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The natural course of traumatic myocardial infarction in a young patient with angiographically normal coronary arteries
The natural course of traumatic myocardial infarction in a young patient with angiographically normal coronary arteries Shi-Wei Yang, MDa, Yu-Jie Zhou, MD, FACC, FSCAI, FHRSa,*, Zhen-Feng Guo, MDb, Da-Yi Hu, MD, FACC, FESC, FHRSc a
Department of Cardiology, Beijing Anzhen Hospital Affiliated to Capital Medical University, Beijing, China Department of Cardiology, Benq Medical Center Affiliated to Nanjing Medical University, Nanjing, China c Department of Cardiology, People’s Hospital Affiliated to Peking University, Beijing, China
b
article info
abstract
Article history: Received 19 May 2011 Revised 3 July 2011 Accepted 12 July 2011 Online 19 October 2011
A 23-year-old man with no history of heart disease was admitted to Beijing Anzhen Hospital Affiliated to Capital Medical University for an abnormal electrocardiogram of ST-T changes mimicking myocardial infarction. Catheterization revealed normal coronary and peripheral arteries. The echocardiogram and delayed enhancement cardiovascular magnetic resonance imaging indicated a markedly reduced left ventricular function and enlarged left ventricular cavity with evidence of fibrous tissue. Given the patient’s history of multiple blunt trauma 7 years previously and acute myocardial infarction diagnosis at that time, he was diagnosed with traumatic myocardial infarction (TMI). We describe the natural course of such a patient with TMI. There is a possibility of spontaneous healing of coronary artery dissection induced by trauma. Although early revascularization may be helpful for preventing cardiac remodeling after TMI in some cases, more data are needed to compare the long-term outcome among different interventions in large sample cases.
Traumatic myocardial infarction (TMI) is a rare but fatal disease, and current understanding of this disease mainly originates from case reports. Intimal tearing and dissection are thought to be the initial mechanisms of TMI.1 Optimal treatment for this condition remains open to debate. Coronary revascularization has been performed successfully in selected cases and
provides good results.2-6 Conservative management has also been advocated because there is a possibility of spontaneous healing of coronary artery dissection.7,8 We describe the natural course of a young patient with TMI, with an onset from multiple blunt trauma 7 years previously. Currently, the patient has a markedly reduced left ventricular function and
Funding: The case report was supported by a grant from the Beijing Municipal Education Commission (No. KZ201110025031). Conflicts of Interest: none. * Corresponding author: Yu-Jie Zhou, MD, FACC, FSCAI, FHRS, Department of Cardiology, Beijing Anzhen Hospital Affiliated to Capital Medical University, An Ding Men Wai, Chao Yang District, Beijing 100029, China. E-mail address: [email protected] (Y.-J. Zhou). 0147-9563/$ - see front matter Ó 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.hrtlng.2011.07.001
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Figure 1 e ECG on admission shows poor R-wave progression and ST-elevation in precordial leads V1-V4 mimicking MI.
Figure 2 e Echocardiogram shows an enlarged left ventricular cavity and a decreased left ventricular ejection fraction of 37% with segmental wall-motion abnormalities.
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Figure 3 e Angiography shows normal coronary and peripheral arteries. (A-C, coronary artery angiography; D, forearm artery angiography; E, subclavian artery angiography; F, brachiocephali trunk and common carotid artery angiography; G, mesentery artery angiography; H, I, renal artery angiography)
enlarged left ventricular cavity with angiographically normal coronary arteries.
Case Report A 23-year-old man with no history of heart disease was admitted to Beijing Anzhen Hospital Affiliated to Capital Medical University for an abnormal electrocardiogram (ECG) noted in a general health check-up. His ECG revealed poor R-wave progression and ST-elevation in precordial leads V1-V4 (Figure 1). The patient had no symptoms of chest pain, chest distress, or shortness of breath. He had good exercise tolerance and could do more than 100 sit-ups continuously with no discomfort before admission. He had no history of hypertension, diabetes mellitus, hyperlipidemia, or other cardiovascular risk factors. He had no history of any emotional or psychiatric disease or chronic fever. According to the patient’s description, he had a motorcycle accident 7
years previously that resulted in multiple blunt trauma to his head, face, and neck, but not the chest. He underwent operation for mandibular fractures. We reviewed the patient’s medical history records and found that there were no skin wound, ecchymoma, rib/ sternal fracture, pneumothorax, mediastinal hematoma, or significant neurologic injuries at that time. On arrival at the trauma center, the patient reported left-sided chest pain and was diagnosed with acute myocardial infarction (AMI). He did not receive coronary angiography (CAG). The patient denied any history of recent trauma or illicit drug use. The patient was not taking any prescription medication and had no known allergies. He drank on rare occasions and did not smoke. For the current admission, and not the prior admission, his pulse was regular at 82 beats/min and blood pressure was 112/64 mm Hg. He had no visible external chest injuries, and there was no left-sided cardiac enlargement on cardiorespiratory examination. Laboratory values showed troponin I of 0.05 ng/ mL (normal range 0-0.05 ng/mL), low-density
h e a r t & l u n g 4 1 ( 2 0 1 2 ) 2 9 4 e3 0 0
297
Figure 4 e No significant anomalies are shown on multislice computed tomography.
lipoprotein cholesterol of 1.68 mmol/L, creatinine of 102 mmol/L, fasting plasma glucose of 5.22 mmol/L, postprandial (2 hours) plasma glucose of 8.6 mmol/L, hemoglobin A1c of 5.2%, brain natriuretic peptide of 63.2 pg/mL (normal range 0-125 pg/mL), erythrocyte sedimentation rate of 2 mm/h, and high-sensitivity Creactive protein of 0.84 mg/L. His thyroid hormone levels were normal. Antigen and antibody screening tests for EpsteineBarr virus, cytomegalovirus, hepatitis B virus, human immunodeficiency virus, and treponema pallidum all showed negative results. Immunofluorescence assays for antinuclear antibodies, anti-extractable nuclear antigen antibodies, antiedouble-stranded DNA antibodies, and anticardiolipin antibodies were all normal. A transthoracic echocardiogram (Figure 2) revealed an enlarged left ventricular cavity (left ventricular enddiastolic dimension 68 mm, left ventricular endsystolic dimension 55 mm) and a decreased left
ventricular ejection fraction of 37% with segmental wall-motion abnormalities: hypokinesis in the anterior wall and the septum. Prior anterior myocardial infarction (MI) was suspected because of the patient’s history, ECG, and echocardiogram, and the patient was scheduled for CAG. Cardiac catheterization showed normal coronary arteries (Figure 3A-C). No coronary artery spasm, coronary artery dissection, muscular bridge, plaque, or thrombus was observed. The peripheral arteries angiography showed a normal right forearm artery (Figure 3D), subclavian artery (Figure 3E), brachiocephalic trunk (Figure 3F), common carotid artery (Figure 3F), mesentery artery (Figure 3G), and renal artery (Figure 3H, I). Multislice computed tomography was used to complement CAG in the diagnosis and characterization of coronary artery anomalies,9 and no significant anomalies were found (Figure 4). The normal results of CAG and multislice computed tomography did not show
298
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Figure 5 e Delayed enhancement cardiovascular magnetic resonance imaging shows full-thickness infarction and markedly reduced left ventricular function with dyskinesis and aneurysmatic bulging of the thinned anterior wall (arrows).
the prior anterior MI. After gadolinium-DTPA contrast injection, delayed enhancement cardiovascular magnetic resonance imaging was performed to assess necrotic myocardium (Figure 5).10 There was predominant transmural hyperenhancement of the anterolateral myocardial wall, indicating full-thickness infarction, with marked subendocardial extension. Cine imaging demonstrated markedly reduced left ventricular function with dyskinesis and aneurysmatic bulging of the thinned anterior wall. After all the tests were completed, the patient was diagnosed with TMI. Because he had asymptomatic left ventricular dysfunction, we treated him with angiotensin-converting enzyme inhibitor perindopril 8 mg 4 times per day and carvedilol 10 mg 4 times per day. The patient was discharged with no complications. He has continued to be virtually symptom-free over a 3-year period of follow-up.
Discussion This report describes a young man with angiographically normal coronary arteries in whom ECG STT changes mimicked MI. The specificity of the ECG diagnosis for prior MI is greatest when Q-waves occur in several leads or lead groupings.11 However, ST deviations and T-wave inversions alone are nonspecific findings for myocardial necrosis.12 Under such conditions, imaging techniques play roles. The echocardiogram revealed segmental wall-motion
abnormalities, and delayed enhancement cardiovascular magnetic resonance indicated full-thickness infarction with marked subendocardial extension.10 According to the universal definition of MI, this patient was satisfied with the diagnosis of prior MI.13 Of individuals with MI who undergo CAG, 1% to 12% are found to have angiographically normal coronary arteries.14-16 This wide range can be explained by differing definitions of angiographically normal arteries: “without any endoluminal irregularity” and “no significant stenosis (eg, stenosis < 30%).”17 Other interpretations may include markedly different definitions of MI or the type of MI (ST-segment elevated MI and noneST-segment elevated MI). If we use the restrictive definition “without any endoluminal irregularity,” 1.1% of patients with MI were in this category.18 The cause of MI with normal coronary arteries is not clear. It has been reported that myocardial bridge,19 coronary spasm,20 coronary anomalies,21 spontaneous coronary dissection,22 anticardiolipin syndrome,23 Kawasaki disease,24 collagen disease,25 Takayasu’s aortitis,26 Buerger’s disease,27 and other diseases may contribute to the genesis of MI. For the patient described, no evidence could verify the above diagnoses. Given the history of a motorcycle accident 7 years previously and AMI diagnosis at that time, a diagnosis of TMI was made. TMI is a rare disease, and current understanding of this disease mainly originates from case reports. Christensen et al28 performed a Medline search from 1974 to 2006 and found 65 articles describing 77 cases
h e a r t & l u n g 4 1 ( 2 0 1 2 ) 2 9 4 e3 0 0
of TMI. There is no clear relationship between the severity of trauma and the development of coronary lesions. In fact, AMI has been reported after low- and high-speed traffic accidents and as direct chest trauma caused by a kick while playing sports.29 The mechanism of TMI is thought to be shearing of the coronary vessel wall, causing intimal tearing, dissection, and subintimal hemorrhage. Platelet aggregation and intraluminal thrombosis then follow.1 Other probable mechanisms of thrombotic coronary injury include vessel rupture and external compression by epicardial hematoma, occlusive dissection of the artery, or hemorrhage into a preexisting atheromatous plaque.30 Overall, the left anterior descending (LAD) coronary artery is most commonly affected (76%), followed by the right coronary artery (12%) and circumflex artery (6%).31 The higher incidence of LAD involvement may relate to its proximity to the sternum and vertebral column. Dramatic acceleration/ deceleration forces probably cause intimal tears of the most vulnerable part of the LAD, the junction of its proximal and mid-portions.32,33 Early recognition and diagnosis of TMI are of great importance to choose appropriate and prompt treatment. This case illustrates the importance of appropriately investigating patients with blunt chest injury to rule out MI. A screening 12-lead ECG should be performed in patients presenting with blunt trauma to the chest. CAG is the best test for coronary artery injury, although transesophageal echocardiography and intravascular ultrasound are also helpful.26 Normal coronary arteries after TMI were found in 15.8% and occlusion of 1 coronary artery in 56.6% of patients with other normal coronary arteries.28 When coronary arteries are found to be normal on angiography, the probable explanation is spasm or spontaneous clot lysis. Optimal treatment for TMI remains open to debate. Individualized intervention should be based on the patient’s presentation and angiographic findings. Coronary artery bypass grafting has been reported to provide good results in some selected cases; however, such a major operation may be accompanied by a higher risk of postoperative complications in patients with multiple traumas.2,3 Percutaneous coronary intervention has also been performed in some cases.4 Although complete healing of these lesions may occur, some patients may develop aneurysmal disease or late coronary occlusion as a result of progression of intimal disruption with dissection.5,6 Other authors advocate conservative management in the absence of ongoing ischemia. Several cases with follow-up have shown that a coronary artery dissection can heal spontaneously over 6 months with medical therapy alone.7,8 Would early revascularization be better than conservative management? Although this may be the case, it may not be of benefit in many trauma cases. More data are needed to compare the long-term outcome among different interventions, which is difficult considering the rarity of these events.
299
Conclusions There is a possibility of spontaneous healing of coronary artery dissection induced by trauma. Although early revascularization may be helpful for preventing cardiac remodeling after TMI in some cases, more data are needed to compare the long-term outcome among different interventions in large sample cases.
References 1. Marcum JL, Booth DC, Sapin PM. Acute myocardial infarction caused by blunt chest trauma: successful treatment by direct coronary angioplasty. Am Heart J 1996;132:1275-7. 2. Yoon SJ, Kwon HM, Kim DS, Hong BK, Kim DY, Cho YH, et al. Acute myocardial infarction caused by coronary artery dissection following blunt chest trauma. Yonsei Med J 2003;44:736-9. 3. Lai CH, Ma T, Chang TC, Chang MH, Chou P, Jong GP. A case of blunt chest trauma induced acute myocardial infarction involving two vessels. Int Heart J 2006;47:639-43. 4. Thorban S, Ungeheuer A, Blasini R, Siewert JR. Emergent interventional transcatheter revascularization in acute right coronary artery dissection after blunt chest trauma. J Trauma 1997;43:365-7. 5. Westaby S, Drossos G, Giannopoulos N. Posttraumatic coronary artery aneurysm. Ann Thorac Surg 1995;60: 712-3. 6. Rubin DA, Denys BG. Delayed and spontaneous coronary artery rupture following nonpenetrating chest trauma. Am Heart J 1992;124:1635-7. 7. Cherng WJ, Bullard MJ, Chang HJ, Lin FC. Diagnosis of coronary artery dissection following blunt chest trauma by transesophageal echocardiography. J Trauma 1995;39:772-4. 8. Chun JH, Lee SC, Gwon HC, Lee SH, Hong KP, Seo JD, et al. Left main coronary artery dissection after blunt chest trauma presented as acute anterior myocardial infarction: assessment by intravascular ultrasound: a case report. J Korean Med Sci 1998;13:325-7. 9. Hamon M, Biondi-Zoccai GG, Malagutti P, Agostoni P, Morello R, Valgimigli M. Diagnostic performance of multislice spiral computed tomography of coronary arteries as compared with conventional invasive coronary angiography: a meta-analysis. J Am Coll Cardiol 2006;48:1896-910. 10. West AM, Kramer CM. Cardiovascular magnetic resonance imaging of myocardial infarction, viability, and cardiomyopathies. Curr Probl Cardiol 2010;35: 176-220. 11. Wagner GS, Macfarlane P, Wellens H, Josephson M, Gorgels A, Mirvis DM, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part VI: Acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society For Computerized Electrocardiology. J Am Coll Cardiol 2009;53:1003-11.
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12. Rautaharju PM, Surawicz B, Gettes LS, Bailey JJ, Childers R, Deal BJ, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part IV: The ST segment, T and U waves, and the QT interval: a Scientific Statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol 2009;53:982-91. 13. Thygesen K, Alpert JS, White HD. Universal definition of myocardial infarction. J Am Coll Cardiol 2007;50:2173-95. 14. Zainea M, Duvernoy WF, Chauhan A, David S, Soto E, Small D. Acute myocardial infarction in angiographically normal coronary arteries following induction of general anesthesia. Arch Intern Med 1994;154:2495-8. 15. Alpert JS. Myocardial infarction with angiographically normal coronary arteries. Arch Intern Med 1994;154: 265-9. 16. Alpert JS. Myocardial infarction with angiographically normal coronary arteries. A personal perspective. Arch Intern Med 1994;154:245. 17. Sharifi M, Frohlich TG, Silverman IM. Myocardial infarction with angiographically normal coronary arteries. Chest 1995;107:36-40. 18. Ammann P, Marschall S, Kraus M, Schmid L, Angehrn W, Krapf R, et al. Characteristics and prognosis of myocardial infarction in patients with normal coronary arteries. Chest 2000;117:333-8. 19. Ishikawa Y, Akasaka Y, Suzuki K, Fujiwara M, Ogawa T, Yamazaki K, et al. Anatomic properties of myocardial bridge predisposing to myocardial infarction. Circulation 2009;120:376-83. 20. Ong P, Athanasiadis A, Borgulya G, Voehringer M, Sechtem U. 3-year follow-up of patients with coronary artery spasm as cause of acute coronary syndrome: the CASPAR (coronary artery spasm in patients with acute coronary syndrome) study followup. J Am Coll Cardiol 2011;57:147-52. 21. Gallagher SM, Jain AK, Archbold RA. Primary percutaneous coronary intervention for st-elevation myocardial infarction in a patient with a single coronary artery arising from the right aortic sinus. J Invasive Cardiol 2011;23:E61-2. 22. Paraskevaidis S, Theofilogiannakos EK, Chatzizisis YS, Mantziari L, Economou F, Ziakas A, et al. Spontaneous dissection of right coronary artery manifested with
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
acute myocardial infarction. Open Cardiovasc Med J 2010;4:178-80. Urbanus RT, Siegerink B, Roest M, Rosendaal FR, de Groot PG, Algra A. Antiphospholipid antibodies and risk of myocardial infarction and ischaemic stroke in young women in the ratio study: a casecontrol study. Lancet Neurol 2009;8:998-1005. Inaba S, Higaki T, Nagashima M, Nishimura K, Ogimoto A, Higaki J, et al. Successful revascularization by pulse infusion thrombolysis in a patient with kawasaki disease combined with acute myocardial infarction. JACC Cardiovasc Interv 2010;3:1091-2. Meune C, Touze E, Trinquart L, Allanore Y. High risk of clinical cardiovascular events in rheumatoid arthritis: levels of associations of myocardial infarction and stroke through a systematic review and meta-analysis. Arch Cardiovasc Dis 2010;103:253-61. Roghi A, Pedrotti P, Milazzo A, Vignati G, Martinelli L, Paino R, et al. Acute myocardial infarction and cardiac arrest in atypical takayasu aortitis in a young girl: unusual diagnostic role of cardiac magnetic resonance imaging in emergency setting. Circulation 2010;121:e370-5. Rodriguez-Fernandez J, Rangel A, Chavez E. [Myocardial infarction simultaneous with buerger disease (obliterating thromboangiitis). A case report]. Arch Cardiol Mex 2002;72:306-10. Christensen MD, Nielsen PE, Sleight P. Prior blunt chest trauma may be a cause of single vessel coronary disease; hypothesis and review. Int J Cardiol 2006; 108:1-5. Kawahito K, Hasegawa T, Misawa Y, Fuse K. Right coronary artery dissection and acute infarction due to blunt trauma: report of a case. Surg Today 1998;28: 971-3. Atalar E, Acil T, Aytemir K, Ozer N, Ovunc K, Aksoyek S, et al. Acute anterior myocardial infarction following a mild nonpenetrating chest traumada case report. Angiology 2001;52:279-82. Ginzburg E, Dygert J, Parra-Davila E, Lynn M, Almeida J, Mayor M. Coronary artery stenting for occlusive dissection after blunt chest trauma. J Trauma 1998;45:157-61. Bjornstad JL, Pillgram-Larsen J, Tonnessen T. Coronary artery dissection and acute myocardial infarction following blunt chest trauma. World J Emerg Surg 2009;4:14. Fu M, Wu CJ, Hsieh MJ. Coronary dissection and myocardial infarction following blunt chest trauma. J Formos Med Assoc 1999;98:136-40.
Department of Cardiology, Beijing Anzhen Hospital Affiliated to Capital Medical University, Beijing, China Department of Cardiology, Benq Medical Center Affiliated to Nanjing Medical University, Nanjing, China c Department of Cardiology, People’s Hospital Affiliated to Peking University, Beijing, China
b
article info
abstract
Article history: Received 19 May 2011 Revised 3 July 2011 Accepted 12 July 2011 Online 19 October 2011
A 23-year-old man with no history of heart disease was admitted to Beijing Anzhen Hospital Affiliated to Capital Medical University for an abnormal electrocardiogram of ST-T changes mimicking myocardial infarction. Catheterization revealed normal coronary and peripheral arteries. The echocardiogram and delayed enhancement cardiovascular magnetic resonance imaging indicated a markedly reduced left ventricular function and enlarged left ventricular cavity with evidence of fibrous tissue. Given the patient’s history of multiple blunt trauma 7 years previously and acute myocardial infarction diagnosis at that time, he was diagnosed with traumatic myocardial infarction (TMI). We describe the natural course of such a patient with TMI. There is a possibility of spontaneous healing of coronary artery dissection induced by trauma. Although early revascularization may be helpful for preventing cardiac remodeling after TMI in some cases, more data are needed to compare the long-term outcome among different interventions in large sample cases.
Traumatic myocardial infarction (TMI) is a rare but fatal disease, and current understanding of this disease mainly originates from case reports. Intimal tearing and dissection are thought to be the initial mechanisms of TMI.1 Optimal treatment for this condition remains open to debate. Coronary revascularization has been performed successfully in selected cases and
provides good results.2-6 Conservative management has also been advocated because there is a possibility of spontaneous healing of coronary artery dissection.7,8 We describe the natural course of a young patient with TMI, with an onset from multiple blunt trauma 7 years previously. Currently, the patient has a markedly reduced left ventricular function and
Funding: The case report was supported by a grant from the Beijing Municipal Education Commission (No. KZ201110025031). Conflicts of Interest: none. * Corresponding author: Yu-Jie Zhou, MD, FACC, FSCAI, FHRS, Department of Cardiology, Beijing Anzhen Hospital Affiliated to Capital Medical University, An Ding Men Wai, Chao Yang District, Beijing 100029, China. E-mail address: [email protected] (Y.-J. Zhou). 0147-9563/$ - see front matter Ó 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.hrtlng.2011.07.001
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Figure 1 e ECG on admission shows poor R-wave progression and ST-elevation in precordial leads V1-V4 mimicking MI.
Figure 2 e Echocardiogram shows an enlarged left ventricular cavity and a decreased left ventricular ejection fraction of 37% with segmental wall-motion abnormalities.
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Figure 3 e Angiography shows normal coronary and peripheral arteries. (A-C, coronary artery angiography; D, forearm artery angiography; E, subclavian artery angiography; F, brachiocephali trunk and common carotid artery angiography; G, mesentery artery angiography; H, I, renal artery angiography)
enlarged left ventricular cavity with angiographically normal coronary arteries.
Case Report A 23-year-old man with no history of heart disease was admitted to Beijing Anzhen Hospital Affiliated to Capital Medical University for an abnormal electrocardiogram (ECG) noted in a general health check-up. His ECG revealed poor R-wave progression and ST-elevation in precordial leads V1-V4 (Figure 1). The patient had no symptoms of chest pain, chest distress, or shortness of breath. He had good exercise tolerance and could do more than 100 sit-ups continuously with no discomfort before admission. He had no history of hypertension, diabetes mellitus, hyperlipidemia, or other cardiovascular risk factors. He had no history of any emotional or psychiatric disease or chronic fever. According to the patient’s description, he had a motorcycle accident 7
years previously that resulted in multiple blunt trauma to his head, face, and neck, but not the chest. He underwent operation for mandibular fractures. We reviewed the patient’s medical history records and found that there were no skin wound, ecchymoma, rib/ sternal fracture, pneumothorax, mediastinal hematoma, or significant neurologic injuries at that time. On arrival at the trauma center, the patient reported left-sided chest pain and was diagnosed with acute myocardial infarction (AMI). He did not receive coronary angiography (CAG). The patient denied any history of recent trauma or illicit drug use. The patient was not taking any prescription medication and had no known allergies. He drank on rare occasions and did not smoke. For the current admission, and not the prior admission, his pulse was regular at 82 beats/min and blood pressure was 112/64 mm Hg. He had no visible external chest injuries, and there was no left-sided cardiac enlargement on cardiorespiratory examination. Laboratory values showed troponin I of 0.05 ng/ mL (normal range 0-0.05 ng/mL), low-density
h e a r t & l u n g 4 1 ( 2 0 1 2 ) 2 9 4 e3 0 0
297
Figure 4 e No significant anomalies are shown on multislice computed tomography.
lipoprotein cholesterol of 1.68 mmol/L, creatinine of 102 mmol/L, fasting plasma glucose of 5.22 mmol/L, postprandial (2 hours) plasma glucose of 8.6 mmol/L, hemoglobin A1c of 5.2%, brain natriuretic peptide of 63.2 pg/mL (normal range 0-125 pg/mL), erythrocyte sedimentation rate of 2 mm/h, and high-sensitivity Creactive protein of 0.84 mg/L. His thyroid hormone levels were normal. Antigen and antibody screening tests for EpsteineBarr virus, cytomegalovirus, hepatitis B virus, human immunodeficiency virus, and treponema pallidum all showed negative results. Immunofluorescence assays for antinuclear antibodies, anti-extractable nuclear antigen antibodies, antiedouble-stranded DNA antibodies, and anticardiolipin antibodies were all normal. A transthoracic echocardiogram (Figure 2) revealed an enlarged left ventricular cavity (left ventricular enddiastolic dimension 68 mm, left ventricular endsystolic dimension 55 mm) and a decreased left
ventricular ejection fraction of 37% with segmental wall-motion abnormalities: hypokinesis in the anterior wall and the septum. Prior anterior myocardial infarction (MI) was suspected because of the patient’s history, ECG, and echocardiogram, and the patient was scheduled for CAG. Cardiac catheterization showed normal coronary arteries (Figure 3A-C). No coronary artery spasm, coronary artery dissection, muscular bridge, plaque, or thrombus was observed. The peripheral arteries angiography showed a normal right forearm artery (Figure 3D), subclavian artery (Figure 3E), brachiocephalic trunk (Figure 3F), common carotid artery (Figure 3F), mesentery artery (Figure 3G), and renal artery (Figure 3H, I). Multislice computed tomography was used to complement CAG in the diagnosis and characterization of coronary artery anomalies,9 and no significant anomalies were found (Figure 4). The normal results of CAG and multislice computed tomography did not show
298
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Figure 5 e Delayed enhancement cardiovascular magnetic resonance imaging shows full-thickness infarction and markedly reduced left ventricular function with dyskinesis and aneurysmatic bulging of the thinned anterior wall (arrows).
the prior anterior MI. After gadolinium-DTPA contrast injection, delayed enhancement cardiovascular magnetic resonance imaging was performed to assess necrotic myocardium (Figure 5).10 There was predominant transmural hyperenhancement of the anterolateral myocardial wall, indicating full-thickness infarction, with marked subendocardial extension. Cine imaging demonstrated markedly reduced left ventricular function with dyskinesis and aneurysmatic bulging of the thinned anterior wall. After all the tests were completed, the patient was diagnosed with TMI. Because he had asymptomatic left ventricular dysfunction, we treated him with angiotensin-converting enzyme inhibitor perindopril 8 mg 4 times per day and carvedilol 10 mg 4 times per day. The patient was discharged with no complications. He has continued to be virtually symptom-free over a 3-year period of follow-up.
Discussion This report describes a young man with angiographically normal coronary arteries in whom ECG STT changes mimicked MI. The specificity of the ECG diagnosis for prior MI is greatest when Q-waves occur in several leads or lead groupings.11 However, ST deviations and T-wave inversions alone are nonspecific findings for myocardial necrosis.12 Under such conditions, imaging techniques play roles. The echocardiogram revealed segmental wall-motion
abnormalities, and delayed enhancement cardiovascular magnetic resonance indicated full-thickness infarction with marked subendocardial extension.10 According to the universal definition of MI, this patient was satisfied with the diagnosis of prior MI.13 Of individuals with MI who undergo CAG, 1% to 12% are found to have angiographically normal coronary arteries.14-16 This wide range can be explained by differing definitions of angiographically normal arteries: “without any endoluminal irregularity” and “no significant stenosis (eg, stenosis < 30%).”17 Other interpretations may include markedly different definitions of MI or the type of MI (ST-segment elevated MI and noneST-segment elevated MI). If we use the restrictive definition “without any endoluminal irregularity,” 1.1% of patients with MI were in this category.18 The cause of MI with normal coronary arteries is not clear. It has been reported that myocardial bridge,19 coronary spasm,20 coronary anomalies,21 spontaneous coronary dissection,22 anticardiolipin syndrome,23 Kawasaki disease,24 collagen disease,25 Takayasu’s aortitis,26 Buerger’s disease,27 and other diseases may contribute to the genesis of MI. For the patient described, no evidence could verify the above diagnoses. Given the history of a motorcycle accident 7 years previously and AMI diagnosis at that time, a diagnosis of TMI was made. TMI is a rare disease, and current understanding of this disease mainly originates from case reports. Christensen et al28 performed a Medline search from 1974 to 2006 and found 65 articles describing 77 cases
h e a r t & l u n g 4 1 ( 2 0 1 2 ) 2 9 4 e3 0 0
of TMI. There is no clear relationship between the severity of trauma and the development of coronary lesions. In fact, AMI has been reported after low- and high-speed traffic accidents and as direct chest trauma caused by a kick while playing sports.29 The mechanism of TMI is thought to be shearing of the coronary vessel wall, causing intimal tearing, dissection, and subintimal hemorrhage. Platelet aggregation and intraluminal thrombosis then follow.1 Other probable mechanisms of thrombotic coronary injury include vessel rupture and external compression by epicardial hematoma, occlusive dissection of the artery, or hemorrhage into a preexisting atheromatous plaque.30 Overall, the left anterior descending (LAD) coronary artery is most commonly affected (76%), followed by the right coronary artery (12%) and circumflex artery (6%).31 The higher incidence of LAD involvement may relate to its proximity to the sternum and vertebral column. Dramatic acceleration/ deceleration forces probably cause intimal tears of the most vulnerable part of the LAD, the junction of its proximal and mid-portions.32,33 Early recognition and diagnosis of TMI are of great importance to choose appropriate and prompt treatment. This case illustrates the importance of appropriately investigating patients with blunt chest injury to rule out MI. A screening 12-lead ECG should be performed in patients presenting with blunt trauma to the chest. CAG is the best test for coronary artery injury, although transesophageal echocardiography and intravascular ultrasound are also helpful.26 Normal coronary arteries after TMI were found in 15.8% and occlusion of 1 coronary artery in 56.6% of patients with other normal coronary arteries.28 When coronary arteries are found to be normal on angiography, the probable explanation is spasm or spontaneous clot lysis. Optimal treatment for TMI remains open to debate. Individualized intervention should be based on the patient’s presentation and angiographic findings. Coronary artery bypass grafting has been reported to provide good results in some selected cases; however, such a major operation may be accompanied by a higher risk of postoperative complications in patients with multiple traumas.2,3 Percutaneous coronary intervention has also been performed in some cases.4 Although complete healing of these lesions may occur, some patients may develop aneurysmal disease or late coronary occlusion as a result of progression of intimal disruption with dissection.5,6 Other authors advocate conservative management in the absence of ongoing ischemia. Several cases with follow-up have shown that a coronary artery dissection can heal spontaneously over 6 months with medical therapy alone.7,8 Would early revascularization be better than conservative management? Although this may be the case, it may not be of benefit in many trauma cases. More data are needed to compare the long-term outcome among different interventions, which is difficult considering the rarity of these events.
299
Conclusions There is a possibility of spontaneous healing of coronary artery dissection induced by trauma. Although early revascularization may be helpful for preventing cardiac remodeling after TMI in some cases, more data are needed to compare the long-term outcome among different interventions in large sample cases.
References 1. Marcum JL, Booth DC, Sapin PM. Acute myocardial infarction caused by blunt chest trauma: successful treatment by direct coronary angioplasty. Am Heart J 1996;132:1275-7. 2. Yoon SJ, Kwon HM, Kim DS, Hong BK, Kim DY, Cho YH, et al. Acute myocardial infarction caused by coronary artery dissection following blunt chest trauma. Yonsei Med J 2003;44:736-9. 3. Lai CH, Ma T, Chang TC, Chang MH, Chou P, Jong GP. A case of blunt chest trauma induced acute myocardial infarction involving two vessels. Int Heart J 2006;47:639-43. 4. Thorban S, Ungeheuer A, Blasini R, Siewert JR. Emergent interventional transcatheter revascularization in acute right coronary artery dissection after blunt chest trauma. J Trauma 1997;43:365-7. 5. Westaby S, Drossos G, Giannopoulos N. Posttraumatic coronary artery aneurysm. Ann Thorac Surg 1995;60: 712-3. 6. Rubin DA, Denys BG. Delayed and spontaneous coronary artery rupture following nonpenetrating chest trauma. Am Heart J 1992;124:1635-7. 7. Cherng WJ, Bullard MJ, Chang HJ, Lin FC. Diagnosis of coronary artery dissection following blunt chest trauma by transesophageal echocardiography. J Trauma 1995;39:772-4. 8. Chun JH, Lee SC, Gwon HC, Lee SH, Hong KP, Seo JD, et al. Left main coronary artery dissection after blunt chest trauma presented as acute anterior myocardial infarction: assessment by intravascular ultrasound: a case report. J Korean Med Sci 1998;13:325-7. 9. Hamon M, Biondi-Zoccai GG, Malagutti P, Agostoni P, Morello R, Valgimigli M. Diagnostic performance of multislice spiral computed tomography of coronary arteries as compared with conventional invasive coronary angiography: a meta-analysis. J Am Coll Cardiol 2006;48:1896-910. 10. West AM, Kramer CM. Cardiovascular magnetic resonance imaging of myocardial infarction, viability, and cardiomyopathies. Curr Probl Cardiol 2010;35: 176-220. 11. Wagner GS, Macfarlane P, Wellens H, Josephson M, Gorgels A, Mirvis DM, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part VI: Acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society For Computerized Electrocardiology. J Am Coll Cardiol 2009;53:1003-11.
300
h e a r t & l u n g 4 1 ( 2 0 1 2 ) 2 9 4 e3 0 0
12. Rautaharju PM, Surawicz B, Gettes LS, Bailey JJ, Childers R, Deal BJ, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part IV: The ST segment, T and U waves, and the QT interval: a Scientific Statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol 2009;53:982-91. 13. Thygesen K, Alpert JS, White HD. Universal definition of myocardial infarction. J Am Coll Cardiol 2007;50:2173-95. 14. Zainea M, Duvernoy WF, Chauhan A, David S, Soto E, Small D. Acute myocardial infarction in angiographically normal coronary arteries following induction of general anesthesia. Arch Intern Med 1994;154:2495-8. 15. Alpert JS. Myocardial infarction with angiographically normal coronary arteries. Arch Intern Med 1994;154: 265-9. 16. Alpert JS. Myocardial infarction with angiographically normal coronary arteries. A personal perspective. Arch Intern Med 1994;154:245. 17. Sharifi M, Frohlich TG, Silverman IM. Myocardial infarction with angiographically normal coronary arteries. Chest 1995;107:36-40. 18. Ammann P, Marschall S, Kraus M, Schmid L, Angehrn W, Krapf R, et al. Characteristics and prognosis of myocardial infarction in patients with normal coronary arteries. Chest 2000;117:333-8. 19. Ishikawa Y, Akasaka Y, Suzuki K, Fujiwara M, Ogawa T, Yamazaki K, et al. Anatomic properties of myocardial bridge predisposing to myocardial infarction. Circulation 2009;120:376-83. 20. Ong P, Athanasiadis A, Borgulya G, Voehringer M, Sechtem U. 3-year follow-up of patients with coronary artery spasm as cause of acute coronary syndrome: the CASPAR (coronary artery spasm in patients with acute coronary syndrome) study followup. J Am Coll Cardiol 2011;57:147-52. 21. Gallagher SM, Jain AK, Archbold RA. Primary percutaneous coronary intervention for st-elevation myocardial infarction in a patient with a single coronary artery arising from the right aortic sinus. J Invasive Cardiol 2011;23:E61-2. 22. Paraskevaidis S, Theofilogiannakos EK, Chatzizisis YS, Mantziari L, Economou F, Ziakas A, et al. Spontaneous dissection of right coronary artery manifested with
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
acute myocardial infarction. Open Cardiovasc Med J 2010;4:178-80. Urbanus RT, Siegerink B, Roest M, Rosendaal FR, de Groot PG, Algra A. Antiphospholipid antibodies and risk of myocardial infarction and ischaemic stroke in young women in the ratio study: a casecontrol study. Lancet Neurol 2009;8:998-1005. Inaba S, Higaki T, Nagashima M, Nishimura K, Ogimoto A, Higaki J, et al. Successful revascularization by pulse infusion thrombolysis in a patient with kawasaki disease combined with acute myocardial infarction. JACC Cardiovasc Interv 2010;3:1091-2. Meune C, Touze E, Trinquart L, Allanore Y. High risk of clinical cardiovascular events in rheumatoid arthritis: levels of associations of myocardial infarction and stroke through a systematic review and meta-analysis. Arch Cardiovasc Dis 2010;103:253-61. Roghi A, Pedrotti P, Milazzo A, Vignati G, Martinelli L, Paino R, et al. Acute myocardial infarction and cardiac arrest in atypical takayasu aortitis in a young girl: unusual diagnostic role of cardiac magnetic resonance imaging in emergency setting. Circulation 2010;121:e370-5. Rodriguez-Fernandez J, Rangel A, Chavez E. [Myocardial infarction simultaneous with buerger disease (obliterating thromboangiitis). A case report]. Arch Cardiol Mex 2002;72:306-10. Christensen MD, Nielsen PE, Sleight P. Prior blunt chest trauma may be a cause of single vessel coronary disease; hypothesis and review. Int J Cardiol 2006; 108:1-5. Kawahito K, Hasegawa T, Misawa Y, Fuse K. Right coronary artery dissection and acute infarction due to blunt trauma: report of a case. Surg Today 1998;28: 971-3. Atalar E, Acil T, Aytemir K, Ozer N, Ovunc K, Aksoyek S, et al. Acute anterior myocardial infarction following a mild nonpenetrating chest traumada case report. Angiology 2001;52:279-82. Ginzburg E, Dygert J, Parra-Davila E, Lynn M, Almeida J, Mayor M. Coronary artery stenting for occlusive dissection after blunt chest trauma. J Trauma 1998;45:157-61. Bjornstad JL, Pillgram-Larsen J, Tonnessen T. Coronary artery dissection and acute myocardial infarction following blunt chest trauma. World J Emerg Surg 2009;4:14. Fu M, Wu CJ, Hsieh MJ. Coronary dissection and myocardial infarction following blunt chest trauma. J Formos Med Assoc 1999;98:136-40.