inversion recovery technique uses a prepulse to create high T1 tissue contrast which is important for infarct imaging. This sequence and contrast-enhanced magnetic resonance angiography (CE-MRA) require use of a contrast agent. MRI contrast agents are commonly based on chelates of gadolinium which are paramagnetic, one example being gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA). All gadolinium chelates currently approved for clinical use are extravascular and therefore become distributed within the interstitium following initial intravenous delivery.

CMR is performed by applying these main sequences and their variants to evaluate cardiovascular physiology and anatomy, characterize tissue, and perform vascular angiography. Additionally, cardiac metabolism can be determined with magnetic resonance spectroscopy (MRS). MRS is not covered in this book and the interested reader is referred to the further reading section.

Most CMR scans are timed with respect to the ECG (ECG-gated) to minimize cardiac motion artefact, and subjects are asked to suspend their breathing in end expiration (breath-hold) to minimize respiratory motion artefact. In some cases scans can be linked to the respiratory cycle using diaphragmatic monitoring techniques (respiratory-gated), allowing subjects to breathe normally (free breathing). High signal from fat can be reduced by the application of a frequency-selective prepulse (fat suppression).

Patients are advised that data are being acquired during the time when the scanner is making a noise. This noise is generated by coils within the magnet. Headphones are worn by subjects during a CMR study and this serves to minimize their discomfort during noisy periods, facilitate hearing instructions from scanner operators, and allow music to be heard throughout if requested.

Imaging planes and protocols

CMR can obtain images in any plane but standard planes of reference are used to enable normal ranges to be defined. Subjects are generally scanned in the supine position and the most important planes in cardiac imaging are four-chamber, two-chamber, short-axis, LVOT and right ventricular outflow tract (RVOT). Suggested steps in obtaining these standard planes are shown sequentially in Figures 1.41.9, and a protocol incorporating them into routine cardiac evaluation is shown in Table 1.1.

Table 1.1 A standard CMR protocol which typically takes 30 minutes to perform

Pre-contrast
Five-slice SSFP pilot
Free breathing, low-resolution transaxial FSE
Breath-hold, low-resolution coronal (+ sagittal) FSE
Two-chamber pilot
Four short-axial pilots
Four-chamber and two-chamber cines
LVOT and RVOT cines
Ventricular short-axis stack cines
Post-contrast
Early gadolinium enhancement (1–5 minutes)
(a) Rpt four-chamber
(b) Rpt two-chamber
(c) Rpt LVOT
Late gadolinium enhancement (5–15 minutes)
(a) Rpt four-chamber
(b) Rpt two-chamber
(c) Rpt ventricular short-axis stack

Protocols for cardiac imaging involve four stages:

The initial pilot images are performed in a breath-hold and are used to optimize subject placement within the magnetic field using the table-positioning tool—the centre of the heart should be at the centre of the field. The pilot scan also enables the user to check that the correct coils are activated and other system requirements are satisfactory. Subsequent low-resolution anatomical coverage using FSE acquires one image per cardiac cycle. This allows a ‘quick-look’ for cardiac and extracardiac pathology at the start of the study and resulting images must be reviewed prior to further acquisitions. A series of transaxial FSE images usually consists of 35–40 slices, performed in free breathing over 1–2 minutes. A 12- to 15-slice series of coronal and sagittal FSE images encompass the heart and can be performed in a breath-hold. Breath-hold images do enable more accurate positioning of subsequent slices, but respiratory variations are small within the transaxial plane. Acquisition of the standard planes has been detailed in Figures 1.41.9. Additional targeted planes and sequences are chosen depending on the referral request, and presence and type of other pathology.

Normal ranges

The normal ranges for end-diastolic volumes (EDV), end-systolic volumes (ESV), stroke volumes (SV), ejection fraction (EF) and myocardial mass indexes in males and females are presented in Table 1.2. These values are calculated using semi-automated software analysis tools applied to the ventricular short-axis stack of GE cines. Calculation of LV parameters is performed in approximately 5 minutes while RV parameters take longer because of the more complex anatomy. Quantification of LV parameters is mandatory for CMR reporting and RV parameters are calculated as required, for example in patients with congenital heart disease, arrhythmogenic right ventricular cardiomyopathy (ARVC), dilated cardiomyopathy (DCM) and cases of valvular regurgitation. Normal ranges are age and body surface area dependent and normatized values are also available.

Other important cardiovascular normal ranges, including dimensions for the aorta and pulmonary vessels, are currently based on echocardiographic data, since CMR specific values are yet to be published (Table 1.3).

Table 1.3 Normal ranges for cardiovascular structures by echocardiography

Cardiovascular structure Range (cm)
Aorta dimensions (end-diastole)
Aortic annulus 1.4–2.6
Sinus of Valsalva 2.1–3.5
Sinotubular junction 1.7–3.4
Ascending aorta (at MPA bifurcation) 2.1–3.4
Aortic arch 2.0–3.6
Descending thoracic aorta (at MPA bifurcation) 1.4–3.0
Distal descending thoracic aorta 1.3–2.8
LVOT (diastole) 1.4–2.6
RVOT (diastole) 1.8–3.4
PA dimensions (end-diastole)
Pulmonary annulus 1.0–2.2
MPA 0.9–2.9
RPA 0.7–1.7
LPA 0.6–1.4
Venous dimensions
Pulmonary 0.7–1.6
Inferior vena cava 1.2–2.3
Superior vena cava 0.8–2.0
Hepatic 0.5–1.1

Indications

The European Society of Cardiology published guidelines in November 2004 on the clinical indications for CMR (Tables 1.41.8) with the usefulness of this imaging technique in specific diseases classified as follows:

Table 1.4 Indications for CMR in CAD

Indication Class
1. Assessment of global ventricular (left and right) function and mass I
2. Detection of CAD  
  Regional LV function at rest and during dobutamine stress II
  Assessment of myocardial perfusion II
  Coronary MRA (CAD) III
  Coronary MRA (anomalies) I
  Coronary MRA of bypass graft patency II
  CMR flow measurements in the coronary arteries Inv
  Arterial wall imaging Inv
3. Acute and chronic myocardial infarction (MI)  
  Detection and assessment I
  Myocardial viability I
  Ventricular septal defect III
  Mitral regurgitation (acute MI) III
  Ventricular thrombus II
  Acute coronary syndromes Inv

Table 1.5 Indications for CMR in patients with pericardial disease, cardiac tumours, cardiomyopathies and cardiac transplants

Indication Class
1. Pericardial effusion III
2. Constrictive pericarditis II
3. Detection and characterization of cardiac and pericardiac tumours I
4. Ventricular thrombus II
5. Hypertrophic cardiomyopathy  
  Apical I
  Non-apical II
6. DCM Inv
  Differentiation from dysfunction related to coronary artery disease I
7. ARVC I
8. Restrictive cardiomyopathy II
9. Siderotic cardiomyopathy (in particular thalassaemia) I
10. Non-compaction II
11. Post-cardiac transplantation rejection Inv

Table 1.6 Indications for CMR in patients with valvular heart disease

Indication Class
1. Valve morphology  
  Bicuspic AV II
  Other valves III
  Vegetations Inv
2. Cardiac chamber anatomy and function I
3. Quantification of regurgitation I
4. Quantification of stenosis III
5. Detection of paravalvular abscess Inv
6. Assessment of prosthetic valves Inv

Table 1.7 Indications for CMR in congenital heart disease

Indication Class
General indications
1. Initial evaluation and follow-up of adult congenital heart disease I
Specific indications
1. Assessment of shunt size (Qp/Qs) I
2. Anomalies of the viscero-atrial situs I
  Isolated situs anomalies II
  Situs anomalies with complex congenital heart disease I
3. Anomalies of the atria and venous return  
  Atrial septal defect (secundum and primum) II
  Anomalous pulmonary venous return, especially in complex anomalies and cor triatriatum I
  Anomalous systemic venous return I
  Systemic or pulmonary venous obstruction following intra-atrial baffle repair or correction of anomalous pulmonary venous return I
4. Anomalies of the atrioventricular valves  
  Anatomic anomalies of the mitral and tricuspid valves II
  Functional valvular anomalies II
  Ebstein’s anomaly II
  Atrioventricular septal defect II
5. Anomalies of the ventricles  
  Isolated ventricular septal defect (VSD) III
  VSD associated with complex anomalies I
  Ventricular aneurysms and diverticula II
  Supracristal VSD I
  Evaluation of right and left ventricular volumes, mass and function I
6. Anomalies of the semilunar valves  
  Isolated valvular pulmonary stenosis and valvular dysplasia III
  Supravalvular pulmonary stenosis II
  Pulmonary regurgitation I
  Isolated valvular AS III
  Subaortic stenosis III
  Supravalvular AS I
7. Anomalies of the arteries  
  Malpositions of the great arteries II
  Post-operative follow-up of shunts I
  Aortic (sinus of Valsalva) aneurysm I
  Aortic coarctation I
  Vascular rings I
  Patent ductus arteriosus III
  Aortopulmonary window I
  Coronary artery anomalies in infants Inv
  Anomalous origin of coronary arteries in adults and children I
  Pulmonary atresia I
  Central pulmonary stenosis I
  Peripheral pulmonary stenosis Inv
  Systemic to pulmonary collaterals I

Table 1.8 Indications for CMR in acquired diseases of the vessels

Indication Class
1. Diagnosis and follow-up of thoracic aortic aneurysm including Marfan disease I
2. Diagnosis and planning of stent treatment for abdominal aortic aneurysm II
3. Aortic dissection  
  Diagnosis of acute aortic dissection II
  Diagnosis and follow-up of chronic aortic dissection I
4. Diagnosis of aortic intramural haemorrhage I
5. Diagnosis of penetrating ulcers of the aorta I
6. PA anatomy and flow I
7. Pulmonary emboli  
  Diagnosis of central pulmonary emboli III
  Diagnosis of peripheral pulmonary emboli Inv
8. Assessment of thoracic, abdominal and pelvic veins I
9. Assessment of leg veins II
10. Assessment of renal arteries I
11. Assessment of mesenteric arteries II
12. Assessment of iliac, femoral and lower leg arteries I
13. Assessment of thoracic great vessel origins I
14. Assessment of cervical carotid arteries I
15. Assessment of atherosclerotic plaque in carotid artery/aorta III
16. Assessment of pulmonary veins I
17. Endothelial function Inv

CMR also has an important role in research and development and is being increasingly used by the pharmaceutical industry in preclinical trials.

Tables 1.4, 1.5, 1.6, 1.7 and 1.8 used with kind permission of European Society of Cardiology from Pennell et al Clinical Indications for Cardiovascular Magnetic Resonance (CMR): Consensus Panel Report, European Heart Journal, 2004, 25 (21), 1940–1965.

Contraindications and issues of safety

The environment in which CMR is performed must be constantly protected from the inadvertent introduction of ferromagnetic metallic objects and electronic equipment near the powerful magnetic field, with safety failures possibly leading to injury and rare cases of mortality. Potential subjects fill out a checklist as shown in Figure 1.10, which is then reviewed by trained personnel prior to placement within the magnet. Regular cardiorespiratory arrest scenario training in the safe and speedy removal of subjects undergoing CMR to nearby, designated resuscitation areas are advocated for clinical and allied MRI staff.