80 yo F with PMH of HTN, HLD, DM, CVAwith a history of continuous chest pain x 2weeks. Patient was found to have a LBBB onunknown duration. Cardiac enzymes werenegative. The patient was transferred toWHC 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. Mahrholdt, et al. Heart 2007
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