American Journal of Emergency Medicine 33 (2015) 1538.e1–1538.e4
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Myocardial hypoperfusion on conventional contrast computed tomography☆,☆☆,★ Abstract Non–electrocardiogram (ECG)–gated contrast computed tomography (CT) is commonly performed to exclude aortic dissection in chest pain patients. Besides evaluating the aorta for dissection flap, attention should be paid to the myocardium for areas of hypoenhancement that may suggest ischemia. Current models of multidetector CT enable assessment of myocardial perfusion with minimal motion artifact even without ECG gating. Transmural hypoenhancement with preserved wall thickness in a coronary distribution is highly specific for acute myocardial infarction. We report 2 cases of acute chest pain with initial nondiagnostic studies that underwent CT aortogram to exclude dissection. Instead, the CT showed myocardial hypoenhancement in left anterior descending artery territory. Myocardial hypoenhancement occurred before ST-segment elevation on ECG, suggesting that recognition of this important finding may lead to earlier revascularization decisions. Conventional computed tomography (CT) is an imaging modality of choice for patients of suspected aortic dissection. Although a negative study excludes acute aortic syndrome, the images should be carefully reviewed for alternative causes of chest pain. In particular, the myocardium is assessed for any areas of hypoenhancement that conform to a coronary artery distribution, which is strong evidence for acute myocardial infarction. We report 2 cases of acute chest pain; both had initial nondiagnostic electrocardiograms (ECGs) and cardiac enzymes and underwent CT to exclude aortic dissection that instead confirmed myocardial infarction. A 67-year-old man with history of hypertension, dyslipidemia, and diabetes presented with chest and back pain for 2 hours. Blood pressure was 130/75 mm Hg; pulse was 60 and regular. Physical examination was unremarkable. Electrocardiogram (Fig. 1A) showed right bundlebranch block, Q waves in inferior (II, III, and aVF), and precordial leads (V2-V4). Initial creatine kinase was 79 IU/L (reference, 39-308 IU/L); troponin T, 21 ng/L (reference, b13 ng/L; N 100 ng/L defines myocardial infarction). Chest radiograph was notable for mediastinal widening; therefore, CT aortogram was performed (Fig. 2A and B). Atherosclerotic plaques and a penetrating aortic ulcer were noted in the aortic arch (Fig. 2A, arrows), which was thought to be the cause of chest pain. The patient was transferred to a tertiary institution for presumed acute aortic syndrome but shortly developed cardiogenic shock. An electrocardiogram was repeated (Fig. 1B) showing ST-segment elevation in precordial leads (V2-V6). Urgent coronary angiogram showed an occluded left anterior descending artery and severe triple-vessel disease. Primary stenting was ☆ No funding is received to produce this work. ☆☆ All authors have access to the data and role in writing this manuscript. ★ We report no conflict of interests regarding this work.
0735-6757/© 2015 Elsevier Inc. All rights reserved.
performed to left anterior descending and right coronary arteries; left circumflex artery was stented in a staged fashion. In retrospect, myocardial hypoenhancement in septal, apical, and lateral wall (Fig. 2B, arrowheads) was already apparent on initial CT. A 72-year-old man with history of treated pulmonary tuberculosis presented with chest pain radiating to back for 3 hours. Blood pressure was 113/63 mm Hg; pulse was 64 and regular. Absent breath sound was noted over left upper lung field. Electrocardiogram (Fig. 3) showed Twave inversion in lateral leads (I and aVL) and equivocal ST-segment deviation in anterior leads (V2-V4). Initial creatine kinase was 73 IU/L (reference, 39-308 IU/L); troponin T, 52 ng/L (reference, b 13 ng/L; N100 ng/L defines myocardial infarction). Chest radiograph showed left apical capping; CT aortogram was performed for suspected aortic dissection (Fig. 4A and B). No dissection flap was seen. The patient was treated as non– ST-segment elevation myocardial infarction with aspirin, clopidogrel, and heparin; he shortly developed cardiogenic shock. Electrocardiogram showed ST-segment elevation in precordial leads (V2-V5). Urgent coronary angiogram showed subtotal occlusion at proximal left anterior descending (Fig. 4C and D) that was stented. In hindsight, myocardial hypoenhancement in septal, apical, and anterior wall (Fig. 4A and B, arrowheads) was already evident on CT. The presentations of acute myocardial infarction and acute aortic syndrome are similar enough that CT is used to exclude dissection in suspicious cases. Although the images are not ECG gated, current models of multidetector CT acquire images of the heart in 100 to 200 milliseconds with minimal motion artifact. The images are usually taken 30 to 60 seconds after contrast injection in the CT aortogram protocol, thus allowing simultaneous, albeit crude, assessment of myocardial perfusion. Transmural hypoenhancement in a coronary artery distribution with preserved wall thickness is highly specific for acute myocardial infarction [1,2]. It is already recognizable a few hours after onset, before the rise of cardiac enzymes [3-5]. In case 1, incidental finding of penetrating aortic ulcer is a distractor, whereas myocardial hypoperfusion in left anterior descending artery distribution was overlooked, resulting in delayed revascularization. In case 2, the initial equivocal ECG and cardiac enzymes, as well as the CT showing no dissection, were falsely reassuring and led to less vigilance to scrutinize CT images for alternative causes of chest pain. Common to both cases is the belief that conventional, non–ECG-gated contrast CT is inadequate to assess myocardial perfusion. Instead, we observe that the CT myocardial perfusion defect was present even before STsegment elevation on ECG. It vindicates the ischemia cascade, which describes hypoperfusion preceding ECG changes in myocardial ischemia. However, revascularization decisions are currently made based on STsegment change on ECG. It is unclear whether transmural hypoperfusion on CT should be treated as an ST-segment elevation equivalent.
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S. Ching, T.S. Chung / American Journal of Emergency Medicine 33 (2015) 1538.e1–1538.e4
Fig. 1. A, Electrocardiogram showed right bundle-branch block, Q waves in inferior (II, III, and aVF), and precordial leads (V2-V4). B, Electrocardiogram later showed ST-segment elevation in anterior and lateral leads (I, aVL, and V2-V6).
S. Ching, T.S. Chung / American Journal of Emergency Medicine 33 (2015) 1538.e1–1538.e4
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Fig. 2. A, Atherosclerotic plaques (arrows) and a penetrating aortic ulcer (arrowhead) are present in aortic arch. B, Myocardial hypoenhancement in septal, apical, and lateral wall (arrowheads). Fig. 4. A and B, Myocardial hypoenhancement in septal, apical, and anterior wall (arrowheads). C and D, Coronary angiogram showing subtotal occlusion at proximal left anterior descending artery (arrows).
Fig. 3. Electrocardiogram showed T-wave inversion in lateral leads (I and aVL) and equivocal ST-segment deviation in anterior leads (V2-V4).
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S. Ching, T.S. Chung / American Journal of Emergency Medicine 33 (2015) 1538.e1–1538.e4
Recognition of myocardial hypoenhancement is particularly important in patients with initial nondiagnostic ECG and cardiac enzymes and in patients with a competing cause of chest pain, potentially leading to earlier diagnosis and revascularization. Shing Ching, MBBS⁎ Tak Shun Chung, MBBS Division of Cardiology, Department of Medicine and Geriatrics United Christian Hospital, Hong Kong, China ⁎Corresponding author at: Department of Medicine and Geriatrics United Christian Hospital, Kwun Tong, Kowloon, Hong Kong, China Email address: [email protected] http://dx.doi.org/10.1016/j.ajem.2015.07.072
References [1] Gosalia A, Haramati LB, Sheth MP, Spindola-Franco H. CT detection of acute myocardial infarction. Am J Roentgenol 2004;182(6):1563–6. [2] Patel R, Lewis D, Dubinsky TJ. Myocardial infarction on non–ECG synchronized contrast-enhanced multi-detector computed tomography. Emerg Radiol 2005; 11(5):301–5. [3] Hecht HS, Bhatti T. Multislice coronary computed tomographic angiography in emergency department presentations of unsuspected acute myocardial infarction. J Cardiovasc Comput Tomogr 2009;3(4):272–8. [4] Ichinose T, Yamase M, Yokomatsu Y, Kawano Y, Konishi H, Tanimoto K, et al. Acute myocardial infarction with myocardial perfusion defect detected by contrastenhanced computed tomography. Intern Med 2009;48(14):1235–8. [5] Lo S, Kwok WK. Acute myocardial infarction found by multi-detector computed tomography ordered for suspected aortic dissection. Hong Kong Med J 2008;14(3): 233–5.
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Myocardial hypoperfusion on conventional contrast computed tomography☆,☆☆,★ Abstract Non–electrocardiogram (ECG)–gated contrast computed tomography (CT) is commonly performed to exclude aortic dissection in chest pain patients. Besides evaluating the aorta for dissection flap, attention should be paid to the myocardium for areas of hypoenhancement that may suggest ischemia. Current models of multidetector CT enable assessment of myocardial perfusion with minimal motion artifact even without ECG gating. Transmural hypoenhancement with preserved wall thickness in a coronary distribution is highly specific for acute myocardial infarction. We report 2 cases of acute chest pain with initial nondiagnostic studies that underwent CT aortogram to exclude dissection. Instead, the CT showed myocardial hypoenhancement in left anterior descending artery territory. Myocardial hypoenhancement occurred before ST-segment elevation on ECG, suggesting that recognition of this important finding may lead to earlier revascularization decisions. Conventional computed tomography (CT) is an imaging modality of choice for patients of suspected aortic dissection. Although a negative study excludes acute aortic syndrome, the images should be carefully reviewed for alternative causes of chest pain. In particular, the myocardium is assessed for any areas of hypoenhancement that conform to a coronary artery distribution, which is strong evidence for acute myocardial infarction. We report 2 cases of acute chest pain; both had initial nondiagnostic electrocardiograms (ECGs) and cardiac enzymes and underwent CT to exclude aortic dissection that instead confirmed myocardial infarction. A 67-year-old man with history of hypertension, dyslipidemia, and diabetes presented with chest and back pain for 2 hours. Blood pressure was 130/75 mm Hg; pulse was 60 and regular. Physical examination was unremarkable. Electrocardiogram (Fig. 1A) showed right bundlebranch block, Q waves in inferior (II, III, and aVF), and precordial leads (V2-V4). Initial creatine kinase was 79 IU/L (reference, 39-308 IU/L); troponin T, 21 ng/L (reference, b13 ng/L; N 100 ng/L defines myocardial infarction). Chest radiograph was notable for mediastinal widening; therefore, CT aortogram was performed (Fig. 2A and B). Atherosclerotic plaques and a penetrating aortic ulcer were noted in the aortic arch (Fig. 2A, arrows), which was thought to be the cause of chest pain. The patient was transferred to a tertiary institution for presumed acute aortic syndrome but shortly developed cardiogenic shock. An electrocardiogram was repeated (Fig. 1B) showing ST-segment elevation in precordial leads (V2-V6). Urgent coronary angiogram showed an occluded left anterior descending artery and severe triple-vessel disease. Primary stenting was ☆ No funding is received to produce this work. ☆☆ All authors have access to the data and role in writing this manuscript. ★ We report no conflict of interests regarding this work.
0735-6757/© 2015 Elsevier Inc. All rights reserved.
performed to left anterior descending and right coronary arteries; left circumflex artery was stented in a staged fashion. In retrospect, myocardial hypoenhancement in septal, apical, and lateral wall (Fig. 2B, arrowheads) was already apparent on initial CT. A 72-year-old man with history of treated pulmonary tuberculosis presented with chest pain radiating to back for 3 hours. Blood pressure was 113/63 mm Hg; pulse was 64 and regular. Absent breath sound was noted over left upper lung field. Electrocardiogram (Fig. 3) showed Twave inversion in lateral leads (I and aVL) and equivocal ST-segment deviation in anterior leads (V2-V4). Initial creatine kinase was 73 IU/L (reference, 39-308 IU/L); troponin T, 52 ng/L (reference, b 13 ng/L; N100 ng/L defines myocardial infarction). Chest radiograph showed left apical capping; CT aortogram was performed for suspected aortic dissection (Fig. 4A and B). No dissection flap was seen. The patient was treated as non– ST-segment elevation myocardial infarction with aspirin, clopidogrel, and heparin; he shortly developed cardiogenic shock. Electrocardiogram showed ST-segment elevation in precordial leads (V2-V5). Urgent coronary angiogram showed subtotal occlusion at proximal left anterior descending (Fig. 4C and D) that was stented. In hindsight, myocardial hypoenhancement in septal, apical, and anterior wall (Fig. 4A and B, arrowheads) was already evident on CT. The presentations of acute myocardial infarction and acute aortic syndrome are similar enough that CT is used to exclude dissection in suspicious cases. Although the images are not ECG gated, current models of multidetector CT acquire images of the heart in 100 to 200 milliseconds with minimal motion artifact. The images are usually taken 30 to 60 seconds after contrast injection in the CT aortogram protocol, thus allowing simultaneous, albeit crude, assessment of myocardial perfusion. Transmural hypoenhancement in a coronary artery distribution with preserved wall thickness is highly specific for acute myocardial infarction [1,2]. It is already recognizable a few hours after onset, before the rise of cardiac enzymes [3-5]. In case 1, incidental finding of penetrating aortic ulcer is a distractor, whereas myocardial hypoperfusion in left anterior descending artery distribution was overlooked, resulting in delayed revascularization. In case 2, the initial equivocal ECG and cardiac enzymes, as well as the CT showing no dissection, were falsely reassuring and led to less vigilance to scrutinize CT images for alternative causes of chest pain. Common to both cases is the belief that conventional, non–ECG-gated contrast CT is inadequate to assess myocardial perfusion. Instead, we observe that the CT myocardial perfusion defect was present even before STsegment elevation on ECG. It vindicates the ischemia cascade, which describes hypoperfusion preceding ECG changes in myocardial ischemia. However, revascularization decisions are currently made based on STsegment change on ECG. It is unclear whether transmural hypoperfusion on CT should be treated as an ST-segment elevation equivalent.
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S. Ching, T.S. Chung / American Journal of Emergency Medicine 33 (2015) 1538.e1–1538.e4
Fig. 1. A, Electrocardiogram showed right bundle-branch block, Q waves in inferior (II, III, and aVF), and precordial leads (V2-V4). B, Electrocardiogram later showed ST-segment elevation in anterior and lateral leads (I, aVL, and V2-V6).
S. Ching, T.S. Chung / American Journal of Emergency Medicine 33 (2015) 1538.e1–1538.e4
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Fig. 2. A, Atherosclerotic plaques (arrows) and a penetrating aortic ulcer (arrowhead) are present in aortic arch. B, Myocardial hypoenhancement in septal, apical, and lateral wall (arrowheads). Fig. 4. A and B, Myocardial hypoenhancement in septal, apical, and anterior wall (arrowheads). C and D, Coronary angiogram showing subtotal occlusion at proximal left anterior descending artery (arrows).
Fig. 3. Electrocardiogram showed T-wave inversion in lateral leads (I and aVL) and equivocal ST-segment deviation in anterior leads (V2-V4).
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S. Ching, T.S. Chung / American Journal of Emergency Medicine 33 (2015) 1538.e1–1538.e4
Recognition of myocardial hypoenhancement is particularly important in patients with initial nondiagnostic ECG and cardiac enzymes and in patients with a competing cause of chest pain, potentially leading to earlier diagnosis and revascularization. Shing Ching, MBBS⁎ Tak Shun Chung, MBBS Division of Cardiology, Department of Medicine and Geriatrics United Christian Hospital, Hong Kong, China ⁎Corresponding author at: Department of Medicine and Geriatrics United Christian Hospital, Kwun Tong, Kowloon, Hong Kong, China Email address: [email protected] http://dx.doi.org/10.1016/j.ajem.2015.07.072
References [1] Gosalia A, Haramati LB, Sheth MP, Spindola-Franco H. CT detection of acute myocardial infarction. Am J Roentgenol 2004;182(6):1563–6. [2] Patel R, Lewis D, Dubinsky TJ. Myocardial infarction on non–ECG synchronized contrast-enhanced multi-detector computed tomography. Emerg Radiol 2005; 11(5):301–5. [3] Hecht HS, Bhatti T. Multislice coronary computed tomographic angiography in emergency department presentations of unsuspected acute myocardial infarction. J Cardiovasc Comput Tomogr 2009;3(4):272–8. [4] Ichinose T, Yamase M, Yokomatsu Y, Kawano Y, Konishi H, Tanimoto K, et al. Acute myocardial infarction with myocardial perfusion defect detected by contrastenhanced computed tomography. Intern Med 2009;48(14):1235–8. [5] Lo S, Kwok WK. Acute myocardial infarction found by multi-detector computed tomography ordered for suspected aortic dissection. Hong Kong Med J 2008;14(3): 233–5.
