P572Characterization of microvascular injury after acute ST elevation myocardial infarction

Abstract

INTRODUCTION: Microvascular injury (MVI) is a combination of microvascular obstruction and intramyocardial hemorrhage (IMH), usually seen after reperfusion of prolonged coronary occlusion due to damage and dysfunction of the microvasculature. Accurate detection of MVI is of great importance, since it has been identified as an independent predictor of poor prognostic outcome following myocardial infarction. We present a case that illustrates how cardiovascular magnetic resonance imaging (CMR) with different modalities plays an important role in visualization and identifying actual size of MVI and infarct area. CASE: A 45-years-old male with history of smoking presented to the coronary care unit, 7 hours after onset of chest pain. On admission, blood pressure was 110/70mmHg with a pulse rate of 96/min, electrocardiography showed ST segment elevation in the inferior leads. Primary percutaneous intervention with stenting was performed in the proximal and mid circumflex artery, with normal post procedural TIMI flow. CMR was performed 3 days after admission to assess cardiac function and infarct characterization on a clinical 1.5T MR system. First, established techniques were used. Volumetric analysis of the cine images (A) revealed an LVEDV of 174mL and LVEF of 48%. T2w imaging showed a well demarcated area of high signal intensity(white arrow) consistent with myocardial edema with an attenuated signal in the infarct core (blue arrow) suggesting IMH.(B) After administration of gadolinium-based contrast agent, the late enhancement images confirmed the previous findings, with delayed wash-out of contrast in the infarcted myocardium (white arrow), normal wash-out in remote (asterisk), and lack of contrast diffusion into the infarct core (blue arrow) due to the injured microvasculature.(C) Recent developments in CMR sequences provide the ability to further characterize the infarcted area. Pre-contrast T1 mapping showed normal T1 values in remote myocardium with long T1 relaxation times (1284 +/- 55ms) in the infarcted myocardium due to the increased extracellular space and myocardial injury, and shorter T1 values (777 +/- 24ms) in the core due to IMH.(D) Additionally, T2 mapping was used to quantify the extent of edema which demonstrated long T2 relaxation time in the infarcted myocardium (82 +/- 1.9ms); a shorter T2 relaxation time was found in the core which could not be discriminated from remote (54 +/- 2.9ms versus 52 +/- 2.4ms).(E) Thus, T2* imaging was used to confirm the presence of IMH in the infarct core, by measuring a very short T2* relaxation time of 5ms(F), indicative of iron deposition due to degradation of hemoglobin. CONCLUSION(S): CMR is an established technique to evaluate patients after acute myocardial infarction. Using traditional sequences, function, edema and infarct size can be measured. However, the newer tissue mapping techniques provide incremental value, by quantification and discrimination of the different areas of myocardial injury.