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Non–ST-Segment Elevation Acute Coronary Syndromes

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Presentation on theme: "Non–ST-Segment Elevation Acute Coronary Syndromes"— Presentation transcript:

1 Non–ST-Segment Elevation Acute Coronary Syndromes
by Henry Chang, James K. Min, Sunil V. Rao, Manesh R. Patel, Orlando P. Simonetti, Giuseppe Ambrosio, and Subha V. Raman Circ Cardiovasc Imaging Volume 5(4): July 17, 2012 Copyright © American Heart Association, Inc. All rights reserved.

2 The typical pathogenesis of non–ST-segment elevation acute coronary syndromes begins with an atherosclerotic plaque. The typical pathogenesis of non–ST-segment elevation acute coronary syndromes begins with an atherosclerotic plaque. Disruption of the vulnerable plaque results in thrombus formation as coagulation factors come into contact with intraplaque elements. Embolic debris may travel downstream and lodge in microvessels. Injured myocardium develops edema and subsequent necrosis that begins in the subendocardium and may extend outward if at-risk regions are not salvaged. Henry Chang et al. Circ Cardiovasc Imaging. 2012;5: Copyright © American Heart Association, Inc. All rights reserved.

3 ECG, cardiac magnetic resonance (CMR), ultrasound, and angiographic findings are shown in a 69-year-old woman with chest and epigastric pain that had resolved by the time she presented to the emergency department. ECG, cardiac magnetic resonance (CMR), ultrasound, and angiographic findings are shown in a 69-year-old woman with chest and epigastric pain that had resolved by the time she presented to the emergency department. Her ECG was a concern for injury (A), and initial troponin was mildly elevated at 0.14 ng/mL. However, because of the lack of symptoms by the time of presentation, invasive angiography was deferred to the following morning. T2-CMR in vertical-long axis (B) and horizontal long-axis (C) planes showed increased signal intensity in apical myocardium, beyond T2 increase in the stagnant apical blood. Apical dyskinesis was also evident (end-diastolic [D and E] and end-systolic [F and G] frames), and late gadolinium enhancement (H and I) showed a large area of signal enhancement in the apical myocardium as well as thrombus in the apical left ventricle (LV). Echocardiography without contrast (J) was also concerning for LV apical thrombus. Invasive coronary angiography (K) showed serial nonobstructive plaques in the left anterior descending coronary artery. The acute coronary syndrome event evident by myocardial imaging was ascribed to plaque erosion (online-only Data Supplement Movies I–IV). Henry Chang et al. Circ Cardiovasc Imaging. 2012;5: Copyright © American Heart Association, Inc. All rights reserved.

4 A 59-year-old man with a history of coronary stent placement in the left anterior descending (LAD) artery presented to the emergency department (ED) for evaluation of atypical chest pain. A 59-year-old man with a history of coronary stent placement in the left anterior descending (LAD) artery presented to the emergency department (ED) for evaluation of atypical chest pain. Cardiac magnetic resonance showed a perfusion abnormality with stress (A) not present at rest (B) and corresponding to a region of infarct scar by late gadolinium-enhancement (C). Single-photon emission computed tomography imaging demonstrated a perfusion defect under stress (E) compared with at rest (F). Invasive coronary angiography (D) showed patent LAD stent. The presence of a perfusion abnormality in the absence of an anatomic target for repeat intervention led to his medical regimen being intensified. At a subsequent ED visit for chest pain, coronary computed tomographic angiography was performed, which demonstrated a patent stent with mild proximal malapposition (G, arrow). As a result of imaging, the medical regimen was further optimized, and repeat catheterization was deemed unnecessary (online-only Data Supplement Movies V–VII). Henry Chang et al. Circ Cardiovasc Imaging. 2012;5: Copyright © American Heart Association, Inc. All rights reserved.

5 Coronary computed tomographic angiography demonstrates adverse atherosclerotic plaque characteristics such as (A) stenosis of the lumen, where luminal diameter at the site of stenosis shows significant and progressive narrowing compared with the proximal more normal-appearing coronary segment, (B) low x-ray attenuation plaques (LAP) indicated by intraplaque Hounsfield unit (HU) values <30, and (C) positive remodeling (PR) of vessel wall defined by an intraplaque arterial diameter-to-normal coronary segment diameter >1.10. Coronary computed tomographic angiography demonstrates adverse atherosclerotic plaque characteristics such as (A) stenosis of the lumen, where luminal diameter at the site of stenosis shows significant and progressive narrowing compared with the proximal more normal-appearing coronary segment, (B) low x-ray attenuation plaques (LAP) indicated by intraplaque Hounsfield unit (HU) values <30, and (C) positive remodeling (PR) of vessel wall defined by an intraplaque arterial diameter-to-normal coronary segment diameter >1.10. Henry Chang et al. Circ Cardiovasc Imaging. 2012;5: Copyright © American Heart Association, Inc. All rights reserved.

6 ECG, cardiac magnetic resonance (CMR), and angiographic findings are shown in a 50-year-old man with diabetes mellitus who presented with intermittent chest pressure; initial troponin-I values were 0.44 and then 0.21 ng/mL (limit <0.11), with no symptoms on arrival after transfer from a regional medical center. ECG, cardiac magnetic resonance (CMR), and angiographic findings are shown in a 50-year-old man with diabetes mellitus who presented with intermittent chest pressure; initial troponin-I values were 0.44 and then 0.21 ng/mL (limit <0.11), with no symptoms on arrival after transfer from a regional medical center. Invasive angiography was planned for the following morning, preceded by CMR with T2-weighted imaging as part of a research protocol. Although ECG was unremarkable (A), T2-CMR in vertical-long axis (B) and horizontal long-axis (C) planes showed increased signal intensity in septal and apical myocardium. Regional wall motion appeared normal in these planes (end-diastolic [D and E] and end-systolic [F and G] frames), and late gadolinium-enhancement (H and I) showed no evident myocardial injury. Invasive coronary angiography later that morning (J) showed high-grade stenoses in the left anterior descending artery and first diagonal branch treated with percutaneous coronary interventions. Interventions aimed at rescuing the imaged salvageable myocardium were considered, and another stent was placed in the proximal right coronary artery (K) the following day (online-only Data Supplement Movies VIII and IX). Henry Chang et al. Circ Cardiovasc Imaging. 2012;5: Copyright © American Heart Association, Inc. All rights reserved.

7 A 56-year-old man with a history of myocardial infarction (MI), coronary artery disease, and multiple coronary stents presented to the emergency department for evaluation of chest pain with epigastric symptoms. A 56-year-old man with a history of myocardial infarction (MI), coronary artery disease, and multiple coronary stents presented to the emergency department for evaluation of chest pain with epigastric symptoms. ECG showed right bundle branch block as well as ST-segment depression and T-wave inversion in leads V1 and V2 (A). His Thrombolysis in MI score was 4, and initial troponins were ­negative. On cardiac magnetic resonance examination, mild wall motion abnormalities were seen (end-diastolic [B] and end-systolic [C] frames in the vertical long-axis view). T2 mapping revealed elevated T2 values in areas absent of any late gadolinium-enhancement (LGE), suggestive of myocardium at risk (T2 and LGE images with vertical long-axis [D and E], 3-chamber [F and G], and short-axis [H and I] views). Note the region of LGE hyperenhancement in (I) without a corresponding T2 elevation in (H), indicating the presence of an old infarct and enabling identification of myocardium at risk amid multiple anatomic targets for revascularization. Invasive angiography showed severe triple-vessel disease with chronic total occlusion of mid right coronary artery with collateral flow and moderate in-stent restenosis throughout the circumflex territory (J). Henry Chang et al. Circ Cardiovasc Imaging. 2012;5: Copyright © American Heart Association, Inc. All rights reserved.

8 Limitations of current diagnostic and treatment approaches are highlighted in this 44-year-old nonsmoking man who presented with stable angina. Limitations of current diagnostic and treatment approaches are highlighted in this 44-year-old nonsmoking man who presented with stable angina. Computed tomographic angiography identified single-vessel coronary stenosis (A, arrow) in the right coronary artery (RCA), prompting immediate institution of aggressive medical therapy. After several weeks, he presented to the emergency department with unstable symptoms, and emergent coronary angiography identified plaque rupture at the site of RCA atherosclerotic plaque characteristics that included low-attenuation plaque with Hounsfield unit (HU) <30 (B, arrow) and positive remodeling (C) indicated by greater vessel wall diameter at the site of plaque (distal open arrows) vs the reference segment (proximal closed arrows). Henry Chang et al. Circ Cardiovasc Imaging. 2012;5: Copyright © American Heart Association, Inc. All rights reserved.


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