Predictive Value of Cardiac MRI After STEMI
Role of Late Enhancement
Irnizarifka, MD.
Resident of Departement of Cardiology and Vascular Medicine
Faculty of Medicine, Universitas Indonesia
ABSTRACT
Background: Cardiovascular diseases are currently the leading cause of and are expected to become so in emerging countries by 2020. Among these, CAD is the most prevalent manifestation and is associated with high mortality and morbidity. Nowadays, at least 70% of patients hospitalized with AMI survive the acute hospital phase. Unfortunately, after STEMI, patients who develop heart failure carry worse prognosis. Strategies for the earliest possible risk assessment after STEMI have become essential not only to better target therapies but also to introduce these therapies in the timeliest manner while benefits still be greatest and to monitor the effects of therapy.
Objectives: This case report aimed to review a case of autolysis acute STEMI and discuss the role of Late Enhancement to predicts further cardiovascular risk.
Case Illustration: A fifty-three years old male was referred to the Emergency Department of NCCHK after 11 hours chief complaint of typical chest pain. He was previously diagnosed with acute STEMI at Sari Asih hospital. Occasionally there were no ST segment changes on admission at NCCHK, but his cardiac enzymes were elevated. He underwent coroangiography with the result of total occlusion at LCx. T2W-STIR revealed myocardial edema with total volume of 38% whereas LGE exhibited necrotic tissue at inferolateral wall from apex to base, with transmurality of 70%, necrotic volume of 20%, and late MVO.
Discussion: As a promising non-invasive imaging tool, CE-MRI provides more information such as infarct size, AAR, myocardial viability, MVO, and myocardial hemorrhage. Hence, lately it was associated with predictive value for outcomes. Available data suggest that LGE quantification very early during STEMI predicts late heart failure and adverse events beyond several traditional risk factors. A second major finding is that during the hyperacute phase of STEMI, LGE volume incurred the strongest association to LV function change. Alternate approaches including the assessment of late MVO which is prognostic marker for combined clinical endpoints after STEMI.
Keywords : acute STEMI, contrast-enhanced MRI, LGE, prognostic.
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Acute coronary syndrome represents the clinically manifest acute myocardial ischemia. Acute ischemia is usually, but not always, caused by atherosclerotic plaque rupture, fissuring, erosion, or a combination with superimposed intracoronary thrombosis, and is associated with an increased risk of cardiac death and myonecrosis.5, 6 Nowadays, at least 70% of patients hospitalized with acute myocardial infarction (AMI) survive the acute hospital phase.7 Despite optimal contemporary invasive and medical treatment, the coronary event rate in patients with ACS remains increased, compared with patients with stable symptoms. Growing evidence suggest that this phenomenon could be a consequence of multiple destabilized and vulnerable plaques throughout the coronary tree.8
Timely diagnosis of STEMI is a key to successful management. A 12-lead ECG must be performed as soon as possible to establish the diagnosis. The diagnosis of STEMI is based on any two of (1) typical chest pain, (2) ECG changes or new LBBB and (3) raised myocardial biomarkers.5, 9 ECG monitoring also should be initiated as soon as possible in all patients with suspected STEMI to detect life-threatening arrhythmias and allow prompt defibrillation if indicated. Typically, ST-segment elevation in acute myocardial infarction, measured at the J point, should be found in two contiguous leads and be ≥0.25 mV in men below the age of 40 years, ≥ 0.2 mV in men over the age of 40 years, or ≥0.15 mV in women in leads V2–V3 and/or ≥ 0.1 mV in other leads (in the absence of left ventricular (LV) hypertrophy or left bundle branch block (LBBB).9
Markers of myocardial necrosis are useful in corroborating the diagnosis, so it must be emphasized that they may not be elevated early after the onset of symptoms. Cardiac troponin (CTn) is the biomarker of choice because it is the most sensitive and specific marker of myocardial injury/necrosis available. Troponin levels usually increase after 3-4 hours.5 Troponin level may remain elevated up to 2 weeks. Elevated CTn values signal a higher acute risk and an adverse long term prognosis.10 Creatine Kinase Myocardial Band (CKMB) is less sensitive and specific. However, it remains useful for the diagnosis of early infarct extension (reinfarction) and peri-procedural MI because of its short half life.5 The level of CKMB and CTn at administration was elevated.
Acute MI has variable impact on long-term survival. After STEMI, patients who develop heart failure carry worse prognosis. Potential benefits might arise from earlier prediction and initiation of preventive treatment for heart failure during STEMI.3 Strategies for the earliest possible risk assessment after STEMI have become essential not only to better target therapies but also to introduce these therapies in the timeliest manner while benefits still be greatest and to monitor the effects of therapy.3, 4
If in spite of angiography performed in the acute phase at the time of PCI there are concerns about inducible ischaemia in the infarct or non-infarct area, outpatient exercise testing (bicycle or treadmill) or stress imaging (using scintigraphy, echocardiography, or MRI) within 4–6 weeks is appropriate. LV dysfunction after STEMI may be due to necrosis, to stunning of viable myocardium remaining in the infarct territory, to hibernation of viable myocardium, or to a combination of all three. Simple stunning should usually recover within 2 weeks of the acute ischaemic insult if reperfusion has been established, but, if ischaemic episodes persist, recurrent stunning may become hibernation and requires revascularization for recovery of function. Hence, several diagnostic techniques can detect myocardial viability, especially MRI.1
Myocardial oedema in the acute phase of myocardial infarction can be visualized as a bright signal on T2-weighted images, defining ‘myocardium at risk’. The major advantages of this technique are to distinguish chronic from acute infarction and to quantify the proportion of myocardial salvaged by comparing T2-weighted oedematous size and late enhancement images.11 This case showed myocardial edema at anteroseptal and inferoseptal wall. Meanwhile, LGE images are T1-weighted inversion recovery sequences acquired about 10 min after intravenous administration of gadolinium. Gadolinium enhances its distribution volume in certain conditions such as necrotic or fibrotic myocardium (hyperenhancement). 11
However, LVEF assessment performed very early after STEMI does not reliably predict late heart failure, because of heterogeneous LV remodeling and healing. LGE measured by cardiac MRI identifies necrosis burden in the chronic phase after MI. In this context, LGE predicts functional recovery after revascularization. However, suggestions of “infarct shrinkage” observed between the first week after infarction and later follow-up has raised the concern that LGE might not accurately assess myocardial damage due to overestimation in the very early STEMI period, because it might represent a combination of necrosis and edema comprising the area at risk. Alternate strategies including the assessment of late MVO and myocardial salvage have been proposed.3 Early and late MVO assessed by MRI are prognostic markers for combined clinical endpoints after STEMI.11 This case showed late MVO embedded inside the necrotic tissue at LGE sequential of cardiac MRI.
Microvascular cell damage causes leakage of blood out of the injured vessel and the subsequent healing process is characterized by haemoglobin degradation in which dark areas on post-contrast sequences indicate not only the presence of microvascular obstruction, but also of intramyocardial haemorrhage. The extent of the hemorrhagic area correlates with the size of ‘dark zones’ on LGE sequences.11
As a promising non-invasive imaging tool, CE-MRI can detect the pathological consequences of reperfusion strategies in vivo and provide more information such as infarct size, myocardial AAR, myocardial viability, MVO, and myocardial hemorrhage. Findings by Jiangqiang et al in 2012 added some knowledges in which the median infarct size was significantly smaller in the NSTEMI group than in the STEMI group (10.7% [5.6–18.1] vs. 19.2% [10.3–30.7], P<0.001). The NSTEMI group also had a significantly lower extent of microvascular obstruction and a smaller number of segments with >75% of infarct transmurality relative to the STEMI group (0% [0–0.6] vs. 0.9% [0–2.3], P<0.001 and 3.0 ± 2.3 vs. 4.6 ± 2.9, P = 0.001, respectively). Myocardial hemorrhage was detected less frequently in the NSTEMI group than the STEMI group (22.6% vs. 43.8%, P = 0.029).2
Another research by Larose et al discovered that LGE quantification very early during STEMI predicts late heart failure and adverse events beyond traditional risk factors such as infarct territory, maximum CK-MB rise, pain-to-balloon time, presence of Q waves, and LVEF during STEMI. A second major finding is that, during the hyperacute phase of STEMI, LGE volume incurred the strongest association to LV function change, beyond infarct transmurality, MVO, and salvaged myocardium (SM).3 IS within 1 week from AMI was directly related to LV remodelling and was a stronger predictor of future events than measures of LV systolic performance. The occurrence of LV dysfunction at 6 months increased with greater LGE: a cut-off of ≥ 23% LGE measured on hyperacute MRI showed the best accuracy for late LV dysfunction (sensitivity 89%, specificity 74%). In the assessment of myocardial viability in AMI patients, when the extent of LGE is <50% the likelihood for functional recovery is efficient.12 This patient had 20% LGE volume so the possibility of LV dysfunction in the near future is low, but the likelihood for functional recovery was decreased since the necrosis transmurality was 70%.
SUMMARY
A fifty-three years old male was reported of having 11 hours chief complaint of typical chest pain. He was presented with non-ST segment elevation ECG after prior inferior ST segments elevation. There was elevation of cardiac enzymes. He underwent coroangiography which revealed total occlusion at LCx. CE-MRI was done and showed sign of sign of stress-inducible ischemia at inferolateral, septal, anterior walls and sign of acute myocardial infarction with late MVO at the same area.
This case report emphasizes the promising non-invasive imaging tool, CE-MRI, in providing more information such as infarct size, AAR, myocardial viability, MVO, and myocardial hemorrhage. This modality can be use to detect residual ischemia at culprit lesion, stress-inducible ischemia of remote lesion, infarct size, and late MVO. Available data suggest that LGE quantification very early during STEMI predicts late heart failure and adverse events beyond traditional risk factors such as infarct territory, maximum CK-MB rise, pain-to-balloon time, presence of Q waves, and LVEF during STEMI. Another major finding is that, during the hyperacute phase of STEMI, LGE volume incurred the strongest association to LV function change, beyond infarct transmurality, MVO, and salvaged myocardium (SM). Late MVO assessed by MRI also become prognostic markers for combined clinical endpoints after STEMI.
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