Clinical Imaging 39 (2015) 897–900
Contents lists available at ScienceDirect
Clinical Imaging journal homepage: http://www.clinicalimaging.org
Acute left circumflex coronary artery occlusion detected on nongated CT☆ Netanel S. Berko ⁎, Elana T. Clark, Jeffrey M. Levsky Department of Radiology, Albert Einstein College of Medicine, Montefiore Medical Center, 111 East 210th Street, Bronx, NY 10467-2490
a r t i c l e
i n f o
Article history: Received 9 February 2015 Received in revised form 11 May 2015 Accepted 15 May 2015 Keywords: Myocardial infarction CT Hypoperfusion Left circumflex coronary artery
a b s t r a c t We describe a patient with chest pain and a nondiagnostic electrocardiogram in whom computed tomographic (CT) aortography demonstrated myocardial hypoperfusion in the distribution of the circumflex artery as well as an abrupt cutoff of contrast in the left circumflex artery. Subsequent cardiac catheterization confirmed occlusion of the circumflex artery and led to revascularization. The diagnosis of acute myocardial infarction on CT can dramatically alter the clinical management of a patient, especially in cases in which other tests are equivocal. © 2015 Elsevier Inc. All rights reserved.
1. Introduction Chest pain is one of the most common complaints in patients presenting to the emergency department. Imaging studies play an important role in the evaluation of chest pain, particularly in cases when aortic dissection or pulmonary embolism is suspected. We present a case in which an unsuspected diagnosis of acute myocardial infarction with a large-branch coronary occlusion was made on nongated computed tomography (CT).
2. Case report A 63-year-old man presented to the emergency department with “squeezing,” intermittent, intense chest pain radiating to the neck and left shoulder for a few hours. The patient had no history of coronary disease and had never experienced similar pain. He had a 40-pack-year smoking history and known hypertension. On physical examination, the patient was in moderate distress, with a blood pressure of 220/120, pulse of 73 beats per minute, and oxygen saturation of 100% on room air. There were no other significant physical findings. The initial electrocardiogram demonstrated normal sinus rhythm with nonspecific flattening of T waves in leads V5 and V6. Serum cardiac enzyme levels were within normal range, with a troponin T b0.01 ng/ml (normal b0.11 ng/ml), creatine phosphokinase (CPK) of
☆ Conflicts of interest: none. ⁎ Corresponding author. Department of Radiology, Albert Einstein College of Medicine, Montefiore Medical Center, 111 East 210th Street, Bronx, NY 10467-2490. Tel.: +1 718 920 4872; fax: +1 718 920 4854. E-mail address: [email protected] (N.S. Berko). http://dx.doi.org/10.1016/j.clinimag.2015.05.007 0899-7071/© 2015 Elsevier Inc. All rights reserved.
178 U/L (normal 20–200 U/L), and creatine kinase MB (CK-MB) of 2.8 ng/ml (normal b5.1 ng/ml). A portable chest radiograph was unremarkable, and further evaluation with CT aortography was requested for possible aortic dissection. CT examination was performed on a 64-slice LightSpeed VCT scanner (GE Healthcare, Waukesha, WI, USA). It demonstrated no aortic dissection; however, there was an area of hypoattenuation in the lateral wall of the left ventricle, which raised suspicion for an acute myocardial infarction in the distribution of the left circumflex coronary artery (Fig. 1A–B). Upon further review of multiplanar reformatted thinsection images, there was suggestion of an abrupt cutoff of contrast in the left circumflex artery (Fig. 1C). Of note, the patient’s heart rate was 68 beats per minute at the time of CT scan. Two hours following the CT scan, cardiac enzyme levels were elevated, with a troponin T of 0.34 ng/ml, CPK of 661 U/L, and CK-MB of 47.9 ng/ml, with further increase 12 h later, with levels of 1.85, 1512, and 115.8, respectively. The patient was admitted with a preliminary diagnosis of acute non-ST-elevation myocardial infarction. Cardiac catheterization was performed the following day and confirmed occlusion of the left circumflex artery (Fig. 2A). A bare metal stent was placed with restoration of flow (Fig. 2B). The patient had an uneventful postprocedure course to discharge. 3. Discussion Chest pain is one of the most common symptoms of patients presenting to the emergency department. Multiple possible etiologies, including cardiac, pulmonary, gastrointestinal, and musculoskeletal related problems, may be causative. The electrocardiogram serves as the initial triage method in order to identify patients with ST-elevation myocardial infarction that benefit from immediate
898
N.S. Berko et al. / Clinical Imaging 39 (2015) 897–900
Fig. 2. (A) Initial image from cardiac catheterization demonstrates an occlusion in the midleft circumflex coronary artery. (B) Improved flow is seen in this artery following angioplasty and bare metal stent placement.
Fig. 1. (A) Axial and (B) sagittal-reformatted, contrast-enhanced CT images demonstrate an area of hypoenhancement (arrows) in the lateral wall of the left ventricle. (C) Coronal oblique maximum intensity projection image demonstrates an abrupt cutoff (arrow) in the mid-left circumflex coronary artery.
catheterization and percutaneous intervention. Unfortunately, many cases of cardiac chest pain do not have characteristic electrocardiographic findings. In this setting, serial laboratory values, particularly
serum cardiac troponin levels, are used to confirm the presence of myocardial infarction, though it takes 4–8 h for these markers to become positive. CT is performed emergently in the diagnostic workup of chest pain patients, especially when acute aortic syndromes or pulmonary embolism are suspected. CT is often completed before the patient has been in the emergency department long enough to have positive cardiac biomarkers. In some patients, therefore, CT provides the first evidence of unsuspected myocardial infarction. It is expected that with expanding use of rapid diagnostic algorithms used to exclude a cardiac etiology of chest pain that utilize coronary CT angiography, the finding of unsuspected myocardial infarction in progress will increase. In a study of emergency department patients undergoing coronary CT angiography to assess for coronary artery disease, acute myocardial infarction was diagnosed in 1% of patients [1]. This role of CT can be of particular importance in situations where the diagnosis of myocardial infarction is not clinically obvious. In particular, diagnosis of myocardial infarction of the left circumflex artery territory is frequently difficult. The posterior location of the circumflex artery limits the utility of the standard 12-lead electrocardiogram
N.S. Berko et al. / Clinical Imaging 39 (2015) 897–900
[2,3]. In one study, less than half of patients with acute left circumflex infarct had ST segment elevation on electrocardiogram, compared with greater than 70% in patients with left anterior descending or right coronary artery infarcts [4]. Early detection of left circumflex infarction is significant due to the worse prognosis of patients with involvement of that territory as compared with those with right coronary artery infarcts [5]. This is for uncertain reasons but may be related to resultant mitral regurgitation, which occurs in 22% of patients [6]. Given the difficulty in the clinical diagnosis of some myocardial infarcts, recognition of characteristic imaging features of myocardial ischemia related to coronary occlusion is vital and may contribute to an unsuspected diagnosis. Acute myocardial infarction results in decreased myocardial perfusion which may be seen as an area of decreased myocardial attenuation in a pattern corresponding with the distribution of a coronary artery [7]. The hypoperfused area can frequently be visually detected, although in some cases an acute infarct manifests as an area of decreased attenuation (defined as a decrease in attenuation of 20 or more Hounsfield units less than surrounding myocardium) that is not easily appreciated visually. Use of a narrow window width (100–300) and level of 100 has been suggested to accentuate the hypoperfused myocardium [8,9]. CT has a high sensitivity and specificity in demonstrating acute myocardial infarction [7]. A study in patients admitted with acute chest pain demonstrated a higher rate of detection of myocardial hypoenhancement in circumflex infarcts compared with other coronary artery infarcts [10]. While decreased myocardial attenuation is present in both recent and chronic myocardial infarctions, certain features can be helpful in differentiating between the two. Fatty replacement frequently occurs in myocardial scar tissue, and thus chronic myocardial infarction will have significantly lower myocardial attenuation than an acute infarction [11,12]. Additionally, chronic infarction is also associated with ventricular dilation and wall thinning [13]. Occlusion of the left anterior descending coronary artery will typically result in hypoenhancement of the anterior wall and the apex of the left ventricle. Occlusion of the left circumflex artery often leads to hypoenhancement of the lateral basal wall. Right coronary artery occlusion may result in hypoenhancement of the inferior wall in patients with right dominance. In patients with posterior descending arteries from the left-sided circulation, there may be no obvious region of hypoenhancement. The extent of hypoperfusion depends on the location of coronary occlusion. Infarcts involving branch vessels will result in hypoenhancement that does not correspond to these vascular territories. Recent studies support the ability of resting coronary CT to detect acute myocardial infarction [14,15]. Although these publications focus on detecting abnormal myocardial enhancement on gated cardiac CT, the principle is the same for nongated CT that may be performed for aortic dissection or pulmonary embolism, as in our case. Of note, rest–stress CT perfusion, utilizing both resting CT and CT following stress, is a different developing modality which has been shown to be useful for the detection of myocardial ischemia outside the setting of an acute coronary event [16]. Additionally, the triple-rule-out CT, including evaluation of the pulmonary arteries, aorta, and coronary arteries, is employed in some institutions in patients with chest pain with low to intermediate risk for acute coronary syndrome [17]. CT for the evaluation of the coronary arteries is usually performed with ECG gating, in which imaging is acquired in synchrony with an ECG tracing. This decreases motion artifact, allowing better visualization of the coronary arteries. ECG gating may be performed prospectively, in which images are acquired only during predetermined phases of the cardiac cycle (usually early diastole), or retrospectively, in which data analysis is performed on images acquired during all phases of the cardiac cycle [18]. In contrast, during non-ECG-gated CT, as in our case, image acquisition is not related to the phase of the cardiac cycle, and therefore there
899
are greater motion artifact and typically more limited evaluation of the coronary arteries. Nongated CT is therefore not a reliable method for detecting coronary occlusion. However, myocardial hypoperfusion, which manifests as a region of lower attenuation in the myocardium, may be detected on nongated CT, as in our case. This demonstrates the importance of considering possible myocardial infarction in any chest pain patient and the need to look for signs of myocardial ischemia. When a coronary occlusion is detected, this offers an additional opportunity to advance diagnosis and therapy. Whereas many patients with non-STelevation myocardial infarction do not receive emergent catheterization and some undergo risk stratification by modalities such as nuclear stress testing, when there is strong evidence of acute occlusion of a coronary artery, more rapid intervention may be beneficial. When a CT study demonstrates occlusion of a significant-sized target vessel and there is a compatible clinical chest pain syndrome, we suggest urgent evaluation by an interventional cardiologist to consider catheterization for percutaneous intervention. 4. Conclusion This case illustrates the importance of examining myocardial perfusion and the coronary arteries on nongated CT angiograms. Myocardial hypoattenuation in the distribution of a coronary artery may be the first decisive clue to the presence of myocardial infarction and may suggest the diagnosis hours before laboratory tests become positive. This is of particular importance in situations where other diagnostic tests may be inconclusive, such as early in the course of left circumflex artery territory infarction. When a coronary artery occlusion is detected, the patient should be evaluated for urgent percutaneous intervention.
References [1] Hecht HS, Bhatti T. Multislice coronary computed tomographic angiography in emergency department presentations of unsuspected acute myocardial infarction. J Cardiovasc Comput Tomogr 2009;3:272–8. [2] Fuchs RM, Achuff SC, Grunwald L, Yin FC, Griffith LS. Electrocardiographic localization of coronary artery narrowings: studies during myocardial ischemia and infarction in patients with one-vessel disease. Circulation 1982;66:1168–76. [3] O'Keefe JH, Gibbons RJ. Left circumflex occlusion—underrecognized and undertreated. J Thromb Thrombolysis 2000;10:221–5. [4] Huey BL, Beller GA, Kaiser DL, Gibson RS. A comprehensive analysis of myocardial infarction due to left circumflex artery occlusion: comparison with infarction due to right coronary artery and left anterior descending artery occlusion. J Am Coll Cardiol 1988;12:1156–66. [5] Rasoul S, de Boer MJ, Suryapranata H, Hoorntje JCA, Gosselink ATM, Zijlstra F, et al. Circumflex artery-related acute myocardial infarction: limited ECG abnormalities but poor outcome. Neth Heart J 2007;15:286–90. [6] Matetzky S, Freimark D, Feinberg MS, Novikov I, Rath S, Rabinowitz B, et al. Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7–9: “hidden” ST-segment elevations revealing acute posterior infarction. J Am Coll Cardiol 1999;34:748–53. [7] Gosalia A, Haramati LB, Sheth MP, Spindola-Franco H. CT detection of acute myocardial infarction. AJR Am J Roentgenol 2004;182:1563–6. [8] Techasith T, Cury RC. Stress myocardial CT perfusion: an update and future perspective. JACC Cardiovasc Imaging 2011;4:905–16. [9] Busch JL, Alessio AM, Caldwell JH, Gupta M, Mao S, Kadakia J, et al. Myocardial hypo-enhancement on resting computed tomography angiography images accurately identifies myocardial hypoperfusion. J Cardiovasc Comput Tomogr 2011;5:412–20. [10] Lessick J, Ghersin E, Dragu R, Litmanovich D, Mutlak D, Rispler S, et al. Diagnostic accuracy of myocardial hypoenhancement on multidetector computed tomography in identifying myocardial infarction in patients admitted with acute chest pain syndrome. J Comput Assist Tomogr 2007;31:780–8. [11] Winer-Muram HT, Tann M, Aisen AM, Ford L, Jennings SG, Bretz R. Computed tomography demonstration of lipomatous metaplasia of the left ventricle following myocardial infarction. J Comput Assist Tomogr 2004;28:455–8. [12] Jacobi AH, Gohari A, Zalta B, Stein MW, Haramati LB. Ventricular myocardial fat: CT findings and clinical correlates. J Thorac Imaging 2007;22:130–5. [13] Nieman K, Cury RC, Ferencik M, Nomura CH, Abbara S, Hoffmann U, et al. Differentiation of recent and chronic myocardial infarction by cardiac computed tomography. Am J Cardiol 2006;98:303–8. [14] Branch KR, Busey J, Mitsumori LM, Strote J, Caldwell JH, Busch JH, et al. Diagnostic performance of resting CT myocardial perfusion in patients with possible acute coronary syndrome. AJR Am J Roentgenol 2013;200:W450–7.
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[15] Pursnani A, Lee AM, Mayrhofer T, Ahmed W, Uthamalingam S, Ferencik M, et al. Early resting myocardial computed tomography perfusion for the detection of acute coronary syndrome in patients with coronary artery disease. Circ Cardiovasc Imaging 2015;8:e002404. http://dx.doi.org/10.1161/CIRCIMAGING. 114.002404. [16] Rochitte CE, George RT, Chen MY, Arbab-Zadeh A, Dewey M, Miller JM, et al. Computed tomography angiography and perfusion to assess coronary artery stenosis
causing perfusion defects by single photon emission computed tomography: the CORE320 study. Eur Heart J 2014;35:1120–30. [17] Halpern EJ. Triple-rule-out CT, angiography for evaluation of acute chest pain and possible acute coronary syndrome. Radiology 2009;252:332–45. [18] Flohr TG, De Cecco CN, Schmidt B, Wang R, Schoepf UJ, Meinel FG. Computed tomographic assessment of coronary artery disease: state-of-the-art imaging techniques. Radiol Clin North Am 2015;53:271–85.
Contents lists available at ScienceDirect
Clinical Imaging journal homepage: http://www.clinicalimaging.org
Acute left circumflex coronary artery occlusion detected on nongated CT☆ Netanel S. Berko ⁎, Elana T. Clark, Jeffrey M. Levsky Department of Radiology, Albert Einstein College of Medicine, Montefiore Medical Center, 111 East 210th Street, Bronx, NY 10467-2490
a r t i c l e
i n f o
Article history: Received 9 February 2015 Received in revised form 11 May 2015 Accepted 15 May 2015 Keywords: Myocardial infarction CT Hypoperfusion Left circumflex coronary artery
a b s t r a c t We describe a patient with chest pain and a nondiagnostic electrocardiogram in whom computed tomographic (CT) aortography demonstrated myocardial hypoperfusion in the distribution of the circumflex artery as well as an abrupt cutoff of contrast in the left circumflex artery. Subsequent cardiac catheterization confirmed occlusion of the circumflex artery and led to revascularization. The diagnosis of acute myocardial infarction on CT can dramatically alter the clinical management of a patient, especially in cases in which other tests are equivocal. © 2015 Elsevier Inc. All rights reserved.
1. Introduction Chest pain is one of the most common complaints in patients presenting to the emergency department. Imaging studies play an important role in the evaluation of chest pain, particularly in cases when aortic dissection or pulmonary embolism is suspected. We present a case in which an unsuspected diagnosis of acute myocardial infarction with a large-branch coronary occlusion was made on nongated computed tomography (CT).
2. Case report A 63-year-old man presented to the emergency department with “squeezing,” intermittent, intense chest pain radiating to the neck and left shoulder for a few hours. The patient had no history of coronary disease and had never experienced similar pain. He had a 40-pack-year smoking history and known hypertension. On physical examination, the patient was in moderate distress, with a blood pressure of 220/120, pulse of 73 beats per minute, and oxygen saturation of 100% on room air. There were no other significant physical findings. The initial electrocardiogram demonstrated normal sinus rhythm with nonspecific flattening of T waves in leads V5 and V6. Serum cardiac enzyme levels were within normal range, with a troponin T b0.01 ng/ml (normal b0.11 ng/ml), creatine phosphokinase (CPK) of
☆ Conflicts of interest: none. ⁎ Corresponding author. Department of Radiology, Albert Einstein College of Medicine, Montefiore Medical Center, 111 East 210th Street, Bronx, NY 10467-2490. Tel.: +1 718 920 4872; fax: +1 718 920 4854. E-mail address: [email protected] (N.S. Berko). http://dx.doi.org/10.1016/j.clinimag.2015.05.007 0899-7071/© 2015 Elsevier Inc. All rights reserved.
178 U/L (normal 20–200 U/L), and creatine kinase MB (CK-MB) of 2.8 ng/ml (normal b5.1 ng/ml). A portable chest radiograph was unremarkable, and further evaluation with CT aortography was requested for possible aortic dissection. CT examination was performed on a 64-slice LightSpeed VCT scanner (GE Healthcare, Waukesha, WI, USA). It demonstrated no aortic dissection; however, there was an area of hypoattenuation in the lateral wall of the left ventricle, which raised suspicion for an acute myocardial infarction in the distribution of the left circumflex coronary artery (Fig. 1A–B). Upon further review of multiplanar reformatted thinsection images, there was suggestion of an abrupt cutoff of contrast in the left circumflex artery (Fig. 1C). Of note, the patient’s heart rate was 68 beats per minute at the time of CT scan. Two hours following the CT scan, cardiac enzyme levels were elevated, with a troponin T of 0.34 ng/ml, CPK of 661 U/L, and CK-MB of 47.9 ng/ml, with further increase 12 h later, with levels of 1.85, 1512, and 115.8, respectively. The patient was admitted with a preliminary diagnosis of acute non-ST-elevation myocardial infarction. Cardiac catheterization was performed the following day and confirmed occlusion of the left circumflex artery (Fig. 2A). A bare metal stent was placed with restoration of flow (Fig. 2B). The patient had an uneventful postprocedure course to discharge. 3. Discussion Chest pain is one of the most common symptoms of patients presenting to the emergency department. Multiple possible etiologies, including cardiac, pulmonary, gastrointestinal, and musculoskeletal related problems, may be causative. The electrocardiogram serves as the initial triage method in order to identify patients with ST-elevation myocardial infarction that benefit from immediate
898
N.S. Berko et al. / Clinical Imaging 39 (2015) 897–900
Fig. 2. (A) Initial image from cardiac catheterization demonstrates an occlusion in the midleft circumflex coronary artery. (B) Improved flow is seen in this artery following angioplasty and bare metal stent placement.
Fig. 1. (A) Axial and (B) sagittal-reformatted, contrast-enhanced CT images demonstrate an area of hypoenhancement (arrows) in the lateral wall of the left ventricle. (C) Coronal oblique maximum intensity projection image demonstrates an abrupt cutoff (arrow) in the mid-left circumflex coronary artery.
catheterization and percutaneous intervention. Unfortunately, many cases of cardiac chest pain do not have characteristic electrocardiographic findings. In this setting, serial laboratory values, particularly
serum cardiac troponin levels, are used to confirm the presence of myocardial infarction, though it takes 4–8 h for these markers to become positive. CT is performed emergently in the diagnostic workup of chest pain patients, especially when acute aortic syndromes or pulmonary embolism are suspected. CT is often completed before the patient has been in the emergency department long enough to have positive cardiac biomarkers. In some patients, therefore, CT provides the first evidence of unsuspected myocardial infarction. It is expected that with expanding use of rapid diagnostic algorithms used to exclude a cardiac etiology of chest pain that utilize coronary CT angiography, the finding of unsuspected myocardial infarction in progress will increase. In a study of emergency department patients undergoing coronary CT angiography to assess for coronary artery disease, acute myocardial infarction was diagnosed in 1% of patients [1]. This role of CT can be of particular importance in situations where the diagnosis of myocardial infarction is not clinically obvious. In particular, diagnosis of myocardial infarction of the left circumflex artery territory is frequently difficult. The posterior location of the circumflex artery limits the utility of the standard 12-lead electrocardiogram
N.S. Berko et al. / Clinical Imaging 39 (2015) 897–900
[2,3]. In one study, less than half of patients with acute left circumflex infarct had ST segment elevation on electrocardiogram, compared with greater than 70% in patients with left anterior descending or right coronary artery infarcts [4]. Early detection of left circumflex infarction is significant due to the worse prognosis of patients with involvement of that territory as compared with those with right coronary artery infarcts [5]. This is for uncertain reasons but may be related to resultant mitral regurgitation, which occurs in 22% of patients [6]. Given the difficulty in the clinical diagnosis of some myocardial infarcts, recognition of characteristic imaging features of myocardial ischemia related to coronary occlusion is vital and may contribute to an unsuspected diagnosis. Acute myocardial infarction results in decreased myocardial perfusion which may be seen as an area of decreased myocardial attenuation in a pattern corresponding with the distribution of a coronary artery [7]. The hypoperfused area can frequently be visually detected, although in some cases an acute infarct manifests as an area of decreased attenuation (defined as a decrease in attenuation of 20 or more Hounsfield units less than surrounding myocardium) that is not easily appreciated visually. Use of a narrow window width (100–300) and level of 100 has been suggested to accentuate the hypoperfused myocardium [8,9]. CT has a high sensitivity and specificity in demonstrating acute myocardial infarction [7]. A study in patients admitted with acute chest pain demonstrated a higher rate of detection of myocardial hypoenhancement in circumflex infarcts compared with other coronary artery infarcts [10]. While decreased myocardial attenuation is present in both recent and chronic myocardial infarctions, certain features can be helpful in differentiating between the two. Fatty replacement frequently occurs in myocardial scar tissue, and thus chronic myocardial infarction will have significantly lower myocardial attenuation than an acute infarction [11,12]. Additionally, chronic infarction is also associated with ventricular dilation and wall thinning [13]. Occlusion of the left anterior descending coronary artery will typically result in hypoenhancement of the anterior wall and the apex of the left ventricle. Occlusion of the left circumflex artery often leads to hypoenhancement of the lateral basal wall. Right coronary artery occlusion may result in hypoenhancement of the inferior wall in patients with right dominance. In patients with posterior descending arteries from the left-sided circulation, there may be no obvious region of hypoenhancement. The extent of hypoperfusion depends on the location of coronary occlusion. Infarcts involving branch vessels will result in hypoenhancement that does not correspond to these vascular territories. Recent studies support the ability of resting coronary CT to detect acute myocardial infarction [14,15]. Although these publications focus on detecting abnormal myocardial enhancement on gated cardiac CT, the principle is the same for nongated CT that may be performed for aortic dissection or pulmonary embolism, as in our case. Of note, rest–stress CT perfusion, utilizing both resting CT and CT following stress, is a different developing modality which has been shown to be useful for the detection of myocardial ischemia outside the setting of an acute coronary event [16]. Additionally, the triple-rule-out CT, including evaluation of the pulmonary arteries, aorta, and coronary arteries, is employed in some institutions in patients with chest pain with low to intermediate risk for acute coronary syndrome [17]. CT for the evaluation of the coronary arteries is usually performed with ECG gating, in which imaging is acquired in synchrony with an ECG tracing. This decreases motion artifact, allowing better visualization of the coronary arteries. ECG gating may be performed prospectively, in which images are acquired only during predetermined phases of the cardiac cycle (usually early diastole), or retrospectively, in which data analysis is performed on images acquired during all phases of the cardiac cycle [18]. In contrast, during non-ECG-gated CT, as in our case, image acquisition is not related to the phase of the cardiac cycle, and therefore there
899
are greater motion artifact and typically more limited evaluation of the coronary arteries. Nongated CT is therefore not a reliable method for detecting coronary occlusion. However, myocardial hypoperfusion, which manifests as a region of lower attenuation in the myocardium, may be detected on nongated CT, as in our case. This demonstrates the importance of considering possible myocardial infarction in any chest pain patient and the need to look for signs of myocardial ischemia. When a coronary occlusion is detected, this offers an additional opportunity to advance diagnosis and therapy. Whereas many patients with non-STelevation myocardial infarction do not receive emergent catheterization and some undergo risk stratification by modalities such as nuclear stress testing, when there is strong evidence of acute occlusion of a coronary artery, more rapid intervention may be beneficial. When a CT study demonstrates occlusion of a significant-sized target vessel and there is a compatible clinical chest pain syndrome, we suggest urgent evaluation by an interventional cardiologist to consider catheterization for percutaneous intervention. 4. Conclusion This case illustrates the importance of examining myocardial perfusion and the coronary arteries on nongated CT angiograms. Myocardial hypoattenuation in the distribution of a coronary artery may be the first decisive clue to the presence of myocardial infarction and may suggest the diagnosis hours before laboratory tests become positive. This is of particular importance in situations where other diagnostic tests may be inconclusive, such as early in the course of left circumflex artery territory infarction. When a coronary artery occlusion is detected, the patient should be evaluated for urgent percutaneous intervention.
References [1] Hecht HS, Bhatti T. Multislice coronary computed tomographic angiography in emergency department presentations of unsuspected acute myocardial infarction. J Cardiovasc Comput Tomogr 2009;3:272–8. [2] Fuchs RM, Achuff SC, Grunwald L, Yin FC, Griffith LS. Electrocardiographic localization of coronary artery narrowings: studies during myocardial ischemia and infarction in patients with one-vessel disease. Circulation 1982;66:1168–76. [3] O'Keefe JH, Gibbons RJ. Left circumflex occlusion—underrecognized and undertreated. J Thromb Thrombolysis 2000;10:221–5. [4] Huey BL, Beller GA, Kaiser DL, Gibson RS. A comprehensive analysis of myocardial infarction due to left circumflex artery occlusion: comparison with infarction due to right coronary artery and left anterior descending artery occlusion. J Am Coll Cardiol 1988;12:1156–66. [5] Rasoul S, de Boer MJ, Suryapranata H, Hoorntje JCA, Gosselink ATM, Zijlstra F, et al. Circumflex artery-related acute myocardial infarction: limited ECG abnormalities but poor outcome. Neth Heart J 2007;15:286–90. [6] Matetzky S, Freimark D, Feinberg MS, Novikov I, Rath S, Rabinowitz B, et al. Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7–9: “hidden” ST-segment elevations revealing acute posterior infarction. J Am Coll Cardiol 1999;34:748–53. [7] Gosalia A, Haramati LB, Sheth MP, Spindola-Franco H. CT detection of acute myocardial infarction. AJR Am J Roentgenol 2004;182:1563–6. [8] Techasith T, Cury RC. Stress myocardial CT perfusion: an update and future perspective. JACC Cardiovasc Imaging 2011;4:905–16. [9] Busch JL, Alessio AM, Caldwell JH, Gupta M, Mao S, Kadakia J, et al. Myocardial hypo-enhancement on resting computed tomography angiography images accurately identifies myocardial hypoperfusion. J Cardiovasc Comput Tomogr 2011;5:412–20. [10] Lessick J, Ghersin E, Dragu R, Litmanovich D, Mutlak D, Rispler S, et al. Diagnostic accuracy of myocardial hypoenhancement on multidetector computed tomography in identifying myocardial infarction in patients admitted with acute chest pain syndrome. J Comput Assist Tomogr 2007;31:780–8. [11] Winer-Muram HT, Tann M, Aisen AM, Ford L, Jennings SG, Bretz R. Computed tomography demonstration of lipomatous metaplasia of the left ventricle following myocardial infarction. J Comput Assist Tomogr 2004;28:455–8. [12] Jacobi AH, Gohari A, Zalta B, Stein MW, Haramati LB. Ventricular myocardial fat: CT findings and clinical correlates. J Thorac Imaging 2007;22:130–5. [13] Nieman K, Cury RC, Ferencik M, Nomura CH, Abbara S, Hoffmann U, et al. Differentiation of recent and chronic myocardial infarction by cardiac computed tomography. Am J Cardiol 2006;98:303–8. [14] Branch KR, Busey J, Mitsumori LM, Strote J, Caldwell JH, Busch JH, et al. Diagnostic performance of resting CT myocardial perfusion in patients with possible acute coronary syndrome. AJR Am J Roentgenol 2013;200:W450–7.
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[15] Pursnani A, Lee AM, Mayrhofer T, Ahmed W, Uthamalingam S, Ferencik M, et al. Early resting myocardial computed tomography perfusion for the detection of acute coronary syndrome in patients with coronary artery disease. Circ Cardiovasc Imaging 2015;8:e002404. http://dx.doi.org/10.1161/CIRCIMAGING. 114.002404. [16] Rochitte CE, George RT, Chen MY, Arbab-Zadeh A, Dewey M, Miller JM, et al. Computed tomography angiography and perfusion to assess coronary artery stenosis
causing perfusion defects by single photon emission computed tomography: the CORE320 study. Eur Heart J 2014;35:1120–30. [17] Halpern EJ. Triple-rule-out CT, angiography for evaluation of acute chest pain and possible acute coronary syndrome. Radiology 2009;252:332–45. [18] Flohr TG, De Cecco CN, Schmidt B, Wang R, Schoepf UJ, Meinel FG. Computed tomographic assessment of coronary artery disease: state-of-the-art imaging techniques. Radiol Clin North Am 2015;53:271–85.
