Myocardial mapping

Myocardial mapping or parametric mapping of the heart is one of various magnetic resonance imaging techniques, which has evolved and been increasingly used in the last decade for non-invasive tissue characterization of the myocardium ^1-5. Unlike normal T1-, T2- or T2*- images, parametric mapping allows for both visualization and quantification of focal and diffuse disease ^1,2,4.

The technique comprises the generation of a parametric map from a series of co-registered images with different T1, T2  or T2*relaxation times, depending on the mapping technique used. The T1, T2 or T2* values of the myocardium are tissue properties and are encoded in the respective pixels of the map. With the mapping technique, they can be compared to the spared healthy myocardium in focal disease or quantified and evaluated on the basis of normal reference values in diffuse disease ^1,5,22.

The T1-map is generated at different degrees of longitudinal relaxation in order to receive a signal intensity vs time curve, from where T1 can be calculated. In a similar fashion, a T2 or T2*-maps are obtained from a signal intensity vs time curve on the basis of different transverse relaxation times. Different acquisition methods for each T1 and T2 quantification exist ^6-8,15-17.

Myocardial T1 mapping

Native T1

The myocardial T1-map depicts the spin-lattice (longitudinal) relaxation of the myocardium and the T1 value [ms] of a voxel represents the respective time constant for the recovery.

Despite extensive research during the last 15 years, histopathological correlates of myocardial T1 values are still not completely elucidated ². T1-mapping techniques have been studied as a key feature for the assessment of myocardial fibrosis ^5,8,9,12,22. However, native T1 reflects changes in intracellular and extracellular compartments and is not only influenced by collagen, but also by protein, water (oedema), lipids and iron ^{1-5,8,9,13,22}.

Myocardial T1 lengthens at higher magnetic field strength^3,7 and is also influenced by various physiological factors^4,7.

Postcontrast T1

Administration of gadolinium leads to a shortening of the T1 time. Postcontrast T1 can be measured and displayed on a map in equal measure. Since most gadolinium agents spread in the intravascular and interstitial compartments and not within the cells,  a reduced post-contrast T1 value should either reflect an expansion of the interstitial space due to collagen (myocardial fibrosis), protein (amyloidosis) or an access to the intracellular space (in case of myocardial oedema or cell membrane disruption e.g. necrosis, myocardial infarction) ^{1,2,8,9,13,14,22}.  

Myocardial extracellular volume (ECV)

Extracellular volume (ECV) reflects the volume fraction that is not taken by cells. It combines interstitial and intravascular space and represents approximately 25% of the myocardial volume ¹³. If native and post-contrast T1 images are co-registered, quantified and adjusted for haematocrit, extracellular volume(ECV) can be calculated for a specific area or for specific voxels ^1,2.  Likewise, an ECV map can be generated. For this purpose postcontrast T1 should be obtained during a slow continuous infusion or at least 15 min after bolus injection ¹³.

Applications of native T1 mapping

Most diffuse cardiac disorders as diffuse fibrosis, scar tissue, and inflammation result in prolonged native myocardial T1 relaxation time^1-5,8-14, it has proven especially useful in the detection of:

• amyloidosis
• acute inflammation
• acute ischemia
• myocardial necrosis

A few cardiac pathologies or conditions can lead to a shortened native T1 relaxation time^1,3,4,9:

• Anderson-Fabry disease
• iron overload
• myocardial haemorrhage
• fat (e.g. arrhythmogenic right ventricular dysplasia, old chronic infarct)
• athlete’s heart

Applications of myocardial extracellular volume (ECV)

Assessment of extracellular volume (ECV) is considered as reasonable in patients getting an extracellular contrast agent¹. Diffuse fibrosis can lead to an increase^1,4,12of ECV, a moderate to severe increase can be observed in:

• cardiac amyloidosis
• myocardial necrosis
• scar tissue
• myocarditis

A decrease in extracellular volume (ECV) can be observed in athlete's heart ¹.

Myocardial T2 mapping

The myocardial T2-map depicts the spin-spin (transverse) relaxation of the myocardium and T2, encoded in the voxels of the map, is a time constant for the decay of transverse magnetization.

T2 time is related to the water content of the respective tissue, hence the myocardium and thus prolonged T2 reflects myocardial oedema, be it due to inflammation or reperfusion²⁰.

T2-mapping offers the potential for more objective detection and quantification of myocardial oedema than standard black-blood T2 and STIR images, which are often of limited value due to susceptibility or slow flow artifacts²⁰.

Myocardial T2 tends to decrease at higher magnetic field strength ¹⁷.

Applications of T2 Mapping

T2-mapping can detect edematous myocardial territories in a variety of cardiac pathologies ^1,3-5,17-22, including:

• acute and subacute inflammation/myocarditis 
• acute ischemia / myocardial infarction
• Tako-tsubo cardiomyopathy
• heart transplant rejection

Low T2 values will be seen in iron overload and haemorrhage ¹.

Myocardial T2* mapping

T2*-mapping is usually based on gradient echo (GRE) sequences,  T2* results principally from variations in the static magnetic field throughout the tissue which will be added to random mechanisms. Thus T2* is a time constant for the decay of transverse magnetization, it is only shorter ²⁶. 

Applications of T2* mapping

T2* relaxation time is sensitive to magnetic field inhomogeneity and has become useful in the evaluation of myocardial iron overload and assessment of chelation therapy ^3,23-25 and also shows a decrease in myocardial haemorrhage or stress-induced ischemia ^1,3.

Normal values

Normal values of native T1 and T2 times differ depending on magnetic field strength (1,5 and 3 T), acquisition sequence (e.g. MOLLI, shMOLLI, SASHA, SAPPHIRE in case of T1-mapping and T2-SSFP, GraSE in case of T2-mapping). Because of variations between scanners, it is still recommended ^1,2,10, that local reference ranges are primarily used, and if a local reference range is not available quantitative results should not be clinically reported ^1,2.

ECV reference ranges from the literature seem to be considered as acceptable, if the same MR system and pulse sequences are used ¹.

Regarding T2*and iron overload, a 3-tier risk model (low, intermediate and high risk) has been recommended^1,25.

Clinical use

There is proven clinical utility in a setting of myocarditis, amyloidosis ^1,13, Anderson-Fabry disease ^1,13 and iron deposition and potential clinical utility regarding many cardiac diseases as cardiomyopathy, heart failure, congenital heart disease, myocardial ischemia and infarction, transplant rejection athlete’s heart and cardiac masses  ^1,3,13.

Detailed recommendations for indications, utility and clinical implementation including imaging protocols, the use of reference ranges and reporting are given in a consensus statement by the Society for Cardiovascular Magnetic Resonance (SCMR) ¹.

Cardiac magnetic resonance fingerprinting (cMRF)

To overcome the problem that conventional mapping techniques require separate acquisitions for T1 and T2 mapping, of which values are also dependent on different scanner technology, pulse sequences, and various physiological and environmental parameters, cardiac magnetic resonance fingerprinting (cMRF) technique has been introduced for simultaneous measurement of T1 and T2 maps in a single scan ^27,28.

See also

• T1 mapping
• T2 mapping
• T2* mapping
• extracellular volume (ECV)
• MR fingerprinting (MRF)