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Table 1 Characteristics of the included studies in the meta-analysis

From: Cardiovascular magnetic resonance native T2 and T2* quantitative values for cardiomyopathies and heart transplantations: a systematic review and meta-analysis

First author, year

Disease (n)/ Control (n)

T2/T2* (ms) Disease

T2/T2* (ms) Control

P value

ROI placement

Seq.

Qual.

Population

Myocardial Infarction (T2*) 1.5 T Philips

 Durighel 2017 [39]

H+: 30

33.8 ± 14.1a

45.0 ± 9.4c

0.16bc

1 SAx at infarct

GRE

1,0,2

STEMI patients referred for CMR in 7 days post-PCI. Haemorrhagic hypointense LGE infarct (H+) or non-haemorrhagic infarcts (H-). Remote as control.

H-: 30/30

54.0 ± 17.9b

1.5 T Siemens

 Bulluck 2016 [40]

CF0: 15

11.3 ± 1.5

32.3 ± 3.9

 

Segments in 3 SAx

 

1,0,2

STEMI patients 4d (F0) and 5 m (F1) post-PCI. Hypo-core (C) (T2* < 20 ms), infarct (I) 2SD above remote myocardium. Remote as control.

CF1: 15

15.0 ± 1.5

33.3 ± 3.1

IF0: 13

29.7 ± 10.0

IF1: 13/28

32.0 ± 5.8

 Bulluck 2017 [41]

26/26

13 ± 3

33 ± 4

<  0.01

Segments

 

2,0,2

STEMI patients PCI < 2 h, CMR at 4d post-PCI. Hypo-core (T2* < 20 ms) measured. Remote as control.

 Carberry 2017 [42]

CF0: 203

14.2 ± 3.6

31.5 ± 2.4

 

3 SAx

 

2,0,2

STEMI patients 2d (F0) and 6 m (F1) post-PCI. Hypo-core (C) (T2* < 20 ms) and infarct zone (Z). Remote as control.

CF1: 203

16.6 ± 2.1

ZF0: 203

32.4 ± 7.6

ZF1: 203/203

25.7 ± 4.4

 Carrick 2016 [43]

CF0: 30

17.8 ± 6.0

31.9 ± 2.0

 

3 SAx

 

1,0,3

STEMI patients 4–12 h (F0), 3d (F1), 10d (F2) and 7 m (F3) post-PCI. T2* in infarct zone (Z) (T2 > 2SD remote) and infarct core (C) (center in the infarct zone with mean T2/T2* value <2SD T2/T2* periphery). Remote as control.

CF1: 30

14.1 ± 4.1

32.9 ± 1.9

CF2: 30

16.7 ± 5.9

32.6 ± 1.6

CF3: 30

18.9 ± 6.2

32.4 ± 2.3

ZF0: 30

29.2 ± 5.8

ZF1: 30

26.6 ± 4.8

ZF2: 30

28.6 ± 3.3

ZF3: 30/30

29.2 ± 4.0

 Kali 2013 [44]

H+: 7

15.9 ± 4.5a

35.2 ± 2.1c

<  0.01ac

SAx whole LV

GRE

1,0,2

STEMI patients within 3 days post-PCI. LGE+ infarcts. Hypo-cores on the T2*-weighted image <2SD reference ROI (H+), otherwise non-haemorrhagic (H-). Remote as control.

H-: 7/14

37.8 ± 2.5b

<  0.05bc

 Mohammadzadeh 2018 [45]

I: 20

35.5 ± 3.6a

29.4 ± 4.5c

<  0.01ac

3 SAx & 2 LAx

 

1,0,2

NSTEMI patients ≥6 months after MI. T2* from infarct (I) (LGE+) and peri-infarct (P). Remote as control.

P: 20/20

30.7 ± 4.9b

 

NSbc

 

 Robbers 2017 [46]

C: 43

26.3 ± 10.7

27.3 ± 6.9

 

1 SAx at infarct

 

2,0,2

STEMI patients 4-6d post-PCI. Infarct core (C) (LGE+ based) and border zone (B). Remote as control.

B: 43/43

30.7 ± 7.7

 Roghi 2015 [47]

H + F0: 7

17

  

3 SAx at necrotic area

GRE

1,0,1

STEMI patients < 5 days (F0) and 6 m (F1) post-PCI. LGE+ as myocardial haemorrhagic (H+) (dark core at T2*) or non-haemorrhagic (H-).

H + F1: 6

18

H-F0: 8

31

H-F1: 8

31

 Yilmaz 2013 [48]

I: 14

24.0 ± 12.4

32.0 ± 4.9

 

3 SAx at infarct

GRE

1,0,2

STEMI patients 2–7 days post-PCI. Infarct core (LGE+ with hyperenhanced T2 area) and peri-infarct zone (P) (LGE area without hyperenhanced T2 area). Remote as control.

P: 14/14

35.7 ± 10.7

1.5 T GE

 Zia 2012 [49]

F0: 62

32.4a

37.4d

<  0.01ad

3 SAx at infarct

GRE

2,0,2

STEMI patients within 2d (F0), 3w (F1) and 6 m (F2) post-PCI. LGE+ infarct. Remote as control.

F1: 62

37.7b

38.4e

NSbe

F2: 62/62

37.3c

38.2f

NScf

Myocardial Infarction (T2*) 3 T Philips

 Chen 2019 [50]

F0: 22

22.0 ± 3.1

31.2 ± 1.6

 

3 SAx

TFE

2,0,2

STEMI patients 1d (F0), 3d (F1), 7d (F2) and 30d (F3) post-PCI. Infarct values (LGE+ based). Remote as control.

F1: 22

23.9 ± 3.3

30.0 ± 0.7

F2: 22

22.1 ± 4.0

30.4 ± 0.8

F3: 22/22

21.5 ± 2.8

30.3 ± 0.7

 Zaman 2014 [51]

6/15

16.1 ± 7.6

24.2 ± 6.7

 

Stack of SAx

GRE

2,0,2

STEMI patients 2d post-PCI. Intramyocardial haemorrhage (hypo-core on LGE+).

Myocardial Infarction (T2) 1.5 T Philips

 Nakamori 2019 [52]

14

45

  

Mean 16 AHA

 

1,0,1

Patients with coronary artery disease.

 Tahir 2017 [53]

F0: 67

84 ± 10

55 ± 3

 

Mid-SAx

TSE

2,0,3

Acute MI patients 8d (F0), 7w (F1), 3 m (F2) and 6 m (F3) post-PCI. Infarct (LGE+ area without hypo-intense area). Remote as control.

F1: 50

68 ± 9

F2: 44

61 ± 7

F3: 45/67

58 ± 4

1.5 T Siemens

 Bulluck 2016 [40]

F0: 15

49.7 ± 5.7

49.3 ± 2.5

 

3 SAx

 

1,0,2

STEMI patients 4d (F0) and 5 m (F1) post-PCI. Hypo-core (T2* < 20 ms). Remote of another population as control.

F1: 15/13

47.3 ± 4.1

46.7 ± 2.5

 Bulluck 2017 [41]

H + C: 26

50 ± 4

51 ± 3

 

3 SAx

 

2,0,2

STEMI patients 4d post-PCI. Hypo-core (H+) (T2* < 20 ms) and without (H-) in infarct core (C) (LGE+) or salvage (S). Remote as control.

H + S: 26

66 ± 6

50 ± 3

H-C: 13

57 ± 4

H-S: 13

66 ± 7

H + R: 26

H-R: 13

 Carberry 2017 [54]

F0: 283

66.3 ± 6.1a

49.7 ± 2.3c

<  0.01ac

SAx whole LV

T2-prep tFISP

1,0,2

STEMI patients 2d (F0) and 6 m (F1) post-PCI. Infarct (SI > 5SD above remote region). Remote as control.

F1: 283/283

56.8 ± 4.5b

<  0.01bc

 Carrick 2016 [43]

CF0: 30

55.5 ± 6.9

49.5 ± 2.5

 

SAx

T2-prep tFISP

1,1,3

STEMI patients 4-12 h (F0), 3d (F1), 10d (F2) and 7 m (F3) post-PCI. Infarct zone (I) (T2 > 2SD above remote) and infarct core (C) (center infarct with a mean T2/T2* value >2SD below periphery).

CF1: 30

51.8 ± 4.6

CF2: 30

59.2 ± 3.6

IF0: 30

62.8 ± 6.7

IF1: 30

61.4 ± 4.1

IF2: 30

68.1 ± 3.7

IF3: 30/50

54.0 ± 2.8

 Carrick 2016 [55]

171

54 ± 5

  

SAx whole LV

T2-prep tFISP

2,0,2

STEMI patients 2d post-PCI. Infarct core (T1 < 2SD of periphery).

 Haig 2018 [56]

C: 245

53.9 ± 4.8

49.7 ± 2.1

 

SAx whole LV

T2-prep tFISP

1,0,3

STEMI patients 2d post-PCI. Infarct zone (Z) (T2 > 2SD above remote) and core (C) (center infarct with a mean T2/T2* > 2SD below periphery). Remote as control.

Z: 245/245

62.9 ± 5.1

 Hausenloy 2019 [57]

I: 48

66 ± 6

50 ± 3

 

1 SAx

 

1,0,1

STEMI patients 4d post-PCI. Infarct (I) (LGE area+) and salvaged (S) (LGE- epicardial to infarcted). Remote as control.

S: 48/ 48

64 ± 6

 Krumm 2016 [58]

22/10

83 ± 23

50 ± 6

 

3 SAx

FSE

1,0,2

STEMI patients 1-5d post-PCI. Infarct (LGE+ based).

 McAlindon 2014 [59]

40/40

71

54

 

3 SAx

T2-prep SSFP

2,0,2

STEMI patients 1-4d post-PCI. Myocardial edema (area with abnormal SI). Remote as control.

 Masci 2018 [60]

C: 163

47.3 ± 3.8

45.5 ± 3.0

 

1 SAx at infarct

T2-prep SSFP

1,0,2

STEMI patients 2.7 days (median) post-PCI. Infarct (I) (LGE+ SI > 5SD remote) and infarct core (C) (hypo-core in LGE+). Remote as control.

I: 163/163

62.8 ± 6.4

 Park 2013 [61]

20/7

67.9 ± 9.3

52.4 ± 3.0

 

SAx whole LV

T2-prep SSFP

2,0,2

Acute MI patients scanned < 7 days post-PCI. Infarct (LGE+ SI > 5SD remote).

 Tessa 2018 [62]

47/47

69 ± 9

51.9 ± 2.9

<  0.01

3 SAx & 2 LAx

T2-prep tFISP

1,0,2

Acute NSTEMI patients before coronary angiography. Infarct (LGE > 2SD remote). Remote as control.

 Verhaert 2014 [26]

27/21

69 ± 6

55.5 ± 2.3

 

3 SAx & 2 LAx

T2-prep SSFP

2,0,2

STEMI and NSTEMI patients 2.1d (mean) after hospital admission. Infarct (LGE+).

 White 2014 [63]

40/40

73.1 ± 6.1

50.1 ± 2.0

 

SAx whole LV

T2-prep SSFP

2,0,2

STEMI patients 3-6d post-PCI. Infarct (LGE+). Remote as control.

1.5 T GE

 Zia 2012 [49]

F0: 62

56.7a

43.4d

<  0.01ad

5 SAx at infarct

T2-prep SI

2,0,2

STEMI patients 2d (F0), 3w (F1) and 6 m (F2) post-PCI. LGE+ segments. Remote as control.

F1: 62

51.8b

39.5e

<  0.01be

F2: 62/62

39.8c

39.5f

NScf

Myocardial Infarction (T2) 3 T Philips

 An 2018 [64]

F0: 20

66.7 ± 4.7a

53.6 ± 5.3e

<  0.05ae

3 SAx

GraSE

2,0,2

STEMI patients 1d (F0), 3d (F1), 7d (F2) and 30d (F3) post-PCI at infarct.

F1: 20

73.6 ± 4.4b

<  0.05be

F2: 20

68.4 ± 4.2c

<  0.05ce

F3: 20/12

65.0 ± 5.4d

<  0.05de

 Zaman 2014 [51]

6/15

81 ± 52

39.1 ± 6.0

 

SAx whole LV

SE

2,0,2

STEMI patients 2d post-PCI. Edematous myocardium (T2W > 2SD above SI remote).

3 T Siemens

 Bulluck 2016 [65]

21

58.4 ± 7.9

  

SAx whole LV

 

1,0,1

STEMI patients 4-6d post-PCI. Segments ≥50% transmural LGE.

 Fischer 2018 [66]

26/10

40.7 ± 4.0

38.4 ± 1.7

 

Basal and mid-SAx

GRE

3,0,2

Patients with an untreated vascular territory of > 50% diameter stenosis. Territories affected by this stenosis.

 Layland 2017 [67]

73/73

57 ± 5

45 ± 3

<  0.01

3 SAx

T2-prep tFISP

1,0,2

NSTEMI patients 6.5d (mean) after invasive management. Infarct (LGE+ > 2SD remote). Remote as control.

 Van Heeswijk 2012 [68]

11/10

61.2 ± 10.1

38.5 ± 4.5

 

Mid-SAx

T2-prep GRE

1,0,2

STEMI patients in subacute phase post-PCI. Infarct (area on LGE+ > 3SD remote).

Heart Transplantation (T2) 1.5 T Siemens

 Butler 2015 [69]

B-: 58

57 ± 6

  

Septal SAx

FSE

2,0,1

Heart transplant patients classified on EMB grades between negative (B-) and positive (B+) biopsy.

B+: 15

63 ± 6

 Dolan 2018 [70]

61/14

50.5 ± 3.4

45.2 ± 2.3

<  0.01

Mean 16 AHA

T2-prep SSFP

1,1,2

Heart transplant patients for regular follow-up.

 Dolan 2019 [71]

R-: 36

49.2 ± 4.0

45.2 ± 2.3

 

Mean 16 AHA

T2-prep SSFP

1,2,2

Heart transplant patients classified between without (R-) and with acute cardiac allograft rejection (R+).

R+: 23/14

52.4 ± 4.7

 Markl 2013 [72]

0R: 8

53.4 ± 1.8

52.2 ± 1.8

 

Mean 16 AHA

T2-prep SSFP

1,1,2

Heart transplant patients with no rejection (0R) or mild rejection (1R).

1R: 2/14

56.1 ± 1.5

 Miller 2014 [73]

0&1R: 22

57.0 ± 3.2a

54.1 ± 2.0c

<  0.01ac

Mean mid-SAx

T2-prep SSFP

3,2,2

Heart transplant patients classified based on biopsy: 0&1R = absence of rejection and 2R = presence of rejection.

2R: 22/10

58.8 ± 3.5b

<  0.01bc

 Miller 2019 [74]

R-: 26

47.0 ± 1.7

  

Mid-SAx excluding LGE+

T2-prep SSFP

2,0,1

Heart transplant patients classified as no rejection (R-), biopsy negative rejection (BNR; allograft rejection with normal biopsy), acute cellular rejection (ACR; 2R or 3R cellular rejection, or treated 1R) and anti-body mediated rejection (AMR; biopsy with grade 2 or 1 with clinically impression of AMR).

BNR: 12

51.8 ± 2.4

ACR: 5

53.4 ± 3.1

AMR: 3

55.2 ± 2.8

 Usman 2012 [27]

0R: 46

52.5 ± 2.2

52.2 ± 3.4

 

Mean 16 AHA

T2-prep SSFP

1,0,2

Heart transplant patients classified based on EMB transplant rejection grades: 0R = no rejection, 1R = mild rejection, 2R = moderate rejection and 3R = severe rejection.

1R: 17

53.1 ± 3.3

2R: 3

59.6 ± 3.1

3R: 1/14

60.3

 Vermes 2018 [75]

B-: 24

51.8 ± 2.8a

51.0 ± 3.1c

NSac

Mean 16 AHA

T2-prep SSFP

1,0,2

Heart transplant patients classified based on EMB transplant rejection grades between negative (B-) and positive (B+).

B+: 7/34

56.5 ± 5.2b

<  0.05bc

 Yuan 2018 [76]

58/20

47.7 ± 2.8

44.5 ± 1.6

<  0.01

Mean basal and mid-SAx

T2-prep SSFP

3,2,2

Heart transplant patients without EMB proven rejection.

1.5 T GE

 Bonnemains 2013 [77]

0R: 14

55.0 ± 2.3

  

Septal mid-SAx

FSE

2,0,1

Heart transplant patients classified based on EMB transplant rejection grades: 0R = no rejection, 1R = mild rejection and 2&3R = moderate & severe rejection.

1R: 42

64.1 ± 11.0

2&3R: 19

72.1 ± 9.0

 Odille 2015 [78]

9

62.2 ± 11.2

  

Mean mid-SAx

FSE

1,0,1

Heart transplant patients without biopsy.

Iron Overload (T2*) 1.5 T Philips

 Desai 2015 [79]

38/13

41.6 ± 13.4

38.4 ± 14.4

0.91

Septal mid-SAx

 

1,2,2

Clinically stable sickle cell disease subjects.

 Fragasso 2011 [80]

TM: 99

27 ± 15

  

Mean septal 3 SAx

 

2,0,1

Three groups of multi-transfused patients: all TM, all TI patients and 60% of the acquired anemia patients were on chelation therapy.

TI: 20

30 ± 11

AA: 10

33 ± 11

 Kritsaneepaiboon 2017 [81]

42/20

35.7 ± 6.9

36.7 ± 3.0

0.63

Septal mid-SAx

GRE

1,0,2

Iron-overloaded patients suffering from primary or secondary hemochromatosis referred for cardiac siderosis screening or follow up.

 Krittayaphong 2017 [82]

200

37.8 ± 7.0

  

Septal mid-SAx

GRE

1,0,1

Thalassemia patients treated with blood transfusions (85%) and chelation therapy (76%).

 Portillo 2013 [83]

16

28.7 ± 5.7

  

Mean septal 3 SAx

GRE

1,0,1

Polytransfused patients and one anemia patient.

 Saiviroonporn 2011 [84]

50

31.4 ± 13.8

  

Septal mid-SAx

GRE

1,0,1

Regular transfused TM patients on iron chelation therapy.

 Seldrum 2011 [85]

19/8

22 ± 11

40 ± 10

<  0.01

Septal mid-SAx

GRE

3,1,2

Chronic anaemia patients on transfusion treatment.

 Soltanpour 2018 [86]

60

23.8 ± 12.1

   

GRE

2,0,1

Regular transfused ß-TM patients receiving chelation therapy.

1.5 T Siemens

 Acar 2012 [87]

22

23.7 ± 11.2

  

Mean mid-SAx

GRE

1,0,1

Regular transfused ß-TM diagnosed patients (every 3–4 weeks) and receiving chronic chelation therapy.

 Alam 2016 [88]

104/20

30.0 ± 10.5

32.7 ± 6.4

0.20

Septal mid-SAx

 

2,0,2

Transfusion dependent anemia patients referred for siderosis screening.

 Alp 2014 [89]

38

22.9 ± 13.3

    

1,0,1

Regular transfused ß-TM patients (≥ 15/year) and receiving chelation therapy.

 Azarkeivan 2013 [90]

156

24.6 ± 15.1

  

Septal mid-SAx

GRE

1,0,1

Regular transfused TM patients and receiving chelation therapy.

 Barzin 2012 [91]

33

20.4 ± 12.1

  

Septal mid-SAx

GRE

1,0,1

TM patients transfused for a least 15 years.

 Bayraktaroglu 2011 [92]

47

14.1

  

Mean septum

 

1,0,1

Regular transfused TM patients and receiving chelation therapy with cardiac involvement (T2* < 20 ms).

 Camargo 2016 [93]

7/17

15.4 ± 6.0

28.0 ± 4.0

<  0.01

Septal mid-SAx

GRE

3,0,2

Patients with myocardial iron overload (T2* < 20 ms), regardless of chelating therapy status.

 Cassinerio 2012 [94]

67

24.5 ± 12.7

  

Septal mid-SAx

GRE

1,0,1

ß-TM patients treated with iron chelators

 Delaporta 2012 [95]

44/143

11.0 ± 5.6

33.5 ± 5.1

<  0.01

  

1,0,2

ß-TM patients with LVEF < 50%, regularly transfused (2–3 weeks), on chelation therapy and cardiac siderosis (T2* < 20 ms). ß-TM patients without cardiac siderosis (T2* ≥ 20 ms) as controls.

 Di Odoardo 2017 [96]

21/34

12.1 ± 4.7

35.7 ± 9.5

<  0.01

Septal mid-SAx

GRE

2,0,2

ß-TM patients on long-term iron-chelation therapy with cardiac involvement (T2* < 20 ms). ß-TM patients without cardiac involvement (T2* ≥ 20 ms) as controls.

 Djer 2013 [97]

30

24.3 ± 11.2

  

Mean septum

 

2,0,1

TM patients with at least 13 years transfusion history and chelation therapy.

 Ebrahimpour 2012 [98]

TM: 49

24.9 ± 13.6

  

Septal mid-SAx

GRE

2,0,1

ß-TM and TI patients on regular transfusion therapy.

TI: 29

29.7 ± 12.8

 Eghbali 2017 [99]

56

22.9 ± 7.3

    

1,0,1

TM patients on chelation therapy.

 Fahmy 2015 [100]

70

32.1 ± 12.1

  

Mean septal 3 mid-SAx

GRE

1,0,1

ß-TM and sickle cell anaemia patients on regular transfusion program and iron chelation therapy referred for cardiac/liver siderosis.

 Feng 2013 [101]

106

22.3 ± 24.0

  

Septal mid-SAx

GRE

1,0,1

Regularly transfused TM patients receiving iron chelation therapy.

 Fernandes 2011 [102]

60

31.2 ± 10.3

  

Septal mid-SAx

GRE

2,0,1

TM patients receiving chronic transfusion therapy and iron chelation regimen.

 Fernandes 2016 [103]

56

34.7 ± 11.8

   

GRE

1,0,1

TM, hemochromatosis and sickle cell anemia patients on transfusion therapy.

 Garceau 2011 [104]

22/23

11 ± 4

33 ± 8

 

Mean septal basal and mid-SAx

 

2,0,2

Chronically transfused ß-TM patients or Diamond-Blackfan anaemia, with cardiac involvement (T2* < 20 ms). Patients without cardiac involvement (T2* ≥ 20 ms) as controls.

 Git 2015 [105]

50

25.3 ± 1.6

  

Mid-SAx

GRE

1,0,1

Patients (80% TM) referred for iron overload assessment.

 Hanneman 2013 [106]

108

24.3 ± 11.5

  

Mean 16 AHA

GRE

1,0,1

Transfusion dependent anaemia patients receiving iron chelation therapy.

 Hanneman 2015 [107]

19/10

24.1 ± 9.2

35.1 ± 5.4

<  0.01

Septal mid-SAx

GRE

3,0,2

TM patients receiving regularly blood transfusions and treatment with iron chelation therapy.

 Junqueira 2013 [108]

30

37.6 ± 7.1

  

Septal mid-SAx

 

2,0,1

Sickle cell disease patients referred of whom 27 receiving transfusions.

 Kayrak 2012 [109]

22

21.7 ± 9.0

  

Mid-SAx

GRE

1,0,1

ß-TM patients regularly transfused (every 3–4 weeks) and receiving chronic chelation therapy.

 Kirk 2011 [110]

45

23.7 ± 16.9

  

Septal mid-SAx

 

1,0,1

ß-TM patients receiving chelation therapy (except 1).

 Kucukseymen 2017 [111]

56

28.3 ± 13.7

    

1,0,1

TM patients transfused every 3–4 weeks.

 Li 2017 [112]

24

32.7 ± 16.7

  

Septal mid-SAx

 

1,0,1

Transfusion-dependent ß-TM patients.

 Liguori 2015 [113]

41/145

11.0 ± 8.1

32.1 ± 5.7

 

Septal mid-SAx

GRE

1,0,2

Regular transfused TM patients under iron chelation therapy and occasionally transfused TI patients with cardiac involvement (T2* < 20 ms). Patients without cardiac involvement (T2* ≥ 20 ms) as controls.

 Mehrzad 2016 [114]

S: 11

8.1 ± 1.4

26.9 ± 6.4

 

Mid-SAx

 

1,0,2

Transfusion dependent ß-TM patients with LVEF > 50% classified between severe (S) (T2* < 10 ms) and moderate (M) (10 ms < T2* < 20 ms) cardiac iron overload. Patients without cardiac involvement (T2* > 20 ms) as controls.

M: 23/16

14.1 ± 2.6

 Ozbek 2011 [115]

21

21.7 ± 9.3

  

Mid-SAx

GRE

1,0,1

Regularly transfused (every 3–4 weeks) TM patients receiving chronic chelation treatment.

 Quatre 2014 [116]

48

21.2 ± 10.1

  

Septum

GRE

2,0,1

Multi transfused TM and TI patients. 45/48 were receiving iron chelation therapy.

 Roghi 2015 [117]

43

31 ± 15

  

Septal mid-SAx

GRE

2,0,1

TM patients

 Sado 2015 [118]

88/67

27 ± 11

31 ± 4

<  0.01

Septal mid-sax

 

3,0,2

Suspected iron overload patients with several underlying diseases.

 Sakuta 2010 [119]

19

45.1 ± 22.4

  

Mid-SAx

 

1,0,1

Transfusion-dependent patients without consecutive oral chelation therapy.

 Torlasco 2018 [120]

138

38.5 ± 14.1

  

Septal mid-SAx

 

1,0,1

TM patients.

1.5 T GE

 Chen 2014 [121]

50

26.1 ± 23.0

  

Mean septum

 

2,0,2

TM patients transfused every 2–4 weeks.

 de Assis 2011 [122]

115

25.0 ± 14.2

  

Mean septum

GRE

1,0,1

Chronically transfused TM and TI patients.

 de Assis 2011 [123]

115

14.3 ± 2.4

  

Mean septum

GRE

2,0,1

ß-TM patients transfused every 2–3 weeks.

 de Sanctis 2016 [124]

6/8

17.5 ± 6.9

36.5 ± 12.5

<  0.01

  

3,2,2

Regular transfused TM patients and receiving chelation therapy with acquired hypogonadotropic hypogonadism (AHH). TM patients without AHH and T2* > 20 ms as controls.

 Marsella 2011 [125]

149

19.3 ± 11.9

  

Mean 16 AHA

 

2,0,1

TM patients with transfusions every 2–4 week and iron chelation with heart dysfunction.

 Mavrogeni 2013 [126]

30

37.2

  

Septal mid-SAx

GRE

1,0,1

Transfused TM patients (every 2–3 weeks) and receiving iron chelation therapy.

 Meloni 2012 [127]

38

30.8 ± 11.3

  

Mean 16 AHA

GRE

1,0,2

Transfusion dependent patients enrolled in the myocardial iron overload in thalassemia network.

 Meloni 2014 [128]

138/329

8.9 ± 2.8

38.7 ± 4.5

 

Mean 16 AHA

GRE

2,0,2

Regularly transfused TM patients with homogeneous myocardial iron overload (all segments T2* < 20 ms). TM without (all segments T2* ≥ 20 ms) as controls.

 Pepe 2018 [129]

481

27.4 ± 12.4

  

Mean 16 AHA

GRE

2,0,1

TM patients.

 Pistoia 2019 [130]

HE: 279

35.0 ± 14.0

  

Mean 16 AHA

GRE

2,0,1

TM patients classified: heterozygotes ß+/ ß0, homozygote ß+ and homozygote ß0

ß+: 154

32.0 ± 21.0

ß0: 238

28.5 ± 23.5

 Pizzino 2018 [131]

28

39.0 ± 9.4

  

Mean 16 AHA

 

2,0,1

Regularly transfused TM patients receiving chelation therapy.

 Positano 2015 [132]

S: 20

7.0 ± 2.4

34.3 ± 5.0

 

Mean 16 AHA

 

1,0,2

TM patients were classified as severe (S) (T2* < 10 ms) or mild-moderate (M) (10 ms ≤ T2* ≤ 20 ms) cardiac involvement. TM patients without cardiac involvement (T2* > 20 ms) as controls .

M: 20/20

15.8 ± 2.4

 Russo 2011 [133]

40/40

29 ± 15

55 ± 13

<  0.05

 

GRE

4,2,2

ß-TM patients receiving regular blood transfusions (2–4 week) and iron chelation therapy.

 Wijarnpreecha 2015 [134]

99

44.3 ± 6.8

  

Mid-SAx

GRE

1,0,1

Non-transfusion dependent thalassemia and receiving < 7 transfusions per year.

1.5 T Vendor unknown

 Barbero 2016 [135]

46

37.7 ± 11.0

    

2,0,1

Regular transfused ß-TM patients receiving iron chelation and follow-up after 4 years.

41.0 ± 15.7

 Bayar 2015 [136]

43/60

13 ± 3

33 ± 10

<  0.01

  

1,0,2

TM patients on regular blood transfusion and iron chelators with cardiac involvement (T2* < 20 ms). TM patients without cardiac involvement (T2* ≥ 20 ms) as control.

 Du 2017 [137]

92

31.9 ± 14.1

    

1,0,1

Aplastic anaemia patients and myelodysplastic syndrome patients with cardiac iron overload, with multiple transfusions.

 Ferro 2017 [138]

45

32.5 ± 12.5

    

1,0,1

Transfused ß-TM patients.

 Karakus 2017 [139]

30/72

14.5 ± 2.1

37.3 ± 12

<  0.01

  

1,0,2

ß-TM and TI patients with transfusion and chelation therapy with cardiac or hepatic iron overload (T2* < 20 ms). Patients without cardiac or hepatic iron overload as controls.

 Karami 2017 [140]

6

16.7 ± 15.4

    

1,0,1

ß-TM patients with regular transfusion and chelation therapy and high serum ferritin levels or severe iron overload

 Monte 2012 [141]

27

27.2 ± 12.3

    

1,0,1

TM patients with LVEF > 55% with transfusions every 3 weeks and iron chelation therapy.

 Parsaee 2017 [142]

55

23.5 ± 9.8

    

1,0,2

TM patients receiving blood transfusions and undergoing iron chelation therapy.

 Pennell 2014 [143]

103

11.4 ± 3.5

    

2,0,2

ß-TM patients with myocardial T2* between 6 and 20 ms, LVEF > 55% and transfusion history.

 Piga 2013 [144]

924

30.1 ± 14.6

    

2,0,1

TM patients.

 Porter 2013 [145]

20

7.7 ± 4.6

   

GRE

2,0,1

Transfusion-dependent TM patients with decreased LVEF and cardiac involvement (T2* ≤ 20 ms).

 Vlachaki 2015 [146]

23

32.8 ± 10.9

  

Septal mid-SAx

 

2,0,1

Regularly ß-TM patients excluding patients with decreased LVEF ≤60% or increased cardiac iron overload (T2* < 8 ms).

 Yuksel 2016 [147]

57

27.6 ± 13.9

  

Septal mid-SAx

GRE

1,0,1

ß-TM patients.

Iron overload (T2*) 3 T Philips

 Kritsaneepaiboon 2017 [81]

42/20

21.7 ± 6.1

23.7 ± 2.4

0.07

Septal mid-SAx

GRE

1,0,21

Iron-overloaded patients suffering from primary or secondary hemochromatosis referred for cardiac siderosis screening or follow up.

3 T Siemens

 Alam 2016 [88]

104/20

18.3 ± 9.0

21.0 ± 4.8

0.14

Septal mid-SAx

 

2,0,2

Transfusion dependent anemia patients referred for siderosis screening.

 Gu 2013 [148]

D+: 33

19.9 ± 2.2

  

Septum

GRE

2,0,1

Myelodysplastic syndrome patients defined as transfusion dependent (D+) or independent (D-).

D-: 40

27.0 ± 2.1

3 T GE

 Meloni 2012 [127]

38

27.6 ± 11.8

  

Mean 16 AHA

 

1,0,2

Transfusion dependent patients enrolled in the myocardial iron overload in thalassemia network.

Iron Overload (T2) 1.5 T Philips

 Kritsaneepaiboon 2017 [81]

42/20

60.3 ± 6.9

58.3 ± 3.2

0.23

Septal mid-SAx

TSE

1,0,2

Iron-overloaded patients suffering from primary or secondary hemochromatosis referred for cardiac siderosis screening or follow up.

 Krittayaphong 2017 [82]

200

58.9 ± 7.3

  

Septal mid-SAx

SE

1,0,1

Thalassemia patients referred for CMR.

1.5 T Siemens

 Feng 2013 [101]

106

48.9 ± 22.2

  

Septal mid-SAx

TSE

1,0,1

Regularly transfused TM patients receiving iron chelation therapy.

Iron overload (T2) 3 T Philips

 Kritsaneepaiboon 2017 [81]

42/20

55.7 ± 6.1

58.0 ± 7.2

0.20

Septal mid-SAx

SE

1,0,2

Iron-overloaded patients suffering from primary or secondary hemochromatosis referred for cardiac siderosis screening or follow up.

3 T Siemens

 Camargo 2016 [93]

7/17

37.9 ± 6.0

45.0 ± 2.0

<  0.05

Septal mid-SAx

T2-prep SSFP

3,0,2

Patients with myocardial iron overload (T2* < 20 ms) regardless of chelating therapy.

Sarcoidosis (T2) 1.5 T Siemens

 Greulich 2016 [149]

61/26

52.3 ± 3.8

49.0 ± 1.6

<  0.01

Mean mid-SAx

T2-prep SSFP

2,2,2

Clinically diagnosed or biopsy proven systemic sarcoidosis patients.

Sarcoidosis (T2) 3 T Philips

 Puntmann 2017 [150]

53/36

54.0 ± 12.2

45.0 ± 10.8

<  0.01

Septal mid-SAx

GraSE

3,0,2

Biopsy proven extra cardiac systemic sarcoidosis patients.

Systemic lupus erythematosus (T2) 1.5 T Siemens

 Mayr 2016 [151]

13/20

51.0 ± 3.3

49.3 ± 2.4

<  0.01

Mid-SAx

T2-prep SSFP

3,0,2

SLE patients.

 Zhang 2015 [152]

24/12

58.2 ± 5.6

52.8 ± 4.4

 

Mid-SAx

T2-prep SSFP

3,0,2

SLE patients.

Systemic lupus erythematosus (T2) 3 T Philips

 Hinojar 2016 [153]

76/46

65 ± 8

45 ± 4

<  0.01

Septal mid-SAx

GraSE

3,2,2

SLE patients with clinical suspected myocarditis.

 Winau 2018 [154]

92/78

51 ± 9

44 ± 4

<  0.01

Septal mid-SAx

GraSE

3,2,2

SLE patients without cardiac disease referred for cardiovascular involvement screening.

Amyloidosis (T2) 1.5 T Siemens

 Kotecha 2018 [155]

AL1: 35

53.2 ± 3.6

48.9 ± 2.0

 

Basal to mid-septum of 4CH

T2-prep SSFP

3,0,2

Amyloidosis patients categorized in systemic AL (1. Cardiac with transmural LGE; 2. Cardiac with subendocardial LGE; 3. No signs of cardiac involvement (CA) and ATTR (AT) (1. TTR gene carrier; 2. Possible CA; 3. Definite CA).

AL2: 37

56.3 ± 4.8

AL3: 28

56.2 ± 5.4

AT1: 11

50.4 ± 3.2

AT2: 12

51.5 ± 3.7

AT3: 163/30

54.7 ± 4.0

 Ridouani 2018 [156]

AL: 24

63.2 ± 4.7a

51.1 ± 3.1c

<  0.01ac

Mean mid-SAx and 4CH

T2-prep SSFP

2,0,2

Amyloidosis patients with cardiac involvement classified as AL or ATTR (AT).

AT: 20/40

56.2 ± 3.1b

<  0.01bc

Anderson-Fabry Disease (T2) 1.5 T Philips

 Messalli 2012 [157]

16

81 ± 3

  

Septum 4CH

 

1,0,1

Genetically confirmed Anderson-Fabry disease patients.

1.5 T Siemens

 Knott 2019 [158]

H+: 24

50.4 ± 3.8a

47.5 ± 2.4c

<  0.05ac

Mean 16 AHA

 

2,1,2

Anderson-Fabry disease patients classified between with (H+) (maximum wall thickness > 12 mm) and without left ventricular hypertrophy (H-).

H-: 20/27

47.8 ± 1.7b

 

NSbc

Hypertrophic Cardiomyopathy (T2*) 1.5 T Philips

 Gastl 2019 [159]

LGE: 75

25.2 ± 4.0

31.3 ± 4.3

 

Septal mid-SAx

FFE

2,2,2

HCM patients classified between with (LGE+) and without LV fibrosis (LGE-).

LGE-: 20/28

28.7 ± 5.3

Hypertrophic Cardiomyopathy (T2*) 3 T GE

 Kanzaki 2016 [160]

16/18

22.3 ± 4.1

21.0 ± 6.4

 

Septal mid-SAx

 

2,0,2

HCM patients with hypertrophied non-dilated LV (LV wall thickness > 13 mm) without other cardiovascular diseases.

Hypertrophic Cardiomyopathy (T2) 1.5 T Philips

 Amano 2015 [161]

21/7

59.8 ± 6.4

48.1 ± 3.2

<  0.01

High T2 SAx

GraSE

1,0,2

HCM patients with maximum LV thickness of ≥15 mm and non-dilated LV asymmetrical hypertrophy without other cardiovascular hypertrophy diseases.

1.5 T Siemens

 Park 2018 [162]

88

55.5 ± 3.2

  

Mean 16 AHA

T2-prep SSFP

2,0,1

HCM patients with maximal LV hypertrophy ≥13 mm and ratio 1.3 maximal thickness to posterior wall without other cause hypertrophy.

Dilated Cardiomyopathy (T2*) 3 T Philips

 Nagao 2015 [163]

E+: 13

30.0 ± 4.0

  

Septal mid-SAx

GRE

1,0,2

DCM patients with LVEF < 45% classified between with (E+) and without major adverse cardiac events (E-).

E-: 33

25.7 ± 4.1

3 T GE

 Kanzaki 2016 [160]

48/18

18.7 ± 3.1

21.0 ± 6.4

 

Septal mid-SAx

 

2,0,2

DCM patients diagnosed with World Health Organization criteria.

Dilated Cardiomyopathy (T2) 1.5 T Philips

 Ito 2015 [164]

R+: 12

61.4 ± 3.1

  

Mean 16 AHA

FSE

2,0,1

DCM patients diagnosed with World Health Organization criteria treated by HF guidelines classified as responders (R+) (ΔLVEF > 15% after 6 m) and non-responders (R-).

R-: 10

68.1 ± 7.9

 Kono 2014 [165]

12

64.5 ± 7.0

  

3 SAx

FSE

1,0,1

DCM patients diagnosed on clinical, echocardiographic and nuclear medicine findings.

 Nishii 2014 [166]

M: 12

61.2 ± 0.4a

51.2 ± 1.6c

<  0.01ac

3 SAx

FSE

3,0,2

Mild DCM patients LVEF > 35% (M), severe DCM ≤ 35% (S).

S: 14/15

67.4 ± 6.8b

<  0.01bc

 Spieker 2017 [167]

M: 23

66.2 ± 7.5a

60.0 ± 4.2c

<  0.01ac

Mean 16 AHA

GraSE

1,2,2

Mild DCM patients LVEF > 30% (M), severe DCM ≤ 30% (S).

S: 34/60

65.5 ± 5.3b

<  0.01bc

1.5 T Siemens

 Cui 2018 [168]

12/15

50 ± 3

45 ± 1

<  0.01

Mid-wall

T2-prep SSFP

3,2,1

DCM patients with LV dilatation, LVEF < 35% and without CAD.

 Mordi 2016 [169]

16/21

55.9 ± 4.4

52.9 ± 3.3

<  0.01

Mean septal basal and mid-SAx

T2-prep SSFP

2,1,2

DCM patients (LVEF 40–50% by echocardiography).

Dilated Cardiomyopathy (T2) 3 T Philips

 Child 2018 [170]

32/26

47 ± 5

45 ± 3

 

Septal mid-SAx LGE-

GraSE

2,2,2

Non-ischemic DCM patients with LVEF < 50%.

Myocarditis (T2) 1.5 T Philips

 Baeßler 2017 [171]

I: 31

62 ± 7a

59 ± 4c

<  0.05ac

Mean 16 AHA

GraSE

3,0,2

Initial cohort (I) of CMR-positive myocarditis patients. Validation cohort (V) of CMR-positive myocarditis (n = 22) + clinically diagnosed (n = 31) + no LLC (n = 15).

V: 68/30

64 ± 6b

<  0.01bc

 Baeßler 2018 [172]

26/10

62.1 ± 4.8

55.8 ± 1.8

<  0.01

Mean HLA & mid-SAx

SE

3,0,2

Acute myocarditis patients with infarct like presentation and positive biventricular EMB.

 Baeßler 2019 [173]

AB+: 21

64.3 ± 5.5

  

Mean HLA & mid-SAx

SE

2,0,1

Myocarditis patients defined as acute (A) (symptoms ≤14d) or chronic (C) and classified based on positive (B+) or negative EMB (B-).

AB-: 10

60.2 ± 5.8

CB+: 26

63.4 ± 5.3

CB-: 14

61.1 ± 3.1

 Bohnen 2017 [174]

F0: 48

61.3 ± 4.6a

55.0 ± 3.1b

<  0.05ab

LGE+ in 3 SAx

GraSE

3,0,2

Acute myocarditis patients scanned in acute phase (F0), after 3 months (F1) and after 12 months (F2).

F1: 39

56.7 ± 4.6

F2: 21/27

54.0 ± 4.0

 Bohnen 2015 [175]

16

65.3 ± 7.3

  

3 SAx

SE

2,0,1

Patients with recent-onset HF, LVEF < 45% without CAD and positive EMB (3d before scan).

 Dabir 2019 [176]

50/30

58.0 ± 6.0

51.6 ± 1.9

<  0.01

3 SAx

GraSE

3,0,2

Patients meet diagnostic criteria for clinically acute myocarditis 3d after symptom onset.

 Gatti 2019 [177]

8/30

55.7 ± 4.2

46.8 ± 1.6

<  0.01

3 SAx

GraSE

2,0,2

Patients with clinically acute myocarditis and LVEF ≥55%.

 Luetkens 2017 [178]

48/35

62.2 ± 8.8

52.3 ± 2.5

<  0.01

3 SAx

GraSE

3,0,2

Patients with acute myocarditis 3d after symptom onset.

 Luetkens 2019 [38]

40/26

61.8 ± 8.2

52.8 ± 2.4

<  0.01

3 SAx

GraSE

2,0,2

Patients with clinically defined acute myocarditis 4d after hospital admission.

 Lurz 2016 [179]

A: 43

62.2 ± 4.5

  

1 SAx

 

1,0,1

Confirmed myocarditis patients classified as acute (A) (acute symptoms ≤14d) or chronic (C) (symptoms >14d).

C: 48

62.8 ± 4.5

 Radunski 2014 [180]

104/21

61.3 ± 5.3

56.3 ± 4.8

<  0.01

3 SAx

 

2,0,2

Myocarditis patients 2w (median) after symptom onset.

 Radunski 2017 [181]

20/20

97.3 ± 23.1

56.7 ± 4.8

<  0.01

LGE in 3 SAx

SE

2,0,2

Myocarditis patients with positive LLC 3d (median) after symptom onset.

 Spieker 2017 [182]

46/60

68.1 ± 5.8

60.0 ± 4.2

<  0.01

Mean 16 AHA

GraSE

2,2,2

Suspected acute myocarditis patients on ESC guidelines 5d after onset.

1.5 T Siemens

 Huber 2018 [183]

20/20

53 ± 4a

48 ± 2c

<  0.05ac

Mean basal and mid-SAx

T2-prep SSFP

3,0,2

Acute viral myocarditis patients based on clinical guidelines 5d after symptom onset.

 Mayr 2017 [184]

39/10

65.3 ± 45.4

53.7 ± 31.0

<  0.01

LGE+ in 3 SAx

TSE

1,0,2

Cardiac disease symptoms, evidence of myocardial injury by elevated serum markers, exclusion of CAD 4d (median) after symptom onset.

 Thavendiranathan 2013 [25]

20/30

65.2 ± 3.2

54.5 ± 2.2

 

LGE+ AHA

T2-prep SSFP

3,0,2

Acute myocarditis patients 1d (median) after hospital admission.

 Von Knobelsdorff Brenkenhoff 2017 [185]

F0:18

55.2 ± 3.1a

50.4 ± 2.3d

<  0.01ad

Mean basal and mid-SAx

T2-prep SSFP

1,2,2

Acute myocarditis patients <7d (F0), 40d (F1) and 189d (F2) after symptom onset.

F1: 18

52.4 ± 1.0b

<  0.01bd

F2: 18/18

51.3 ± 3.0c

0.32cd

Myocarditis (T2) 3 T Siemens

 Gang 2019 [186]

35/35

65.5 ± 8.5

55.2 ± 3.6

<  0.05

 

T2-prep SSFP

2,0,2

Clinically suspected myocarditis patients 2.6 ± 1.9d after hospital admission.

 Stirrat 2018 [187]

9/10

57.1 ± 5.3

46.7 ± 1.6

<  0.01

LGE+ SAx & LAx

T2-prep tFISP

2,0,2

Confirmed acute myocarditis patients 1w after diagnosis.

Hypertension (T2*) 1.5 T Philips

 Chen 2018 [188]

H+: 20

23.8 ± 3.1a

30.8 ± 2.7c

<  0.05ac

 

TFE

2,0,2

Hypertension patients with (H+) and without (H-) LV hypertrophy.

H-: 21/23

28.7 ± 4.2b

<  0.05bc

  1. 4CH 4 chamber, AHA American Heart Association, AL amyloid light-chain, ATTR amyloid transthyretin, ß-TM beta thalassemia major, CAD coronary artery disease, CMR cardiovascular magnetic resonance, D days, DCM dilated cardiomyopathy, EMB endomyocardial biopsy, ESC European Society of Cardiology, FFE fast field echo, FSE fast spin echo, GraSE gradient spin echo, GRE gradient echo, H hours, HCM hypertrophic cardiomyopathy, HF heart failure, HLA horizontal long axis, LAx long axis, LGE late gadolinium enhancement, LLC Lake Louis criteria, LV left ventricle, LVEF left ventricular ejection fraction, M months, MI myocardial infarction, NS non-significant, NSTEMI non-ST-elevation myocardial infarction, PCI percutaneous coronary intervention, Qual. outcome Newcastle-Ottawa quality assessment scale, ROI region-of-interest, SAx short axis, SD standard deviation, SE spin echo, Seq. MR sequence, SI spiral imaging, SLE systemic lupus erythematosus, SSFP steady-state free precession, STEMI ST-elevation myocardial infarction, T2-prep. T2-prepared, TFE turbo field echo, tFISP true fast imaging with steady state precession, TI thalassemia intermedia, TM thalassemia major, TSE turbo spin echo, W weeks