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 |