Cardiac MR and viability

Case

Wednesday, April 27, 2011

80 yo F with PMH of HTN, HLD, DM, CVA
with a history of continuous chest pain x 2
weeks. Patient was found to have a LBBB on
unknown duration. Cardiac enzymes were
negative. The patient was transferred to
WHC for further management.


Dobutamine CMR
• Contractile reserve can be assessed using low dose dobutamine stress test
• Allows for superior endocardial border definition facilitating more
accurate wall motion and wall thickening
• Dobutamine CMR vs PET
• 35 patients with mild LV dysfunction
• Sensitivity of 88% and Specificity of 87% for detecting regions of viable
myocardium
• Reduced predictive ability with more severe dysfunction is present at rest
with specificity in the 80% range, but sensitivity limited to 50%
• If contractile function improves with dobutamine the there is likely
viability
• Lack of improvement, however, does may not rule out viability as
ischemia may develop at even low levels of dobutamine administration

Mahrholdt, et al. Heart 2007

Contrast Enhancement
CMR
• Regions of myocardial infarct exhibit signal intensity (contrast
enhancement) on T1-weighted images after administration
gadolinium
• Gadolinium passively diffuses into the intracellular space due to
rupture of myocyte membranes leading to increased contrast
concentration in interstitial space between collagen ﬁbers
• Contrast images are acquired mid-diastole
• The inversion time must be manually selected to null signal from
normal myocardial regions
• This varies btw patients as a function of dose and and time
after administration of contrast due to varying
pharmacokinetics.


Downloaded from heart.bmj.com on October 25, 2010 - Published by group.bmj.com

EDUCATION IN HEART

ce CMR

124

Histology

SPECT

Base Midventricular Apex

Figure 2 Contrast enhanced cardiovascular magnetic resonance (CeCMR), histology and single photon emission computed tomography (SPECT) images
obtained in an animal with a medium sized infarct. There is a nearly perfect match between necrosis defined by histology and ceCMR. Whereas ceCMR
allows the exact assessment of the transmural extent of infarction, SPECT defines segments as either viable or non-viable. Reproduced with permission from
Wagner et al.9


Use of contrast enhanced MRI to identiﬁfy reversible
myocardial dysfunction C O N T R AST- E N H A N C E D M AG N ET I C R E S O N A N C E I M AG I N G TO I D E N T I F Y R EV E R S I B L E M YO C A R D I A L DYS F U N C T I O N

Cine Image Contrast-Enhanced Image

• Methods
• 50 patients prospectively enrolled
11
12 1

2

• Of these 41 patient had MRI before and after
revascularization 10 3
A
B

• Inclusion criteria
9 4

• Scheduled to undergo revascularization
• Had regional wall motion abnormalities bu
8

7 6
5

ventriculogram or echo
The New Eng land Jour nal of Medicine

• Exclusion criteria Figure 1. Typical Cine Image and Contrast-Enhanced Image Obtained by MRI before Revascularization.
Registration of the images was not required, because both types were acquired during the same MRI session. Twelve equal circum-

•
ferential segments were analyzed in each short-axis view. For contrast-enhanced images, the transmural extent of hyperenhance-
Unstable angina ment was determined for each segment with use of the following equation: with
A÷(area A+area B). All Dysfunctional
Segments percentage of area that was hyperenhanced=100¬area
Severe Hypokinesia, Segments with
Segments Akinesia, or Dyskinesia Akinesia or Dyskinesia

• NYHA Class IV heart failure

)
12
of
•

2
Left Anterior Descending

(1
100
Contraindication for MRI

)
48
Coronary Artery Left Circumflex Artery Right Coronary Artery

1
of

)
28
9)

28
•

32

of
(1
Results

3
of

(2
56
80

(2
•

)
Improved Contractility (%)

86
80 percent of patient demonstrated hyperenhancement

3)

of
18

6
(5
of
09
•

(1
60
50 percent with q waves on ekg showed

)
)
0)

20
68
11

of
hyperenhacement

of
of

(9
9
(2
6
(4
40

• Before revascularization, 38 percent of pts had
abnormal contractility and 33 percent had some areas

4)

3)
20

12

10
of hyperenhancement

of

of

)
54
3

0
(1

(1

of
)
58

)
)

(4

46
57
of
•

of
of
(1
Areas with dysfunctional, but non-hyperenhancing

(0
(0
0
0

51 0

00

0

51 0

00

0

51 0

00
26 5

76 75

26 5

76 75

26 5

76 75
myocardium improved signiﬁcantly after
–5

–5

–5
2

2

2
–1

–1

–1
1–

–

1–

–

1–

–
revascularization Transmural Extent of Hyperenhancement (%)
Figure 2. Typical Contrast-Enhanced Transmural Extentby MRI in a Short-Axis View (Upper Panels) and and the Likelihood(Lower
Figure 4. Relation between the Images Obtained of Hyperenhancement before Revascularization a Long-Axis View of
Panels) in Three Patients. after Revascularization.
Increased Contractility
Kim et al NEJM, 2000
Hyperenhancement is present (arrows) in various coronary-perfusion territories462the left anterior descending coronary artery, the
Data are shown for all 804 dysfunctional segments and separately for the — segments with at least severe hypokinesia
left circumflex artery, and the right coronarydyskinesia before revascularization. For all three analyses, there was an inverse
and the 160 segments with akinesia or artery — with a range of transmural involvement.
Wednesday, April 27, 2011 relation between the transmural extent of hyperenhancement and the likelihood of improvement in contractility.

Viability post CABG
1538 Circulation September 21, 2004

• Methods
• 60 patients undergoing mutlivessel
CABG were studies
preoperatively, 6 days and 6
months post op
• Patients were also randomized to
be off pump and on pump
• Exclusion: age > 75 yo, severe pre-
existing LV dysfunction, CKD,
typical MRI contraindications Selvanayagam et al DE-MRI in Predicting Viability After CABG 1539
• Results
• Preoporatively 21% of wall transmural extent of HE correlated closely with the likelihood also analyzed by a s
segments had abnormal regional of improvement in regional function after surgery (Figure 4). to good agreement
When all segments that were dysfunctional preoperatively mural grading of the
function, whereas 14% showed were analyzed, the proportion with improved regional func- the value for asse
evidence of hyperenhancement tion decreased as the transmural grade of HE increased (SE, 0.01; P 0.000
(P 0.001). For example, regional function improved in 156 (Spearman r 0.8; P
• At 6 months, 57% of wall segments of 190 segments (82%) with no preexisting HE but in only 16 by the first and sec
had improved contraction by at of 63 segments (25%) with 51% to 75% HE and 1 of 25
Effects of OPCA
segments (4%) with 76% HE. This relationship between the
least one grade transmural extent of HE and the improvement in regional Global LV Func

• function was present irrespective of the degree of preopera- As previously repor
Strong correlation between the tive segmental dysfunction (Figure 4). was similar in the
transmural extent of 2.9 0.8, OPCABG
CI was significantly
hyperenhancement and ther Relationship of New Perioperative HE to Regional
ONCABG; 3.2 0.8
Function at 6 Months
recovery of in regional function at To investigate the impact of surgery-related irreversible Table, the cardiac in
6 months injury on late regional myocardial function and viability, we · m 2 in the OPCAB
systematically analyzed segments with no or minimal HE in the ONCABG
Selvanayagam et al Circulation, 2004 (pre-CABG) in which the RWM worsened at 6 months. In the improvement in the
Figure 4. Relationship between transmural
Wednesday, April 27, 2011 362 preoperatively dysfunctional segmentsextent of HE before
with no HE or months postoperati
surgery and likelihood of increased regional function after sur-

tivity ofwas LAD or not (AUC: 0.95 for LAD infarct ratio of for (AUC: 0.71; 95% be greatest. We have demo
89%, specificity of 74%, positive likelihood vs. 0.89 benefits might CI: 0.60 to 0.82, p 0.00
non-LAD infarct, p ratio of 0.1. This cutoff waswere with LGE STEMI, LGE percentage is(AUC: 0
3.6, and negative likelihood 0.3) and whether Q waves during percentage), CK-MB rise the stron
selectedpresent or not at STEMI presentation (AUC 0.93 for 0.69 to 0.89, p failure and adverse events, openin
of late heart 0.01), and LVEF during ST
Predicting Late Myocardial Recovery and Outcomes in Early hours
to screen for patients at risk for developing LV
Q waves present vs. 0.88 for Q waves absent, p 0.3).
dysfunction late after STEMI, correctly classifying 80% of 0.84; 95% CI: 0.76 to 0.93,early risk stratific
improved strategies for very
p 0.03) (F
We additionally explored clinical outcomes: over 2.3 LVEF measurement after STEMI. Consi
the population. The 23% LGE cutoff seemed useful in diagnostic accuracy of LGE percentage for pr
of STEMI
0.4 year follow-up, MACE occurred in 23 (22%) subjects (1 has gone toward earlier risk stratification and
dichotomizing 2 groups with widely diverging recoveries in 4 LV dysfunction did not differ, whether the inf
death, 2 MIs, 5 malignant arrhythmias requiring AICD, mentation of prognosis-altering intervention
severe LV dysfunction 35%, 11 hospital stays for heart STEMI (5,26). Treatment strategies based
failure). The previously defined Associations of Variables <50%
Measured During Acute STEMI With
Multivariable Associations of Variables
Multivariable cutoff of 6-Month LVEF
LGE 23% LVEF after STEMI have shown important su
Table 4
measured during hyperacute STEMI incurred a significant
•
Measured During Acute STEMI With 6-Month LVEF <50%
(2– 4,27). However, LVEF measured very ear
Methods risk of adverse events by univariable Cox proportional an imperfect predictor of later LVEF reco
OR 95% CI p Value
hazards regression (hazard ratio: 10.1; 95% CI: 3.7 to 27.3, global EF at the time of STEMI might beg
• 0.0001) (Fig. 4). In addition, LGE Table 3 selection
Best overall multivariable model by stepwise forward
p percentage re-
104 prospectively enrolled patients with including all significant variables from
mained independently ECG Q waves atwith MACE in multiva-
associated presentation
later months—as observed in this study and
as a6.27 of the 0.81–74.9 disappearance of the
result gradual
successfully reperfused STEMI
Presence of 0.08
riable Cox regression that included CK-MB rise and LVEF
LGE during STEMI* increased contractility of healthy segments an
1.33 1.09–1.78 0.002
during STEMI (hazard ratio: 1.72; 95% CI: 1.43 to 2.01, (6,26). In addition, low EF at the time of S
•
Pain-to-balloon time, min 1.15 1.01–1.32 0.09
Exclusion criteria were recent MI p 0.007).Adjusted for LVEF during STEMI, LGE %, and CK-MB beget normal EF after infarct healing, as sys
JACC Vol. 55, No. LVEF2010 STEMI*
22, during
after During 0.20 Larose e
tion0.95 Predicting0.88–1.03
observed early Recovery STEMI mightST
(<6months), shock requiring IABP, June 1, 2010:2459–69
Discussion LGE during STEMI* Late Hyperacute
combination of reversible myocardial stunning
1.36 1.11–1.66 0.004

respiratory failure, contraindications for Maximum CK-MB rise after STEMI, mmol/l
The major finding of this study is that LGE quantification ible1.00
necrosis (28,29). The failure of recent tre
0.99–1.01 0.40

egies such as AICD implantation based on
MRI very early *Values givenSTEMI predicts late heart failure and
during as percentages.
adverse events beyond traditional risk factors such as infarct
Abbreviations as in Tables 1 and 3. LVEF very early after STEMI, contrary t
observed when LVEF was measured 40 d
• Subjects were followed prospectively at 33
territory, maximum CK-MB rise, pain-to-balloon time,
presence of Q waves, and LVEF during STEMI. A second might be due to the observed variability in L
during early infarct healing (3,30).
months and MRI was repeated at 6 months major finding is that, during the hyperacute phase of
STEMI, LGE volume incurred the strongest association to Predictors of residual systolic function after i

• LV function change, beyond infarct transmurality, MVO, and remodeling. Systolic function after STE
Primary endpts were change in LVEF and LV and SM. Significant variability in preload and afterload a function of the infarct territory (31), the
dysfunction at 6 months. conditions and difficulty in discriminating stunned from segment elevation on ECG (32,33), microvas
tion (34,35), time to reperfusion (36), and tim
nonviable myocardium at the time of STEMI have rendered

• Secondary endpt was MACE
most early variables imperfect predictors of late systolic
function and adverse events. However, strategies for the
(37). Although LVEF at the time of STE
correlated to late systolic function in early stu
has since been called into question by m
•
earliest possible risk assessment after STEMI have become
Results essential not only to better target therapies but also to radionuclide (38) and volumetric techniques (9
introduce these therapies in the timeliest manner while remodeling is a particularly heterogeneous pr

• LGE was the best predictor of late LV
dysfunction Figure 2 Relative Change in LVEF From STEMI to 6-Month Follow-Up, Assessed According to Quartiles of LVEF During ST

• LGE > 23% of volume accurately predicted The LGE 23% during STEMI identifies a subgroup of patients with significantly worse functional recovery
compared with those with less LGE, across the entire range of LVEF quartiles during STEMI. Abbreviations as in Figure 1.

late dysfunction (sensitivity 89%, specificity
74%)
• LGE > 23 % carried a hazard ration of 6.1
percent for adverse events (p<0.0001)
Larose et al JACC, 2010
Wednesday, April 27, 2011 Figure 4 Kaplan-Meier Event-Free Survival Estimates for LGE >23% Versus LGE <23% Very Early During STEMI

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