Cardiovasc Imaging Asia. 2018 Jan;2(1):12-18. English.
Published online Jan 31, 2018.
Copyright © 2018 Asian Society of Cardiovascular Imaging
Review

Clinical Application of T1 and T2 Mapping in Cardiac Magnetic Resonance Imaging for Nonischemic Cardiomyopathy: A Case-Based Review

Lulu Said Fundikira,1 Yoo Jin Hong,2 Pan Ki Kim,2 Sang A Lee,2 Kyung Sun Nam,2 Dong Jin Im,2 Chul Hwan Park,3 Hye-Jeong Lee,2 Jin Hur,2 Young Jin Kim,2 Tae Hoon Kim,3 and Byoung Wook Choi2
    • 1Department of Radiology and Imaging, Muhimbili University of Health and Allied Sciences, Dar Es Salaam, Tanzania.
    • 2Department of Radiology and Research Institute of Radiological Science, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
    • 3Department of Radiology and Research Institute of Radiological Science, Gangnam Severance Hospital, Yonsei University Medical Center, Seoul, Korea.
Received November 24, 2017; Revised December 18, 2017; Accepted December 22, 2017.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Cardiac magnetic resonance imaging is instrumental in diagnosing various cardiovascular diseases. Recently introduced T1 mapping and T2 mapping sequences have enabled quantification of the T1 and T2 relaxation times of the myocardium and associated cardiovascular structures, which are intrinsic properties of tissues. These sequences have been increasingly used to diagnose cardiomyopathy based on changes in the T1 and T2 relaxation times and to objectively quantify the severity of cardiomyopathy. As reference values in T1 and T2 mapping sequences are influenced by specific techniques or magnetic field strength, they are limitations. However, parametric imaging with native T1, T2, and extracellular volume fraction (%) values yields a higher diagnostic accuracy than conventional MRI and is useful for diagnosis, treatment, and risk stratification of cardiomyopathy.

Keywords
T1 mapping; T2 mapping; Extracellular space; Magnetic resonance imaging; Cardiomyopathies

INTRODUCTION

Cardiac magnetic resonance imaging (MRI) provides excellent assessment of myocardial function and anatomy and is used in diagnosis of cardiac diseases, including nonischemic cardiomyopathy [1, 2, 3]. Cardiac MRI is considered the gold standard for evaluating ventricular mass, volume, and ejection fraction, as well as for detection of focal myocardial fibrosis using late gadolinium enhancement (LGE). However, LGE has limited value in nonischemic myocardial disease, as the observed disease tends to be diffuse [4]. Moreover, LGE employs qualitative assessment of the myocardium and is susceptible to inter-patient and inter-image variability [5]. Recent innovations in cardiac MRI with the introduction of T1 mapping and T2 mapping sequences, including quantification of the T1 and T2 relaxation times of the myocardium and associated cardiovascular structures, have emerged as promising alternatives [4]. Mapping sequences allow for a per-voxel calculation of the absolute relaxation time of T1 and T2 values in milliseconds, as well as parametric reconstructed images of high spatial resolution [6].

The pixel signal intensity is based on the relaxation of hydrogen nucleus protons in a static magnetic field. T1 relaxation time depends on the molecular environment of the water molecules in the tissue and therefore characterizes each tissue very specifically. T1 relaxation time varies among tissues, but also within the same tissue, depending on its pathophysiological status and the presence of inflammation, edema, fat, fibrosis, etc. [7].

T2 relaxation time is also a tissue-specific time parameter used to differentiate between normal and abnormal myocardial tissue. Increased water content is the main cause of longer T2 relaxation times. Thus, an increased T2 value is mainly noted in myocardial edema [8].

Cardiac MR mapping techniques have an advantage over LGE imaging by eliminating the influences of variations in signal enhancement by directly measuring the underlying T1 and T2 relaxation times [5]. Moreover, mapping enables quantification of the proportion of extracellular volume (ECV). ECV is calculated using a formula that combines native T1 and postcontrast times with hematocrit value. An increased ECV is a marker of myocardial remodeling and is most often due to excessive collagen deposition (in the absence of amyloid or edema) [9, 10].

At a fixed magnetic field strength and in the absence of exogenous contrast agent, such as gadolinium chelate, the native T1 value of normal tissue falls within a predictable range (e.g., at 1.5 T, normal myocardium has a T1 relaxation time of 940–1000 ms) [11]. Normal myocardial T2 values acquired using steady-state free precession MRI have been reported to be 52.18±3.4 ms at 1.5 T [12] and 45.1 ms at 3 T [13].

Kellman and Hansen [14] reported myocardial ECVs in healthy volunteers to be similar at field strengths of 1.5 T (0.25±0.04) and 3 T (0.26±0.04). A “bolus only” injection is sufficient for ECV measurement, while a minimum delay of 15 min is recommended to reach a state of dynamic equilibrium for postcontrast T1 mapping and acquisition of time point data [6, 15].

Studies have shown variability of native T1 relaxation times based on the sequence used, the magnetic field strength (higher native T1 values at higher strength), the image acquisition plane, and the region of myocardium being sampled, as well as the patient's heart rate, age, and sex [8]. The Modified Look-Locker inversion recovery (MOLLI) sequence used for T1 mapping is characterized by data acquisition at a fixed point in the cardiac cycle over successive heartbeats during a single breath-hold (approximately 16–20 s). Multiple Look-Locker image acquisitions are performed at different inversion times and then merged into one dataset to facilitate final analysis [16].

The purpose of this study is to present various cases of nonischemic cardiomyopathy evaluated in our institution using T1 mapping, T2 mapping, and ECV quantification for diagnosis.

CASE SERIES DISCUSSION

Dilated cardiomyopathy

Dilated cardiomyopathy (DCMP) is the most common form of nonischemic cardiomyopathy and is characterized by a dilated and poorly functioning left ventricle. Half of the cases are idiopathic in nature, with the rest secondary to previous infection, alcohol and drug abuse, or toxicity [17, 18].

Cardiac MR LGE shows patchy or diffuse midwall enhancement, which usually does not correspond to any coronary artery distribution, and represents fibrosis in the setting of chronic myocardial remodeling [17, 18, 19].

Buss et al. [20] noted that patients with DCMP usually show increased ECV compared with those in a control group, even in early stages of disease before a significant change in left ventricular (LV) function. Native T1 and ECV values are increased in DCMP (Fig. 1) and are correlated with reduced wall thickness [21].

Fig. 1
Dilated cardiomyopathy. A 62-year-old woman was admitted to the hospital with dyspnea and pitting edema for one month. She underwent cardiac magnetic resonance imaging (Siemens 3 T); her left ventricle was dilated (LV end-diastolic dimension=7.3 cm, volume=235.3 mL/m2) and showed global diffuse hypokinesia; the measured LV ejection fraction was 25%. (A) Subtle LGE was noted at the mid-layer of the interventricular septum of the left mid-ventricle (arrows). (B-E) On the T1 mapping sequence, global native LV T1 was increased (B) (native T1=1434.4 ms, reference value=1203 ms), ECV was increased (D) (30.6%, reference=25%), and T2 was slightly increased (E) (56.2 ms, reference value=48.5 ms; reference values are the same in the following cases). (A) LGE image, (B) native T1 map, (C) post T1 map, (D) ECV map, and (E) T2 map. LV: left ventricular, LGE: late gadolinium enhancement, ECV: extracellular volume.

Hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HCMP) is the most common inheritable cardiac disorder. It is characterized by abnormal thickening of the LV wall in the absence of dilatation. HCMP commonly involves the interventricular septum in an asymmetric manner. Fibrosis occurs through intercellular deposition of collagen fibers and can be diffuse or present as focal scarring [22].

LGE has been reported in up to 75% of patients with HCMP in whom the clear majority have patchy midwall-type enhancement, which is typically most pronounced within the segments most severely affected by hypertrophy [23]. Native T1 sequences can depict the presence and pattern of myocardial fibrosis even in fibrotic areas that are undetected by LGE. Significant increases in native T1 and ECV values are observed in regions affected by HCMP [24] (Fig. 2).

Fig. 2
HCMP. A 34-year-old man was diagnosed with HCMP 12 years prior. On magnetic resonance imaging, the interventricular septum and LV anterior wall were abnormally thickened (maximal thickness, 31 mm at the mid-LV anteroseptal wall). The LV ejection fraction was 70.1%. (A) On LGE images, multifocal, patchy delayed enhancement was noted in a thickened myocardium, mainly located at mid septum (arrows). (B-E) On the T1 mapping sequence, the global native T1 and ECV values were significantly increased (B) (native T1=1234.5 ms) (D) (ECV=41.0%). The T2 values did not increase (E) (T2=50 ms). The native T1 and ECV values of the thickened myocardium were even higher than in other areas (native T1=1273.1 ms, ECV=46%). (A) LGE image, (B) native T1 map, (C) post T1 map, (D) ECV map, and (E) T2 map. HCMP: hypertrophic cardiomyopathy, ECV: extracellular volume, LV: left ventricular, LGE: late gadolinium enhancement.

Myocarditis

Inflammation of the myocardium can have a variety of etiologies, which are commonly viral, but is also caused by toxins, drugs, and autoimmune processes [25].

Findings on MRI include myocardial edema, wall motion abnormalities, and patchy subepicardial (96%) and midwall LGE (84%). The typical location of LGE is the lateral and inferior walls (73%), followed by the anterior wall [26].

T1 mapping provides improved detection of edema in acute myocarditis and subclinical low-grade myocardial inflammation compared to that with conventional T2 and LGE imaging [26].

T1 mapping has also shown sensitivity in identifying myocardial abnormalities caused by inflammation and fibrosis. T2 mapping specifically detects increased myocardial water content [19].

Both native T1 mapping and ECV are superior to the Lake Louise criteria for the diagnosis of myocarditis, although native T1 mapping can be influenced by the time between the onset of symptoms and MRI scanning [27].

A previous study involving patients with suspected systemic lupus erythematosus myocarditis demonstrated significantly increased native T1 and T2 values compared to those in normal control subjects. T1 and T2 mapping provides effective, noninvasive, and radiation- and contrast-free evaluation of myocarditis [28] (Fig. 3).

Fig. 3
Eosinophilic myocarditis. A 65-year-old man with myocarditis presented with symptoms of chest discomfort, dyspnea, and fever for three days. He had increased peripheral blood eosinophils (8.1%). Magnetic resonance imaging showed global LV hypokinesia with reduced systolic function (40%). (A) LGE images showed multifocal, mild patchy delayed enhancement in the mid-LV epicardial layer (arrows). (B-E) T1 mapping showed diffusely increased native T1 (B) (1423.0 ms) and ECV (D) (39.9%) values, probably due to myocardial inflammation and fibrosis; moreover, increased T2 (E) (70.8 ms) values were noted, probably due to myocardial edema. A small pericardial effusion (arrow) and bilateral pleural effusion were also noted. (A) LGE image, (B) native T1 map, (C) post T1 map, (D) ECV map, and (E) T2 map. ECV: extracellular volume, LV: left ventricular, LGE: late gadolinium enhancement.

Peripartum cardiomyopathy

Peripartum cardiomyopathy (PPCM) is defined as the onset of heart failure in the last month of pregnancy or up to five months postpartum without previous history of heart disease [29].

PPCM is probably associated with pregnancy-related reduced suppressor T cell activity, which may trigger autoimmune myocardial inflammation or activation of myocarditis. Recovery usually occurs in 50% of patients within six months [30].

LGE is evident in the mid-myocardium, mainly in the anterior and anterolateral segments [31]. LGE parallels irreversible myocardial injury and may contribute to persistent myocardial dysfunction, hampering recovery in some cases. However, Schelbert et al. [32] noted that LGE was uncommon in PPCM.

T1 mapping will show increased values; this is especially useful in patients with unremarkable LGE. Patients with edema have increased native T2 values compared with those in normal subjects [33, 34] (Figs. 4 and 5).

Fig. 4
PPCM. A 30-year-old woman with PPCM underwent emergency cesarean section due to preterm labor following emergency vascular embolization for uterine atony. Chest pain and dyspnea suddenly developed, and magnetic resonance imaging showed mild LV enlargement with severe hypokinesia and reduced LV systolic function (LV ejection fraction=39.9%). (A) No abnormal delayed enhancement of the myocardium was noted on the LGE image. (B-E) On the T1-mapping sequence, diffusely (not segmentally) increased global myocardial native T1 values (B) (1532.3 ms), ECV (D) (36.7%), and T2 values (E) (60 ms) were suggestive of myocardial edema. A moderate pericardial effusion was also noted. After the management of heart failure, her symptoms subsided. (A) LGE image, (B) native T1 map, (C) post T1 map, (D) ECV map, and (E) T2 map. PPCM: peripartum cardiomyopathy, LV: left ventricular, ECV: extracellular volume, LGE: late gadolinium enhancement.

Fig. 5
Follow-up MRI of peripartum cardiomyopathy. Follow-up MRI performed after two months showed decreased LV size and systolic LV dysfunction (LV ejection fraction=53.6%) without regional wall motion abnormalities. (A) No delayed enhancement of the LV myocardium was noted. (B-E) On T1-mapping, the global native T1 values decreased (B) (1532.3 ms to 1271.7 ms); the global ECV and T2 values also decreased (36.8% to 29.9%, 60 ms to 46.1 ms, respectively). (A) Late gadolinium enhancement image, (B) native T1 map, (C) post T1 map, (D) ECV map, and (E) T2 map. LV: left ventricular, MRI: magnetic resonance imaging, ECV: extracellular volume.

Amyloidosis

Amyloidosis is a systemic disease characterized by the extracellular deposition of pathologic, insoluble amyloid protein in organs and tissues throughout the body.

Cardiac involvement is common, with an immunoglobulin light chain associated with B-cell dyscrasias and transthyretin types of amyloidosis, and is associated with a poor prognosis [8].

Myocardial thickening is an important finding in cardiac amyloidosis with a restrictive diastolic filling pattern. Systolic dysfunction is usually seen in the late phase of the disease [35].

Endomyocardial biopsy is the gold standard for diagnostic testing, revealing infiltration and expansion of the interstitial space by amyloid deposits. However, it is rarely performed due to procedural risks and the possibility of sampling error. Diagnosis is often dependent on non-invasive imaging [36].

LGE imaging typically shows global transmural or subendocardial enhancement with a thickened myocardium and without territorial distribution [29].

ECV expansion in cardiac amyloidosis reaches extremely high values (on the order of 0.5 to 0.6). The myocardial amyloid load also has a relatively strong effect on native T1, which extends the utility of T1 mapping to patients with contraindications to contrast agent [16] (Fig. 6).

Fig. 6
Cardiac amyloidosis. A 62-year-old man diagnosed with transthyretin cardiac amyloidosis presented with generalized weakness and a tingling sensation in his hands. He was suspected to have diffuse infiltrative disease upon echocardiography; magnetic resonance imaging showed a diffusely thickened LV myocardium with normal wall motion and systolic function (LV ejection fraction=60%). (A) LGE images showed diffuse, global subendocardial delayed enhancement of the entire LV and right ventricular side of the interventricular septum (arrows). (B-E) The global native T1 was mildly increased (B) (native T1=1453.8 ms) and ECV LV values were markedly increased (D) (ECV=60.9%) on the T1-mapping sequence. The T2 value was slightly increased (E) (58.1 ms). (A) LGE image, (B) native T1 map, (C) post T1 map, (D) ECV map, and (E) T2 map. ECV: extracellular volume, LV: left ventricular, LGE: late gadolinium enhancement.

Fabry disease

Anderson-Fabry disease is an X-linked metabolic disorder associated with alpha-galactosidase deficiency and intracardiac glycolipid accumulation [37].

The typical cardiac manifestations include concentric biventricular hypertrophy, thickening of the atrioventricular valves, and an inferolateral mid-wall pattern of LGE due to focal fibrosis [21, 38].

The disease process involves intramyocyte accumulation of lipids, which shortens the native T1 time. The extracellular matrix is not altered; thus, ECV is found within a normal range, comparable to that in controls (Fig. 7).

Fig. 7
Fabry disease. A 37-year-old man diagnosed with Fabry disease was suspected to have diffuse infiltrative disease due to a diffuse hypertrophied myocardium with heterogeneous signal on echocardiography. Magnetic resonance imaging showed diffusely thickened LV myocardium with normal wall motion and systolic function (LV ejection fraction=69.7%). (A) LGE images showed subendocardial delayed enhancement in anterior anterolateral segments of the mid-ventricle (arrows). (B-E) Slightly decreased native T1 values on inferolateral and inferior mid-LV segments (B) (1155.7 ms) with mildly increased global native T1 (B) (1215.1 ms) and ECV (D) (29.3%). The T2 value was within normal range (E) (49.4 ms). (A) LGE image, (B) native T1 map, (C) post T1 map, (D) ECV map, and (E) T2 map. ECV: extracellular volume, LV: left ventricular, LGE: late gadolinium enhancement.

Iron overload

Thalassemia is an inherited hemoglobin disorder that requires regular blood transfusions, which may lead to iron overload in tissues including the heart. Patients may develop cardiomyopathy, which is the principal cause of mortality. Most of the observed cardiac problems are reversible in the early stages of the disease through chelation therapy [39].

Voskaridou et al. [40] in a study involving 106 patients with beta thalassemia, found that comparison of heart T2 and serum ferritin values showed a negative correlation. Thalassemia major patients showed a significant negative correlation between the above two parameters; however, T2-values of the myocardium were significantly lower in thalassemia major than in thalassemia intermedia patients. Sado et al. [41] performed T1 mapping in cardiac iron overload patients and noted that T1 values were lower in affected patients than in healthy volunteers (836±138 ms vs. 968±632 ms, p<0.001). They concluded that myocardial T1 mapping is an alternative method for cardiac iron quantification, with potential for improved detection of mild iron loading and with superior reproducibility.

Another study involving 106 patients with thalassemia major compared myocardial T1 against T2 and T2* for myocardial iron characterization. It was observed that, in patients with myocardial iron overload, T1 values were shortened compared to those in normal volunteers, with linear correlations between T2 and T2* (r=0.82; p<0.001) and between T1 and T2* (r=0.83; p<0.001) [42] (Fig. 8).

Fig. 8
Iron overload. A 19-year-old man was diagnosed with beta thalassemia at the age of 18 months. Magnetic resonance imaging showed a diffusely thinned left ventricular myocardium with mildly reduced systolic function (LV ejection fraction=49%). (A) LGE images showed delayed, subtle subepicardial enhancement in the mid-ventricular septum (arrows). (B-E) T1 mapping images showed markedly decreased global native T1 values (B) (758.9 ms), suggesting significant iron overload. The ECV value was significantly increased (D) (35.6%) and the T2 value was significantly decreased (E) (35.1 ms). (A) LGE image, (B) native T1 map, (C) post T1 map, (D) ECV map, and (E) T2 map. ECV: extracellular volume, LV: left ventricular, LGE: late gadolinium enhancement.

Short summary of this manuscript

T1 and T2 mapping are useful techniques to diagnose various nonischemic cardiomyopathies.

Notes

Conflicts of Interest:The authors declare that they have no conflict of interest.

Acknowledgments

This study was supported by a faculty research grant of Yonsei University College of Medicine (6-2016-0077).

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