Cardiovascular magnetic resonance imaging assessment of outcomes in acute myocardial infarction

Table 1 Cardiovascular magnetic resonance studies illustrating the prognostic importance of left ventricular ejection fraction in acute myocardial infarction

Ref.	Year	n	CMR time	Main findings	Follow-up
El Aidi et al[32]	2014	25497	N/A	Meta analysis of prognostic value of CMR surrogate markers. LVEF was only IP for MACE (HR 1.05 per -5%)	N/A
Husser et al[33]	2012	304	7 d	LVEF was IP for MACE (HR 0.95 for each +1% LVEF)	140 wk
Eitel et al[34]	2011	208	3 d	LVEF was IP for MACE (HR 0.95 for each +1% LVEF)	18.5 mo
Amabile et al[35]	2010	114	6 d	LVEF was IP for MACE (HR 0.96 for each +1% LVEF)	12 mo
de Waha et al[36]	2010	438	3 d	LVEF was IP for MACE (OR 1.63) and all-cause mortality (OR 2.51)	19 mo
Cochet et al[37]	2009	127	3-7 d	LVEF of < 40% was IP for MACE (OR 1.20)	12 mo
Hombach et al[6]	2005	110	6 d	LVEF was IP for 9 mo MACE (P = 0.006)	225 d

CMR time: Mean/median time of CMR post acute STEMI; MACE: Major adverse cardiovascular events; IP: Independent predictor; LVEF: Left ventricular ejection fraction; CMR: Cardiovascular magnetic resonance; N/A: Not available.

Table 2 Studies illustrating the prognostic importance of left ventricular volumes and adverse left ventricular remodelling in acute myocardial infarction

Ref.	Year	n	Modality	Main findings	Follow-up
Ahn et al[13]	2013	135	Echo	Adverse LV remodelling (> 20% inc. LVEDV) at 6 mo was IP 3 yr MACE. MACE rate approximately 25% in patients with adverse LV remodelling vs approximately 6% in non-remodelled patients	981 d
Hombach et al[6]	2005	110	CMR	Baseline LVEDV was IP for MACE (P = 0.038)	225 d
St John Sutton et al[39]	2003	512	Echo	Percentage change in LV area (surrogate for LV volume) between baseline echo and follow-up at 12 mo was IP for ventricular ectopy and VT	24 mo
Bolognese et al[12]	2002	284	Echo	Baseline LVESV was IP for cardiac death and MACE. Components of MACE higher in patients with adverse remodelling (> 20% inc. LVEDV: Mortality 14% vs 5%, MACE 18% vs 10%)	5 yr
Otterstad et al[40]	2001	712	Echo	Increase in LVESV between acute scan at 7 d and echo at 3 mo strongest IP for MACE	24 mo
St John Sutton et al[41]	1994	512	Echo	LV end-diastolic area (RR 1.1) and LV end-systolic area (RR 1.1) on baseline echo, and %-change in LV area at 12 mo echo (RR 1.55) were strongest IPs for MACE	12 mo
White et al[30]	1987	605	LV gram	LVESV of LV gram at 4 wk was strongest IP of long-term mortality (P < 0.0001)	78 mo

MACE: Major adverse cardiovascular events; IP: Independent predictor; LVEDV: Left ventricular end-diastolic volume; LVESV: Left ventricular end-systolic volume; Modality: Modality of LV volume assessment (CMR: Cardiovascular MRI; Echo: Echocardiography; LV gram: LV contrast angiography).

Table 3 Studies illustrating the prognostic importance of left ventricular strain in acute myocardial infarction

Ref.	Year	n	Modality	Main findings	Follow-up
Ersbøll et al[56]	2014	1048	TTE	(E-prime divided by peak early diastolic strain rate) strongest IP of MACE and death	29 mo
Ersbøll et al[57]	2013	849	TTE	GLS was IP of MACE	30 mo
Hung et al[58]	2010	610	TTE	GLS and strain-rate, and GCS and strain-rate IPs for MACE in model with WMS, LVEF	25 mo
Antoni et al[59]	2010	659	TTE	GLS (HR 1.2) was IP of mortality. LVEF, wall-motion score and Tissue Doppler mitral valve inflow not	21 mo

TTE: Transthoracic echocardiography; GLS: Global longitudinal strain; MACE: Major adverse cardiovascular events; IP: Independent predictor; HR: Hazard ratio; LVEF: Left ventricular ejection fraction.

Table 4 Temporal changes in cardiovascular magnetic resonance-derived infarct size in acute myocardial infarction

Ref.	Year	n	CMR times post STEMI	Relative LGE IS reduction	LGE method	Main findings
Carrick et al[74]	2016	30	8 h → 3 d → 10 d → 7 mo	26%	Automated	Significant decrease d3 to d10 (20% ± 13% to 14% ± 10% LV mass). No change at 7 mo
Dall’Armelina et al[21]	2011	30	2 d → 6 mo	22%	> 2SD	IS reduced at times from 27% ± 15% LV mass 24 h post PPCI, to 21% ± 11% at 6 mo
Mather et al[18]	2011	48	2 d → 1 wk → 30 d → 3 mo	37%	> 2SD	27% IS drop between d2 and d7 post PPCI, no change at 3 mo
Ganame et al[20]	2011	58	3 d → 4 mo → 12 mo	45%	Manual	33% decrease IS d3 and 4 mo then no further decrease at 12 mo
Ibrahim et al[9]	2010	17	1 d → 1 wk → 1 mo → 6 mo	37%	Manual	34% reduction in IS from d2 to 1 wk, then no further change at 1 and 6 mo
Engblom et al[7]	2009	22	1 d → 1 wk → 12 mo	40%	Automated	28% reduction in IS between d1 and 1 wk
Ripa et al[5]	2007	58	2 d → 1 mo → 6 mo	30%	Manual	14% % reduction in IS from d2 to 1 mo
Hombach et al[6]	2005	110	6 d → 9 mo	28%	Manual	28% reduction in IS from d6 to 9 mo

LGE method: SD: Standard deviations; Total LGE IS Overest: Relative overestimation of final IS (last timepoint) on acute CMR; CMR: Cardiovascular magnetic resonance; LGE: Late gadolinium enhancement; IS: Infarct size; PPCI: Primary percutaneous coronary intervention.

Table 5 Cardiovascular magnetic resonance studies illustrating importance of segmental late gadolinium enhancement extent and functional recovery in acute myocardial infarction

Ref.	Year	n	LGE method	Cutoff (LGE)	Main findings	Time of CMR 1	Time of CMR 2
Khan et al[85]	2016		FWHM	50% SEE	SEE strong predictor or segmental functional improvement (AUC 0.840) and normalisation (AUC 0.887)	2 d	9 mo
Wong et al[54]	2014	45	FWHM	50% SEE	Inverse relationship between TEE and likelihood of functional recovery on WMS at 24 wk (area under curve 0.68)	8 d	13 wk
Natale et al[86]	2011	46	2SD	50% TEE	Inverse relationship TEE and likelihood of functional recovery on SWT (93% sens, 75% spec)	5 d	20 wk
Engblom et al[7]	2008	22	Manual	50% TEE	Inverse relationship between TEE and functional recovery on WMS	7 d	24 wk
Shapiro et al[87]	2007	17	Manual	50% SEE	Inverse relationship between TEE and likelihood of functional recovery on WMS at 26 wk. Odds-ratio of functional recovery 0.2 with each SEE quartile	6 d	26 wk
Kitagawa et al[88]	2007	18	2SD	50% TEE	Inverse relationship between TEE and functional recovery. 31% segments > 50% TEE still improved	5 d	39 wk
Janssen et al[89]	2006	67	Manual	50% TEE	Inverse relationship between TEE and functional recovery on WMS at 12w (51%-75%: 39% segments improved, 76%+: 21% improved)	4 d	12 wk
Motoyasu et al[90]	2004	23	2SD	50% TEE	Inverse relationship between SEE and functional recovery on SWT	25 d	24 wk
Beek et al[19]	2003	30	6SD	50% SEE	Inverse relationship between SEE and functional recovery on WMS	7 d	13 wk

WMS: Wall motion scoring; SWT: Systolic wall thickening; TEE: Transmural extent of enhancement; SEE: Segmental extent of enhancement; SD: Standard deviations.

Table 6 Cardiovascular magnetic resonance studies illustrating importance of infarct size on left ventricular function and remodelling in acute myocardial infarction

Ref.	Year	n	LGE method	Main findings	Time post STEMI of predictive CMR	Follow-up
Ahn et al[13]	2013	135	Manual	IS strongest IP of LVR in model with LVEF and MI location	7 d	6 mo (echocardiogram)
Husser et al[33]	2012	304	> 2SD	IS IP of LVR in model incl. LVEF, IS, LV vols, MVO	6 d	189 d
Monmeneu et al[91]	2012	118	> 2SD	No. segments > 50% transmurality IP for LVR	6 d	6 mo
Ezekowicz et al[92]	2010	64	Manual	IS strongest IP of LVEF in model with MVO, troponins	7 d	3 mo
Ganame et al[25]	2009	98	Manual	IS strongest IP of LVR (>> MVO, AAR, Troponin-I)	2 d	6 mo
Bodi et al[93]	2009	214	> 2SD	Extent of transmural necrosis (no. segments > 50% TEE) strongest IP for LV recovery (+ > 5% LVEF)	7 d	6 mo
Wu et al[94]	2008	122	Manual	IS extent only IP for LVEF and LVR	2 d	4 mo
Hombach et al[6]	2005	110	Manual	IS extent IP of LVR in model with MVO, % transmurality	6 d	225 d

IS: Infarct size; IP: Independent predictor; LVR: LV remodelling; LVEDVI: Left-ventricular end-diastolic volume index; LVEDVI: Left-ventricular end-systolic volume index; LVEF: Left ventricular ejection fraction; MVO: Microvascular obstruction; SD: Standard deviation.

Table 7 Cardiovascular magnetic resonance studies illustrating the prognostic importance of infarct in acute myocardial infarction

Ref.	Year	n	LGE method	Main findings	CMR timepoint	Follow-up
Husser et al[96]	2013	250	> 2SD	Extent of transmural infarction (no. of segments > 50% transmurality) only IP for MACE at 6 mo	7 d	163 wk
Izquierdo et al[97]	2013	440	> 2SD	IS was IP for AACEs (arrhythmic cardiac events: Sudden death, VT, VF, ICD shock) in model including LVEF, hypertension	7 d	123 wk
Eitel et al[34]	2011	208	> 5SD	IS was IP of MACE at 19 mo in model including MVO, LVEF, MSI, Killip, TIMI post-PPCI	3 d	18.5 mo
Miszalski-Jamka et al[98]	2010	77	Manual	LV transmurality index IP (HR 1.03) and IS (HR 1.03) IPs for MACE in a model containing RVEF and RV IS	“3-5 d”	1150 d
Larose et al[67]	2010	103	FWHM	IS strongest IP for MACE (HR 1.36) in model containing LVEF, CK. LGE > 23% had HR 6.1 for MACE	4.5 h	2 yr
Bodi et al[38]	2009	214	> 2SD	Extent of transmural infarction (no. of segments > 50% transmurality) IP for MACE (HR 1.35 if > 5 segs)	7 d	553 d
Wu et al[99]	2008	122	Manual	IS only IP of 2 yr MACE in model containing LVEF, LVESVI	2 d	538 d

LGE: Late gadolinium enhancement; FWHM: Full-width half-maximum; SD: Standard deviations; MACE: Major adverse cardiovascular events; LVEF: Left ventricular ejection fraction; PPCI: Primary percutaneous coronary intervention; LGE method (LGE quantification method): SD: Standard deviations; FWHM: Full-width half-maximum.

Table 8 Temporal changes in cardiovascular magnetic resonance late microvascular obstruction in acute myocardial infarction

Ref.	Year	n	CMR timepoints	LGE method	Main findings
Carrick et al[74]	2016	30	8 h → 3 d → 10 d → 7 mo	Auto	L-MVO in 20%, peaked early at 8 h and stable at d3. Decreased by d10, absent at 7 mo
Mather et al[18]	2011	48	2 d → 1 wk → 30 d → 3 mo	> 2SD	L-MVO in 60%, peak at d2. Decrease at subsequent points. L-MVO absent at 3 mo
Ganame et al[20]	2011	58	3 d → 4 mo → 12 mo	Manual	L-MVO in 64%. L-MVO absent at 4 mo
Ripa et al[5]	2007	58	2 d → 6 mo	Manual	L-MVO in 42%. L-MVO absent at 6 mo
Hombach et al[6]	2005	110	6 d → 9 mo	Manual	46% had L-MVO (2.8% LV mass, 16% of IS) on acute CMR. L-MVO absent at 6 mo

MVO: Microvascular obstruction; LGE method: SD: Standard deviations; IS: Infarct size; LV: Left ventricle; CMR: Cardiovascular magnetic resonance.

Table 9 Cardiovascular magnetic resonance studies illustrating the importance of late microvascular obstruction on left ventricular function and remodelling in acute myocardial infarction

Ref.	Year	n	LGE method	Main findings	Time post STEMI of predictive CMR	Follow-up
Kidambi et al[115]	2013	39	> 2SD	L-MVO only IP of impaired infarct strain. Model with IS, TIMI flow, diabetes, transmurality	3 d	3 mo
Wong et al[103]	2012	40	Manual	L-MVO extent only IP for LVEF at 3 mo in model including E-MVO, IS and myocardial blood flow on perfusion	3 d	3 mo
Ezekowitz et al[92]	2010	64	Manual	L-MVO extent was IP of LVEF in model with IS and NT-proBNP	7 d	4 mo
Weir et al[112]	2010	100	Manual	L-MVO extent was only IP of LVR in model with TIMI post PCI, E-MVO, IS	4 d	6 mo
Ganame et al[25]	2009	98	Manual	L-MVO extent was IP of LVR in model with IS, troponin-I, TTR	2 d	6 mo
Nijveldt et al[111]	2008	60	Manual	L-MVO presence strongest IP of LVEF change and LVR in model with TTR, IS, LVEF, E-MVO	5 d	4 mo
Hombach et al[6]	2005	110	Manual	L-MVO extent IP for LVR in model with baseline IS, infarct transmurality	6 d	225 d

MVO: Microvascular obstruction; IS: Infarct size; IP: Independent predictor; TTR: Time to revascularisation; LVR: Left ventricular remodelling; LVEF: Left ventricular ejection fraction; LVEDVI: Left-ventricular end diastolic volume index; LVESVI: Left-ventricular end systolic volume index.

Table 10 Cardiovascular magnetic resonance studies illustrating the prognostic importance of late microvascular obstruction in acute myocardial infarction

Ref.	Year	n	LGE method	Main findings	Time of prognostic CMR post STEMI	Follow-up
Regenfus et al[117]	2015	249	Manual	L-MVO extent strongest IP for MACE in model including IS, LVEF, TIMI pre and post PPCI and no. diseased vessels	3.7 d	72 mo
Eitel et al[119]	2014	738	> 5SD	Largest multicentre study of L-MVO in PPCI. L-MVO > 1.4% LVM and TIMI risk score only IPs of combined MACE. Adding L-MVO to model with clinical predictors, LVEF and IS increased c-statistic	7 d	6 mo
de Waha et al[120]	2012	438	Manual	L-MVO extent IP for combined MACE in model including IS, LV volumes (only other IP was LVEF). L-MVO/IS strongest IP in model including L-MVO extent, LVEF, IS, LV volumes	3 d	19 mo
de Waha et al[36]	2010	438	Manual	Presence and extent of L-MVO were strongest IPs for MACE and mortality in models with IS, LVEF, ST-res, TIMI-flow post PCI. E-MVO was not an IP	3 d	19 mo
Cochet et al[37]	2009	184	Manual	L-MVO strongest IP for MACE, in models including GRACE score, IS, LVEF. L-MVO stronger IP than E-MVO (OR 8.7 vs 2.5)	“3-7 d”	12 mo
Bruder et al[116]	2008	143	Manual	Only extent of L-MVO > 0.5% LV mass was IP for MACE; model included IS, LVEF, age, DM, sex	4.5 d	12 mo
Hombach et al[6]	2005	110	Manual	L-MVO IP for MACE (P = 0.04) in model including LV end-diastolic volume and LVEF	6 d	268 d

MVO: Microvascular obstruction; LVEF: Left ventricular ejection fraction; IS: Infarct size; PCI: Percutaneous coronary intervention; MACE: Major adverse cardiovascular events; IP: Independent predictor.

Table 11 Cardiovascular magnetic resonance studies illustrating the importance of intramyocardial haemorrhage on left ventricular function and remodelling in acute myocardial infarction

Ref.	Year	n	IMH CMR method	Main findings	CMR time post MI	Mean/median F/U CMR
Carrick et al[74]	2016	245	T2*	IMH strongest IP for LVR. IMH associated with lower LVEF and greater volumes	3 d	7 mo
Kidambi et al[115]	2013	39	T2w-TSE and T2*	IMH associated with attenuation of follow-up infarct strain	3 d	3 mo
Husser et al[33]	2012	304	T2w-TSE	IMH strongest IP for LVR in model with LVEF, IS, LV vol, L-MVO	6 d	189 d
Mather et al[131]	2011	48	T2w-TSE and T2*	IMH strongest IP of LVR in model with IS, LVEF, LVESV, E-MVO, MSI	2 d	3 mo
Beek et al[24]	2010	45	T2w-TSE	IMH was a univariate predictor of LVEF. However no prognostic significance beyond baseline LVEF and MVO in predicting final LVEF	5 d	4 mo
Bekkers et al[121]	2010	90	T2w-TSE	Acute MSI and LVEF increase at follow-up lowest if IMH present. But IMH no prognostic significance beyond MVO in predicting LVEF	5 d	103 d
O’Regan et al[126]	2010	50	T2*	IMH presence univariate predictor of LVEF and LV volumes. However only IS independently predicted LVEF	3 d	N/A
Ganame et al[25]	2009	98	T2w-TSE	IMH extent strongest IP of LVR in model with IS, E-MVO, Troponin-I, AAR, TTR, IS	2 d	4 mo

IS: Infarct size; IP: Independent predictor; LVR: Left ventricular remodelling; MVO: Microvascular obstruction; LVEF: Left ventricular ejection fraction; LVESVI: Left-ventricular end systolic volume index; T2w-TSE: T2-weighted turbo spin-echo; AAR: Area at risk; MSI: Myocardial salvage index; N/A: Not applicable.

Table 12 Temporal changes in cardiovascular magnetic resonance-derived area at risk and myocardial salvage index in acute myocardial infarction

Ref.	Year	n	CMR timepoints post STEMI	AAR, IS method	Main findings
Mather et al[18]	2011	48	2 d → 1 wk → 30 d → 3 mo	> 2SD STIR, > 2SD LGE	AAR reduction at successive timepoints, 1-3 mo (-75%). No change MSI at d2 or 1 wk as IS and AAR decreased proportionally
Dall’Armelina et al[21]	2011	30	2 d → 1 wk → 2 wk → 6 mo	> 2SD T2p-BB, > 2SD LGE	100% had oedema at d2. AAR stable over 1st week (37% vs 39% LVM). Decreased by 2 wk and nearly resolved at 6 mo
Carlsson et al[138]	2009	16	1 d → 1 wk → 6 wk → 6 mo	Manual STIR, and LGE	AAR at all timepoints. AAR stable in 1st week, correlated with 1 wk SPECT. Decrease by 1 mo (10% LVM), nearly gone by 6 mo
Ripa et al[5]	2007	58	2 d → 1 mo → 6 mo	Manual STIR and LGE	All had oedema at d2. AAR decreased at all time points. No data on MSI in this study

AAR: Area at risk; MSI: Myocardial salvage index; AAR, LGE method: SD: Standard deviations; STIR: T2-weighted short-tau inversion recovery imaging; T2p-SS-BB: T2-prepared single-shot bright-blood; 3T: 3.0 tesla field strength; IS: Infarct size.

Table 13 Cardiovascular magnetic resonance studies showing the importance of myocardial salvage index on left ventricular function and remodelling in acute myocardial infarction

Ref.	Year	n	AAR, IS method	Main findings	CMR timepoint post STEMI	Follow-up
Mather et al[131]	2011	48	> 2SD STIR, > 2SD LGE	MSI was IP for LVR (OR 0.95) in model including LV volumes, LVEF, IS, IMH, MVO	2 d	3 mo
Monmeneu et al[91]	2012	118	> 2SD STIR, > 2SD LGE	MSI univariate predictor of LVR and final LVEF. However not IP of LVR in model with LVESVI, IS, no. transmural segs	6 d	6 mo
Masci et al[14]	2011	260	> 2SD STIR, > 5SD LGE	MSI strong univariate predictor of LVR and final LVEF. However not IP in model including IS, MVO	1 wk	4 mo
Masci et al[26]	2010	137	> 2SD STIR, > 5SD LGE	MSI strongest IP for LVR However IS and MSI (r = -0.72) and IS and AAR (r = 0.85) correlated	1 wk	4 mo

IS: Infarct size; IP: Independent predictor; LVR: Left ventricular remodelling; MVO: Microvascular obstruction; LVEF: Left ventricular ejection fraction; LVESVI: Left-ventricular end systolic volume index; STIR: T2-weighted short-tau inversion-recovery; LGE: Late gadolinium enhancement.

Table 14 Cardiovascular magnetic resonance studies illustrating the prognostic importance of myocardial salvage index in acute myocardial infarction

Ref.	Year	n	AAR, IS method	Main findings	CMR timepoint post STEMI	Follow-up
Eitel et al[34]	2011	208	> 2SD -STIR, > 5SD LGE	MSI was only CMR-based IP of mortality in model with age, IS, MVO, LVEF, TIMI- post PPCI, diabetes, age (IS not IP). MSI not IP of MACE (only IS, LVEF, age were)	3 d	19 mo
Eitel et al[161]	2010	208	> 2SD STIR, > 5SD LGE	MSI was only IP for MACE and mortality in model including LVEF, MVO, IS, ST-resolution and TIMI-grade post PCI	3 d	6 mo

IS: Infarct size; PCI: Percutaneous coronary intervention; MACE: Major adverse cardiovascular events; IP: Independent predictor; MVO: Microvascular obstruction; LVEF: Left ventricular ejection fraction.

Table 15 Cardiovascular magnetic resonance studies illustrating the prognostic importance of right ventricular infarction in acute myocardial infarction

Ref.	Year	n	RV LGE analysis method	Main findings	CMR timepoint post STEMI	Follow-up
Jensen et al[184]	2010	50	Manual	RVI only IP of MACE in model with age, sex, LVEF, LV IS	3 d	32 mo
Miszalski-Jamka et al[98]	2010	99	Manual	RVEF (HR 1.46) and RVI extent (HR 1.50) IP for MACE	“3-5 d”	1150 d
Grothoff et al[187]	2012	450	Manual	RVI was IP of MACE (HR 6.70)	“1-4 d”	20 mo

MACE: Major adverse cardiovascular events; IP: Independent predictor; HR: Hazard ratio; RV: Right ventricle; LVEF: Left ventricular ejection fraction; LGE: Late gadolinium enhancement; IS: Infarct size; RVI: Right ventricular infarction.

Table 16 Key studies illustrating the independent predictive value of cardiovascular magnetic resonance markers for left ventricular remodelling

CMR marker	Ref.	Year	n	CMR quantification	Main findings	Acute CMR time	Follow-up CMR time
IS	Husser et al[33]	2012	304	2SD	IS extent IP for LVR in model with LVEF, IS, LV volumes, MVO	6 d	189 d
IS	Monmeneu et al[91]	2012	118	2SD	Number of segments > 50% transmurality IP for LVR	6 d	6 mo
IS	Wu et al[94]	2008	122	Manual	IS extent at 2 d only IP for LVEF and LVR	2 d	4 mo
IS	Hombach et al[6]	2005	110	Manual	IS extent at 6 d was an IP for LVR in model with MVO, % transmurality	6 d	225 d
L-MVO	Weir et al[112]	2010	100	Manual	L-MVO extent was only IP of LVR in model with TIMI post PCI, E-MVO, IS	4 d	6 mo
L-MVO	Hombach et al[6]	2005	110	Manual	L-MVO extent IP of LVR in model with baseline IS, infarct transmurality	6 d	225 d
IMH	Carrick et al[74]	2016	245	T2*	IMH strongest IP of LVR in model with patient/angio characteristics, LVEDVI	3 d	7 mo
IMH	Husser et al[33]	2012	304	T2w-TSE	IMH strongest IP for LVR in model with LVEF, IS, LV volumes, L-MVO	6 d	189 d
MSI	Monmeneu et al[91]	2012	118	2SD LGR/STIR	MSI univariate but not IP of LVR in model with IS, LVESVI, segments > 50%	6 d	6 mo
MSI	Masci et al[14]	2011	260	2SD STIR, 5SD LGE	MSI univariate predictor of LVR and final LVEF. However not IP of either	1 wk	4 mo
MSI	Masci et al[26]	2010	137	> SD STIR, 5SD LGE	MSI strongest IP for LVR. However IS and MSI and IS and AAR correlated	1 wk	4 mo
T1	Carrick et al[177]	2016	300	T1 map, 2SD STIR, 5SD LGE	Infarct core native T1 inverse relationship with LVR (OR 0.91 per -10 ms T1)	2 d	6 mo

Criteria: Individual studies with n≥ 100 and follow-up CMR ≥ 3 mo post-PPCI. IS: Infarct size; L-MVO: Late microvascular obstruction; IMH: Intramyocardial haemorrhage; MSI: Myocardial salvage index; SD: Standard deviations; STIR: T2-weighted short-tau inversion recovery; LGE: Late gadolinium enhancement; IP: Independent predictor; LV: Left ventricular; LVEF: Left ventricular ejection fraction; AAR: Area at risk; LVEDVI: Left ventricular end-diastolic volume; CMR: Cardiovascular magnetic resonance.

Table 17 Key studies illustrating the independent predictive value of cardiovascular magnetic resonance markers for prognosis

CMR marker	Ref.	Year	n	CMR quantification	Main findings	Acute CMR time	Follow-up
IS	Husser et al[96]	2013	250	> 2SD	Extent of transmural infarction was only IP for MACE	7 d	163 wk
IS	Izquierdo et al[97]	2013	440	> 2SD	IS was IP for arrhythmic cardiac events in model including LVEF, hypertension	7 d	123 wk
IS	Eitel et al[34]	2011	208	> 5SD	IS was IP of MACE in model with MVO, LVEF, MSI, Killip, TIMI flow post-PPCI	3 d	18.5 mo
IS	Larose et al[67]	2010	103	FWHM	IS strongest IP for MACE in model with LVEF, CK. LGE > 23% for MACE	4.5 h	2 yr
IS	Bodi et al[38]	2009	214	> 2SD	Extent of transmural infarction (no. of segments > 50% transmurality) IP for MACE	7 d	553 d
IS	Wu et al[99]	2008	122	Manual	IS only IP of 2 yr MACE in model containing LVEF, LVESVI (HR 1.06)	2 d	538 d
L-MVO	Regenfus et al[117]	2015	249	Manual	MVO extent strongest IP for MACE in model with IS, LVEF, TIMI and no. vessels	3.7 d	72 mo
L-MVO	Eitel et al[119]	2014	738	> 5SD	L-MVO > 1.4% LVM IP of MACE in model with LVEDVI, LVEF, clinical markers	7 d	6 mo
L-MVO	de Waha et al[120]	2012	438	Manual	L-MVO extent IP for MACE in model with IS, LV volumes. L-MVO/IS strongest IP	3 d	19 mo
L-MVO	de Waha et al[36]	2010	438	Manual	L-MVO strongest IP of MACE/mortality in model with IS, LVEF, STR, TIMI post	3 d	19 mo
L-MVO	Cochet et al[37]	2009	184	Manual	L-MVO strongest IP for MACE in model with GRACE, IS, LVEF. E-MVO weaker IP	“3-7 d”	12 mo
L-MVO	Bruder et al[116]	2008	143	Manual	L-MVO extent > 0.5% LV mass IP for MACE in model with IS, LVEF, age, DM, sex	4.5 d	12 mo
L-MVO	Hombach et al[6]	2005	110	Manual	L-MVO IP for MACE (P = 0.04) in model with LV end-diastolic volume and LVEF	6 d	268 d
IMH	Carrick et al[74]	2016	245	T2*	IMH strongest IP of CV death and HF. Multivariate model, L-MVO not predictor	3 d	830 d
IMH	Amabile et al[133]	2012	114	T2w-TSE	IMH presence was strongest predictor of MACE in model with MVO, LVEF, STR	4 d	12 mo
IMH	Husser et al[33]	2012	304	T2w-TSE	IMH IP for MACE in model with AAR, IS, L-MVO. T2w. No inc. value with LGE	6 d	140 wk
IMH	Eitel et al[125]	2011	346	T2w-TSE	IMH IP of MACE in model with L-MVO. T2w inc. value with LGE and cine	3 d	6 mo
MSI	Eitel et al[34]	2011	208	> 2SD/> 5SD	MSI only CMR IP of mortality in model with age, IS, MVO, LVEF, TIMI post, IS	3 d	19 mo
MSI	Eitel et al[161]	2010	208	> 2SD/> 5SD	MSI only IP for MACE/mortality in model with LVEF, MVO, IS, STR, TIMI post	3 d	6 mo
T1	Carrick et al[177]	2016	300	T1 map, > 2SD STIR, > 5SD	Infarct core T1 inverse association with risk of mortality and heart failure hospitalisation, in model with LVEF, infarct T2, IMH. Similar prognostic as L-MVO	2 d	2.5 yr

Criteria: Individual studies with n≥ 100 and follow-up CMR ≥ 6 mo follow-up. IS: Infarct size; L-MVO: Late microvascular obstruction; IMH: Intramyocardial haemorrhage; MSI: Myocardial salvage index; SD: Standard deviations; STIR: T2-weighted short-tau inversion recovery; LGE: Late gadolinium enhancement; IP: Independent predictor; LV: Left ventricular; LVEF: Left ventricular ejection fraction; AAR: Area at risk; LVEDVI: Left ventricular end-diastolic volume; CK: Creatine kinase; T2w-TSE: T2-weighted turbo spin echo; MACE: Major adverse cardiovascular events; CV: Cardiovascular.