ILLUSTRATIVE CASE
Acute Myopericarditis in an Adolescent Mimicking Acute Myocardial Infarction Jayendra Sharma, MD, FACC,* Nithi Fernandes, MD,† Dora Alvarez, MD,† and Shefali Khanna, MD† Abstract: Acute myopericarditis is primarily a pericarditic syndrome with variable myocardial involvement, as evidenced by elevated cardiac enzymes. It is a rare entity, exclusively seen in male adolescents and accounts for less than 2% of the cases of inpatient admissions for chest pain/ pericarditis in the pediatric age group. The electrocardiographic changes of pericarditis include J point/ST segment elevation, which needs to be differentiated from the benign early repolarization pattern that is common in young adolescents and the subtle anterior ST segment elevation myocardial infarction. Differentiating acute myopericarditis from acute coronary syndromes can be challenging because they share the presenting triad of acute chest pain, ST segment changes, and elevated cardiac enzymes. The accurate distinction of myopericarditis from acute myocarditis or acute coronary syndrome is important because of their differences in risk for specific complications, prognosis, and treatment implications. We present a case of acute myopericarditis in an adolescent who presented with atypical precordial chest pain, accompanied by inferolateral focal electrocardiographic changes and significant elevation of cardiac enzymes. The differential diagnosis and management of myopericarditis is reviewed with a focus on electrocardiographic changes and troponin assays. Key Words: myopericarditis, acute coronary syndrome, early repolarization pattern, troponin assay, cardiac MRI (Pediatr Emer Care 2015;31: 427–430)
C
hest pain is a common complaint in children and adolescents presented to the emergency department; however, only 0.6% of cases have an underlying cardiac etiology.1 Patients with myopericarditis present with symptoms of pericarditis in the presence of elevated levels of cardiac enzymes and usually with preserved left ventricular systolic function.2 Acute myopericarditis is a rare entity in pediatric age group with a limited data available from literature.3 The diagnosis of pericarditis depends on a triad of typical precordial chest pain, pericardial friction rub, and diffuse ST segment elevation on electrocardiogram. Serum troponin I levels are sometimes significantly elevated in myopericarditis, which is related to the extent of myocardial inflammation and does not predict adverse outcome.3,4 The elevated troponin I levels in context of chest pain and abnormal electrocardiogram raise the need to differentiate the myopericarditis from acute myocarditis and acute coronary syndrome. Such distinction is of utmost importance because their risk of specific complications, prognosis and treatment strategies are different. Electrocardiogram, twodimensional echocardiogram, and cardiac magnetic resonance imaging (MRI) are useful tools in differential diagnosis and management.
From the *Divisions of Pediatric Cardiology and †Pediatric Intensive Care, Department of Pediatrics, Lincoln Medical and Mental health center, Bronx, NY. Disclosure: The authors declare no conflict of interest. Reprints: Jayendra Sharma, MD, FACC, 45, Wiltshire Road, Scarsdale, NY 10583 (e‐mail: [email protected]). Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0749-5161
CASE A 12-year-old boy presented to the pediatric emergency department complaining of the gradual onset of nonradiating midsternal chest pain associated with nausea, vomiting, and chills for a day. The chest pain was worse when lying on the left side and was not exacerbated by respiration and change in position. Having a history of intermittent asthma, his mother gave him an Albuterol nebulizer at home, without relief of his symptoms. His medical history and family history were unremarkable. On arrival, he had normal vital signs except for mildly elevated blood pressure 122/77 mm Hg (95th percentile for age and height) without acute distress. On physical examination, there was no chest wall tenderness, and the heart sounds were normal without murmur, rub, or gallop. The rest of the physical exam was within normal limits. Laboratory evaluation including blood counts, sedimentation rate, electrolyte and lipid profile, and urine toxic screen were unremarkable. A 12 lead electrocardiogram revealed ST segment elevation and PR segment depression in inferolateral leads (Fig. 1A). Troponin level done at that time was elevated at 6.60 ng/mL. Serum creatine kinase and creatine kinase-muscle brain done 8 hours later were also elevated at 1356 U/L and 20.50 ng/mL, respectively. Chest radiograph showed a normal heart size and clear lungs. Echocardiogram showed normal proximal coronaries, normal left ventricular dimensions with good systolic function, and no pericardial effusion. He was admitted for suspected myopericarditis, given anti-inflammatory medication every 6 hours and observed under cardiorespiratory monitoring. He remained afebrile, hemodynamically stable, breathing comfortably but required morphine sulfate twice for pain management in first 24 hours. His serum troponin I level rose to maximum of 24 ng/mL within 24 hours after admission. Electrocardiograms (Fig. 1) and cardiac enzymes (Fig. 2) were repeated at regular intervals over the next 4 days, which showed initially an elevation in cardiac enzymes and worsening ST segment elevations, followed by gradual resolution of both. He was discharged on ibuprofen and follow-up in pediatric cardiology 2 weeks later showed normal electrocardiogram and echocardiogram.
DISCUSSION
Myopericarditis is primarily a “pericarditic syndrome” in which acute pericarditis often is accompanied by some degree of myocarditis, as evident by elevated cardiac enzymes.2 Both pericarditis and myocarditis can coexist in clinical practice because they share common etiologic agents, mainly cardiotropic viruses. The profile of common viral agents include enteroviruses, adenovirus, cytomegalovirus, Epstein-Barr virus, parvo virus and human immunodeficiency virus. The prevalence of myopericarditis is difficult to ascertain because some cases may remain subclinical, and its subtle symptoms may be overshadowed by the systemic manifestation of viral infection. Data on myopericarditis and its outcome in children are scarce.3 Imazio et al2,3 reported that myopericarditis may be present approximately in 15% of all diagnosed cases of acute pericarditis in adults, but in children, it accounts for only 1.4% of cases of inpatient admissions of chest
Pediatric Emergency Care • Volume 31, Number 6, June 2015
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.pec-online.com
427
Sharma et al
Pediatric Emergency Care • Volume 31, Number 6, June 2015
FIGURE 1. (A) Twelve lead electrocardiogram showing ST elevation and PR depression in inferolateral leads on admission. (B) Worsening of ST elevation in first 24 hours. (C) Gradual improvement of ST elevation and PR depression after 4 days.
428
www.pec-online.com
© 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Pediatric Emergency Care • Volume 31, Number 6, June 2015
Myopericarditis With Focal EKG Changes
FIGURE 2. Serial values of serum troponin I, creatine kinase, and CK-MB levels during hospitalization.
pain/pericarditis. Myopericarditis is exclusively seen in male adolescents, as exemplified in our case. The clinical presentation of myopericarditis is varied, reflecting variability of involvement, focal or diffuse.2 The diagnosis of acute pericarditis in the emergency room depends on typical precordial chest pain, presence of pericardial rub, electrocardiographic changes such as diffuse ST segment elevation and new or worsening pericardial effusion on echocardiography. The typical pain of pericarditis is sharp in nature with gradual onset, typically radiates to scapular area, increases with inspiration, and generally eases on getting up and leaning forward. A pericardial friction rub is considered a pathognomic finding, but its absence does not rule out the diagnosis. Pericardial effusion is seen in 60% cases of pericarditis. The presence of left ventricular dilatation, wall motion abnormalities, or systolic dysfunction on echocardiogram should alert about the possibility of developing acute myocarditis or acute coronary syndrome rather than acute myopericarditis. The diffuse ST segment elevation with PR segment depression on electrocardiogram is suggestive of pericarditis. The differential diagnosis of ST segment elevation includes benign early repolarization, pericarditis, myocardial infarction, bundle branch block, and left ventricular aneurysm. Early repolarization pattern is a common electrocardiogram variant characterized by J point elevation, manifested as terminal QRS slurring or notching associated with concave upward ST segment elevation and prominent T wave in at least two contagious leads.5 Early repolarization
pattern is frequently seen in healthy young adolescents and its incidence and degree decreases with age. Isoproterenol and exercise may normalize ST segment, which favors its benign nature. J point/ST segment elevation in the normal heart is because of the differences in Ito-mediated action potential spike and dome between ventricular epicardium and endocardium, resulting in a transmural voltage gradient during early repolarization. The electrocardiographic differentiation of early repolarization from pericarditis and subtle anterior ST segment elevation myocardial infarction is sometimes difficult.6 The typical four phases of electrocardiographic changes of acute pericarditis are seen in 60% of the cases.4 Earliest findings in the first 24 hours include depression of PR segment with diffuse concave ST segment elevation, more so in coexistent myocarditis which is followed by normalization of PR/ST segments. Diffuse negative T wave is seen subsequently, followed by either normalization of electrocardiogram or persistent negative T waves. The diagnosis of acute myocardial infarction in adolescent, presenting with persistent chest pain and elevated troponin I levels, is based on convex ST segment elevations, supported by presence of etiologic risk factors and wall motion abnormalities on echocardiogram. The focal electrocardiographic change is seen in 50% of the cases of myopericarditis, such as in our case, which makes differentiation from ischemic changes difficult.7 PR segment depression is an important but often ignored electrocardiographic finding in myopericarditis and its presence in both limb leads,
© 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.pec-online.com
429
Pediatric Emergency Care • Volume 31, Number 6, June 2015
Sharma et al
especially in lead II and precordial leads as seen in our case give most favorable predictive power (positive 96.7% and negative power 90%) to differentiate myopericarditis from ST elevation myocardial infarction.8 Differentiating acute myopericarditis from acute coronary syndrome can be challenging in some cases and may require coronary angiography or perfusion studies. Because of a lack of data in children, coronary angiography was performed in majority cases of myopericarditis as reflected in the study presented by Kobayashi et al.3 Cardiac MRI with gadolinium contrast seems to offer the best imaging modality to define the extent of myocardial involvement and patency of the coronary system. It can help to differentiate acute myopericarditis from acute myocarditis or acute coronary syndrome in presence of left ventricular systolic dysfunction.9 Both cardiac MRI and coronary angiography were not considered in our case due to the low coronary risk profile of this adolescent with normal proximal coronaries and normal left ventricular dimensions/function on periodic echocardiograms with downward trend of cardiac enzymes after first 24 hours of admission. Cardiac troponin is the most sensitive and specific biochemical marker of myocardial injury, and with the new high sensitivity assay, even a minor damage to the heart muscle can be detected. Troponin leaks out of myocyte only after membrane disruption after myocardial cell death but can also occur with increased cell membrane permeability as demonstrated in strenuous exercise such as marathon running. The troponin assay has been established as a useful screening tool for the evaluation of acute coronary syndrome in adults, but its value in children with chest pain is not well defined, and limited information is available regarding its utility in risk stratification. The latest laboratory assay used for serum troponin is the VITROS troponin I and the 99% upper reference limit of normal is less than 0.034 ng/mL. Subendocardial ischemia is reported with serum troponin level less than 0.01 ng/mL. Serum troponin values between 0.1 and 2 ng/mL are considered borderline and need to be correlated with clinical scenario. Noncoronary causes of elevation of troponin include acute myopericarditis, tachyarrhythmia, sepsis, pulmonary embolism, acute heart failure, cardiac contusion, sympathomimetic drugs, and strenuous exercise. The most common diagnosis associated with elevated serum troponin levels, usually more than 2 ng/mL in children with chest pain, is myocarditis.10 An elevated troponin level in myopericarditis, unlike in acute coronary syndromes does not seem to carry an adverse prognosis in adults as well in children.3.4 The aspirin or nonsteroidal anti-inflammatory drugs, such as ibuprofen are the therapy of choice for acute myopericarditis. In the case of recurrences, Colchicine may be a valid alternative. Nonsteroidal anti-inflammatory therapy appears to be ineffective in cases of predominant myocarditis and has been shown to
430
www.pec-online.com
increase mortality associated with myocardial damage. Corticosteroids should be the last line of treatment as they are independently associated with recurrence but they do have a role in management of pericarditis with significant effusion. Acute myopericarditis is rare in children, seen almost exclusively in male adolescents and presents with the triad of typical pericarditic chest pain, ST segment elevation and PR segment depression on electrocardiogram and elevated serum troponin levels. It is a distinct entity however when accompanied by left ventricular dysfunction, it needs to be differentiated from acute myocarditis and acute coronary syndrome as their management and prognosis are different. Cardiac MRI with gadolinium contrast is the preferred imaging modality for differential diagnosis in the low-risk pediatric population. Serum troponin levels are sometimes markedly elevated at presentation as in our case but they are not associated with adverse prognosis. Acute myopericarditis in children usually follows a benign course with good outcome. REFERENCES 1. Drossner D, Hirsh D, Sturum J, et al. Cardiac disease in pediatric patients presenting to a pediatric ED with chest pain. Am J Emerg Med. 2011;29: 632–638. 2. Imazio M, Trinchero R. Myopericarditis: etiology, management and prognosis. Int J Cardiol. 2008;23:17–26. 3. Kobayashi D, Aggarwal S, Kheiwa A, et al. Myopericarditis in children: elevated troponin I level does not predict outcome. Pediatr Cardiol. 2012;33:1040–1045. 4. Imazio M, Demichellis B, Cecchi E, et al. Cardiac troponin I in acute pericarditis. J Am Coll Cardiol. 2003;42:2144–2148. 5. Klatsky AL, Oehm R, Cooper RA, et al. The early repolarization normal variant electrocardiogram: correlates and consequences. Am J Med. 2003;15:171–177. 6. Smith SW, Khalil A, Henry TD, et al. Electrocardiographic differentiation of early repolarization from subtle anterior ST segment elevation myocardial infarction. Ann Emerg Med. 2012;60:45–56. 7. Nibet BC, Breyer M. Acute myopericarditis with focal ECG findings mimicking acute myocardial infarction. J Emerg Med. 2010;39:153–158. 8. Porela P, Kyto V, Nikus K, et al. PR depression is useful in the differential diagnosis of myopericarditis and ST elevation myocardial infarction. Ann Noninvasive Electrocardiol. 2012;17:141–145. 9. May L, Patton D, Fruitman D. The evolving approach to pediatric myocarditis: a review of the current literature. Cardiol Young. 2011;21: 241–251. 10. Brown J, Hirsh D, Mahle W. Use of troponin as a screen for chest pain in the pediatric emergency department. Pediatr Cardiol. 2012;33:337–342.
© 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Acute Myopericarditis in an Adolescent Mimicking Acute Myocardial Infarction Jayendra Sharma, MD, FACC,* Nithi Fernandes, MD,† Dora Alvarez, MD,† and Shefali Khanna, MD† Abstract: Acute myopericarditis is primarily a pericarditic syndrome with variable myocardial involvement, as evidenced by elevated cardiac enzymes. It is a rare entity, exclusively seen in male adolescents and accounts for less than 2% of the cases of inpatient admissions for chest pain/ pericarditis in the pediatric age group. The electrocardiographic changes of pericarditis include J point/ST segment elevation, which needs to be differentiated from the benign early repolarization pattern that is common in young adolescents and the subtle anterior ST segment elevation myocardial infarction. Differentiating acute myopericarditis from acute coronary syndromes can be challenging because they share the presenting triad of acute chest pain, ST segment changes, and elevated cardiac enzymes. The accurate distinction of myopericarditis from acute myocarditis or acute coronary syndrome is important because of their differences in risk for specific complications, prognosis, and treatment implications. We present a case of acute myopericarditis in an adolescent who presented with atypical precordial chest pain, accompanied by inferolateral focal electrocardiographic changes and significant elevation of cardiac enzymes. The differential diagnosis and management of myopericarditis is reviewed with a focus on electrocardiographic changes and troponin assays. Key Words: myopericarditis, acute coronary syndrome, early repolarization pattern, troponin assay, cardiac MRI (Pediatr Emer Care 2015;31: 427–430)
C
hest pain is a common complaint in children and adolescents presented to the emergency department; however, only 0.6% of cases have an underlying cardiac etiology.1 Patients with myopericarditis present with symptoms of pericarditis in the presence of elevated levels of cardiac enzymes and usually with preserved left ventricular systolic function.2 Acute myopericarditis is a rare entity in pediatric age group with a limited data available from literature.3 The diagnosis of pericarditis depends on a triad of typical precordial chest pain, pericardial friction rub, and diffuse ST segment elevation on electrocardiogram. Serum troponin I levels are sometimes significantly elevated in myopericarditis, which is related to the extent of myocardial inflammation and does not predict adverse outcome.3,4 The elevated troponin I levels in context of chest pain and abnormal electrocardiogram raise the need to differentiate the myopericarditis from acute myocarditis and acute coronary syndrome. Such distinction is of utmost importance because their risk of specific complications, prognosis and treatment strategies are different. Electrocardiogram, twodimensional echocardiogram, and cardiac magnetic resonance imaging (MRI) are useful tools in differential diagnosis and management.
From the *Divisions of Pediatric Cardiology and †Pediatric Intensive Care, Department of Pediatrics, Lincoln Medical and Mental health center, Bronx, NY. Disclosure: The authors declare no conflict of interest. Reprints: Jayendra Sharma, MD, FACC, 45, Wiltshire Road, Scarsdale, NY 10583 (e‐mail: [email protected]). Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0749-5161
CASE A 12-year-old boy presented to the pediatric emergency department complaining of the gradual onset of nonradiating midsternal chest pain associated with nausea, vomiting, and chills for a day. The chest pain was worse when lying on the left side and was not exacerbated by respiration and change in position. Having a history of intermittent asthma, his mother gave him an Albuterol nebulizer at home, without relief of his symptoms. His medical history and family history were unremarkable. On arrival, he had normal vital signs except for mildly elevated blood pressure 122/77 mm Hg (95th percentile for age and height) without acute distress. On physical examination, there was no chest wall tenderness, and the heart sounds were normal without murmur, rub, or gallop. The rest of the physical exam was within normal limits. Laboratory evaluation including blood counts, sedimentation rate, electrolyte and lipid profile, and urine toxic screen were unremarkable. A 12 lead electrocardiogram revealed ST segment elevation and PR segment depression in inferolateral leads (Fig. 1A). Troponin level done at that time was elevated at 6.60 ng/mL. Serum creatine kinase and creatine kinase-muscle brain done 8 hours later were also elevated at 1356 U/L and 20.50 ng/mL, respectively. Chest radiograph showed a normal heart size and clear lungs. Echocardiogram showed normal proximal coronaries, normal left ventricular dimensions with good systolic function, and no pericardial effusion. He was admitted for suspected myopericarditis, given anti-inflammatory medication every 6 hours and observed under cardiorespiratory monitoring. He remained afebrile, hemodynamically stable, breathing comfortably but required morphine sulfate twice for pain management in first 24 hours. His serum troponin I level rose to maximum of 24 ng/mL within 24 hours after admission. Electrocardiograms (Fig. 1) and cardiac enzymes (Fig. 2) were repeated at regular intervals over the next 4 days, which showed initially an elevation in cardiac enzymes and worsening ST segment elevations, followed by gradual resolution of both. He was discharged on ibuprofen and follow-up in pediatric cardiology 2 weeks later showed normal electrocardiogram and echocardiogram.
DISCUSSION
Myopericarditis is primarily a “pericarditic syndrome” in which acute pericarditis often is accompanied by some degree of myocarditis, as evident by elevated cardiac enzymes.2 Both pericarditis and myocarditis can coexist in clinical practice because they share common etiologic agents, mainly cardiotropic viruses. The profile of common viral agents include enteroviruses, adenovirus, cytomegalovirus, Epstein-Barr virus, parvo virus and human immunodeficiency virus. The prevalence of myopericarditis is difficult to ascertain because some cases may remain subclinical, and its subtle symptoms may be overshadowed by the systemic manifestation of viral infection. Data on myopericarditis and its outcome in children are scarce.3 Imazio et al2,3 reported that myopericarditis may be present approximately in 15% of all diagnosed cases of acute pericarditis in adults, but in children, it accounts for only 1.4% of cases of inpatient admissions of chest
Pediatric Emergency Care • Volume 31, Number 6, June 2015
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.pec-online.com
427
Sharma et al
Pediatric Emergency Care • Volume 31, Number 6, June 2015
FIGURE 1. (A) Twelve lead electrocardiogram showing ST elevation and PR depression in inferolateral leads on admission. (B) Worsening of ST elevation in first 24 hours. (C) Gradual improvement of ST elevation and PR depression after 4 days.
428
www.pec-online.com
© 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Pediatric Emergency Care • Volume 31, Number 6, June 2015
Myopericarditis With Focal EKG Changes
FIGURE 2. Serial values of serum troponin I, creatine kinase, and CK-MB levels during hospitalization.
pain/pericarditis. Myopericarditis is exclusively seen in male adolescents, as exemplified in our case. The clinical presentation of myopericarditis is varied, reflecting variability of involvement, focal or diffuse.2 The diagnosis of acute pericarditis in the emergency room depends on typical precordial chest pain, presence of pericardial rub, electrocardiographic changes such as diffuse ST segment elevation and new or worsening pericardial effusion on echocardiography. The typical pain of pericarditis is sharp in nature with gradual onset, typically radiates to scapular area, increases with inspiration, and generally eases on getting up and leaning forward. A pericardial friction rub is considered a pathognomic finding, but its absence does not rule out the diagnosis. Pericardial effusion is seen in 60% cases of pericarditis. The presence of left ventricular dilatation, wall motion abnormalities, or systolic dysfunction on echocardiogram should alert about the possibility of developing acute myocarditis or acute coronary syndrome rather than acute myopericarditis. The diffuse ST segment elevation with PR segment depression on electrocardiogram is suggestive of pericarditis. The differential diagnosis of ST segment elevation includes benign early repolarization, pericarditis, myocardial infarction, bundle branch block, and left ventricular aneurysm. Early repolarization pattern is a common electrocardiogram variant characterized by J point elevation, manifested as terminal QRS slurring or notching associated with concave upward ST segment elevation and prominent T wave in at least two contagious leads.5 Early repolarization
pattern is frequently seen in healthy young adolescents and its incidence and degree decreases with age. Isoproterenol and exercise may normalize ST segment, which favors its benign nature. J point/ST segment elevation in the normal heart is because of the differences in Ito-mediated action potential spike and dome between ventricular epicardium and endocardium, resulting in a transmural voltage gradient during early repolarization. The electrocardiographic differentiation of early repolarization from pericarditis and subtle anterior ST segment elevation myocardial infarction is sometimes difficult.6 The typical four phases of electrocardiographic changes of acute pericarditis are seen in 60% of the cases.4 Earliest findings in the first 24 hours include depression of PR segment with diffuse concave ST segment elevation, more so in coexistent myocarditis which is followed by normalization of PR/ST segments. Diffuse negative T wave is seen subsequently, followed by either normalization of electrocardiogram or persistent negative T waves. The diagnosis of acute myocardial infarction in adolescent, presenting with persistent chest pain and elevated troponin I levels, is based on convex ST segment elevations, supported by presence of etiologic risk factors and wall motion abnormalities on echocardiogram. The focal electrocardiographic change is seen in 50% of the cases of myopericarditis, such as in our case, which makes differentiation from ischemic changes difficult.7 PR segment depression is an important but often ignored electrocardiographic finding in myopericarditis and its presence in both limb leads,
© 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.pec-online.com
429
Pediatric Emergency Care • Volume 31, Number 6, June 2015
Sharma et al
especially in lead II and precordial leads as seen in our case give most favorable predictive power (positive 96.7% and negative power 90%) to differentiate myopericarditis from ST elevation myocardial infarction.8 Differentiating acute myopericarditis from acute coronary syndrome can be challenging in some cases and may require coronary angiography or perfusion studies. Because of a lack of data in children, coronary angiography was performed in majority cases of myopericarditis as reflected in the study presented by Kobayashi et al.3 Cardiac MRI with gadolinium contrast seems to offer the best imaging modality to define the extent of myocardial involvement and patency of the coronary system. It can help to differentiate acute myopericarditis from acute myocarditis or acute coronary syndrome in presence of left ventricular systolic dysfunction.9 Both cardiac MRI and coronary angiography were not considered in our case due to the low coronary risk profile of this adolescent with normal proximal coronaries and normal left ventricular dimensions/function on periodic echocardiograms with downward trend of cardiac enzymes after first 24 hours of admission. Cardiac troponin is the most sensitive and specific biochemical marker of myocardial injury, and with the new high sensitivity assay, even a minor damage to the heart muscle can be detected. Troponin leaks out of myocyte only after membrane disruption after myocardial cell death but can also occur with increased cell membrane permeability as demonstrated in strenuous exercise such as marathon running. The troponin assay has been established as a useful screening tool for the evaluation of acute coronary syndrome in adults, but its value in children with chest pain is not well defined, and limited information is available regarding its utility in risk stratification. The latest laboratory assay used for serum troponin is the VITROS troponin I and the 99% upper reference limit of normal is less than 0.034 ng/mL. Subendocardial ischemia is reported with serum troponin level less than 0.01 ng/mL. Serum troponin values between 0.1 and 2 ng/mL are considered borderline and need to be correlated with clinical scenario. Noncoronary causes of elevation of troponin include acute myopericarditis, tachyarrhythmia, sepsis, pulmonary embolism, acute heart failure, cardiac contusion, sympathomimetic drugs, and strenuous exercise. The most common diagnosis associated with elevated serum troponin levels, usually more than 2 ng/mL in children with chest pain, is myocarditis.10 An elevated troponin level in myopericarditis, unlike in acute coronary syndromes does not seem to carry an adverse prognosis in adults as well in children.3.4 The aspirin or nonsteroidal anti-inflammatory drugs, such as ibuprofen are the therapy of choice for acute myopericarditis. In the case of recurrences, Colchicine may be a valid alternative. Nonsteroidal anti-inflammatory therapy appears to be ineffective in cases of predominant myocarditis and has been shown to
430
www.pec-online.com
increase mortality associated with myocardial damage. Corticosteroids should be the last line of treatment as they are independently associated with recurrence but they do have a role in management of pericarditis with significant effusion. Acute myopericarditis is rare in children, seen almost exclusively in male adolescents and presents with the triad of typical pericarditic chest pain, ST segment elevation and PR segment depression on electrocardiogram and elevated serum troponin levels. It is a distinct entity however when accompanied by left ventricular dysfunction, it needs to be differentiated from acute myocarditis and acute coronary syndrome as their management and prognosis are different. Cardiac MRI with gadolinium contrast is the preferred imaging modality for differential diagnosis in the low-risk pediatric population. Serum troponin levels are sometimes markedly elevated at presentation as in our case but they are not associated with adverse prognosis. Acute myopericarditis in children usually follows a benign course with good outcome. REFERENCES 1. Drossner D, Hirsh D, Sturum J, et al. Cardiac disease in pediatric patients presenting to a pediatric ED with chest pain. Am J Emerg Med. 2011;29: 632–638. 2. Imazio M, Trinchero R. Myopericarditis: etiology, management and prognosis. Int J Cardiol. 2008;23:17–26. 3. Kobayashi D, Aggarwal S, Kheiwa A, et al. Myopericarditis in children: elevated troponin I level does not predict outcome. Pediatr Cardiol. 2012;33:1040–1045. 4. Imazio M, Demichellis B, Cecchi E, et al. Cardiac troponin I in acute pericarditis. J Am Coll Cardiol. 2003;42:2144–2148. 5. Klatsky AL, Oehm R, Cooper RA, et al. The early repolarization normal variant electrocardiogram: correlates and consequences. Am J Med. 2003;15:171–177. 6. Smith SW, Khalil A, Henry TD, et al. Electrocardiographic differentiation of early repolarization from subtle anterior ST segment elevation myocardial infarction. Ann Emerg Med. 2012;60:45–56. 7. Nibet BC, Breyer M. Acute myopericarditis with focal ECG findings mimicking acute myocardial infarction. J Emerg Med. 2010;39:153–158. 8. Porela P, Kyto V, Nikus K, et al. PR depression is useful in the differential diagnosis of myopericarditis and ST elevation myocardial infarction. Ann Noninvasive Electrocardiol. 2012;17:141–145. 9. May L, Patton D, Fruitman D. The evolving approach to pediatric myocarditis: a review of the current literature. Cardiol Young. 2011;21: 241–251. 10. Brown J, Hirsh D, Mahle W. Use of troponin as a screen for chest pain in the pediatric emergency department. Pediatr Cardiol. 2012;33:337–342.
© 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
