- 80 year old female with history of HTN, HLD, DM, and CVA presented with 2 weeks of continuous chest pain and was found to have a LBBB on EKG. Cardiac enzymes were negative. - Dobutamine stress CMR can assess contractile reserve and viability with high sensitivity and specificity. Sensitivity is reduced with more severe dysfunction at rest. - Regions of myocardial infarction exhibit late gadolinium enhancement on CMR which helps identify the extent and location of infarction. The inversion time must be optimized to null normal myocardium.

1. Case

2. 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.

3. 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

4. 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.
Mahrholdt, et al. Heart 2007

5. 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