PEDIATRICS Vol. 120 No. 4 October 2007, pp. e938-e943 (doi:10.1542/peds.2006-3123)
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Myocardial Infarction in Healthy Adolescents
The Heart Center, Akron Children's Hospital, Akron, Ohio
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ABSTRACT |
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OBJECTIVE. Chest pain in children and adolescents is a frequent cause for office or emergency department visits. However, it is unclear whether myocardial infarction occurs in children with no anatomic abnormality presenting with chest pain.
METHODS. Clinical history, electrocardiography, echocardiography, and cardiac enzyme levels were evaluated in patients presenting to the emergency department over a period of 11 years (June 1995 to May 2006). Patients in whom findings were suggestive of acute myocardial infarction, in addition, underwent drug screening, serum lipid profile, and hypercoagulability workup and, when myocardial infarction was diagnosed, heart catheterization with coronary angiography.
RESULTS. Nine patients (8 boys; age range: 12–20 years; mean: 15.5 years) met established criteria for myocardial infarction. Abnormal electrocardiograms were found in 8 patients (6 with ST elevation and 2 with nonspecific ST-T abnormalities), abnormal cardiac enzyme levels in all, and echocardiographic abnormalities in 3. Cardiac dysrhythmias were found in 4 patients, 3 with nonsustained ventricular tachycardia. Drug abuse, lipid profile, and hypercoagulability studies were negative in all. Left ventricular focal hypokinesia was seen by echocardiogram or angiography in 5 patients and abnormal coronary anatomy in none. Cardiac function normalized in 8 patients. One patient had a persistent focal inferior hypokinesis. Calcium channel blocker therapy was initiated in all of the patients with no recurrence of anginal chest pain on follow-up. One patient complained of chest pain distinct from anginal pain.
CONCLUSIONS. Myocardial infarction can occur in adolescents with normal coronary arterial anatomy. Adolescents who present for emergency care with typical chest pain need electrocardiographic and cardiac enzyme workups. Those with results that are suggestive of acute infarction require additional workup. Coronary vasodilation therapy seems helpful, but given the lack of coronary thrombosis in these patients, thrombolytic therapy seems unwarranted. Long-term follow-up is necessary, and adjustments in therapy may be required with time.
Key Words: adolescent • chest pain • coronary vasospasm • myocardial infarction
Abbreviations: ECG—electrocardiogram • CK—creatine kinase • CK-MB—creatine kinase MB fraction
Chest pain in the pediatric population is a frequent complaint and is noncardiac in origin in the vast majority of patients. Myocardial ischemia can occur in childhood, however, and is usually caused by anatomic congenital cardiovascular abnormalities. Several reports of isolated cases of acute ischemia in patients without congenital coronary arterial anomalies have been noted in the literature.1–3 This study reports the occurrence of acute myocardial infarction in a series of patients without congenital coronary anomalies or drug abuse who presented to the emergency department with chest pain. Their workup, clinical course, and treatment are described.
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METHODS |
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Of otherwise healthy adolescent patients presenting to the emergency department with chest pain over the course of 11 years (June 1995 to May 2006), 9 patients met established criteria of acute myocardial ischemia and infarction. Criteria for myocardial infarction included, in addition to typical anginal chest pain, electrocardiogram (ECG) changes including ST elevation of
1 mm or nonspecific ST and T changes, abnormal cardiac wall motion by echocardiographic or angiographic imaging, and elevation in the creatinine kinase (CK) MB fraction (CK-MB) and troponin I levels.4 Eight males and 1 female, who was 4 months postpartum (age range: 12–20 years; mean: 15.5 years), presented with chest discomfort, suggesting myocardial ischemia. History for activity, substance abuse, and family history were obtained. Workup in all of the patients included ECG and echocardiography, obtaining cardiac enzyme levels, and performing a lipid profile and drug screen. Hypercoagulability studies were performed for the last 7 patients in the series. All of the patients with myocardial ischemia were followed with serial ECG tracing and monitored for arrhythmias. Acute treatment for all of the patients included nitroglycerin (sublingual, topical, or intravenous) and aspirin or intravenous heparin. Thrombolytic therapy was not administered to any patient. Diltiazem was started postinfarction and continued postdischarge.
Cardiac catheterization with coronary angiography was performed on all of the patients to assess for congenital heart disease, myocardial wall motion abnormality, and to define coronary arterial anatomy. Patients were assessed after hospitalization by clinical history, ECG, echocardiography, and exercise stress testing.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSREFERENCES |
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In a pediatric adolescent population presenting to the emergency department with chest pain over a period of 11 years, 9 otherwise healthy patients, except for migraine headaches in 2, met criteria for acute myocardial infarction. Eight of the patients were male, and 1 was female.
In 1 patient, the resting ECG was normal. In 2, nonspecific ST and T changes were seen in the inferior leads, and in 6, typical ST elevation of myocardial injury, all in the inferior or inferolateral leads, was seen (Fig 1A). Serial ECG showed evolvement of ST segment abnormalities, including transient T wave inversion, in 7 patients. Diagnostic Q waves developed in 3 patients (Fig 1B), all of which normalized in the course of follow-up (Fig 1C). ECG changes occurred over hours to days. The 1 normal ECG remained normal during follow-up.
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Nonsustained ventricular tachycardia was seen in 3 patients, was not associated with hemodynamic instability, and did not require treatment. An additional patient developed a transient accelerated idioventricular rhythm after resolution of the chest pain.
Echocardiography showed segmental inferior wall motion abnormality in 3 patients, all of whom had inferior lead ST elevation. The remaining 6 patients had normal echocardiograms, including 2 patients with ST segment elevation.
All of the patients had cardiac enzyme elevation of CK and CK-MB; the last 8 patients had their troponin I level determined as well. All of the patients exhibited a single peak and a decay in enzyme level without the recurrence of additional peaks (Fig 2).
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The drug screen was negative for 8 of the 9 patients and was positive for amphetamines in 1 patient who was taking methylphenidate for attention-deficit disorder. The patient denied substance abuse or overdosage of methylphenidate. He had been treated with methylphenidate for years before presentation and has been on methylphenidate subsequently without recurrence of angina.
Laboratory evaluations for hyperlipidemia revealed no significant hypercholesterolemia. Hypercoagulability workup was negative in all 7 patients on whom it was performed.
All of the patients underwent selective coronary angiography, most after resolution of chest pain before hospital discharge and 1 while still experiencing residual chest pain. All of the coronary angiograms were normal. Four of 9 left ventricular angiograms showed inferior wall hypokinesis, and 1 showed mild lateral focal hypokinesia. Left ventricular ejection fraction was normal or near normal in all of the cases. No congenital coronary or cardiac anomalies were found. No coronary thrombi were found. Provocative measures to identify coronary spasm were not performed in the acute infarct period.
All of the patients responded to nitroglycerin therapy (sublingual, topical, or intravenous) with subsidence of their chest pain. Chronic treatment with diltiazem was started after chest pain had subsided. Posthospitalization follow-up showed no recurrence of anginal pain while on diltiazem. One patient presented with atypical chest pain on follow-up different from his previous angina. Maximal exercise stress testing performed on all of the patients after hospitalization showed no evidence of ischemia.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSREFERENCES |
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Chest pain is a frequent complaint among adolescents and is mostly noncardiac in origin. Ischemic chest pain in the pediatric population is uncommon and can be secondary to both congenital defects (coronary arterial anomalies, aortic valvar and supravalvar stenosis, hypoplastic left heart syndrome, pulmonary atresia, or complete transposition of the great arteries)5–15 or acquired diseases (eg, pericarditis, autoimmune vasculitis, Kawasaki disease, drug abuse and medications, trauma, endocarditis, or hyperlipidemia).16–24 Angina with normal coronary anatomy in an otherwise healthy child or adolescent does not usually come to mind in the differential diagnosis of chest pain. The current study presents a series of 9 healthy patients who presented to the emergency department with typical severe retrosternal pain radiating to the left arm or jaw and who had developed acute myocardial infarction. The etiology of infarction is presumed to be because of coronary spasm given the lack of fixed anatomic stenosis or occlusion. The spasm was apparently of sufficient duration to result in myocardial necrosis and enzyme leak. The vasoactive nature of their ischemia was also suggested by effective response to nitroglycerin. Whether the migraines in 2 of the patients are part of a general vasoreactivity is unclear at the present time.
Not all of the patients showed typical ST elevation of myocardial infarction on electrocardiogram, and some showed only nonspecific ST-T changes. Ruling out myocardial infarction, therefore, cannot depend solely on the absence of typical electrocardiographic changes. Obtaining cardiac enzyme levels, therefore, is critical to exclude myocardial infarction when the clinical chest pain suggests myocardial ischemia. The predilection of myocardial infarction to the inferior left ventricular wall segments, as suggested by the electrocardiographic, echocardiographic, and left ventricular angiographic changes in our series, cannot be explained satisfactorily at the present time.
Cardiac enzymes are released and can be assayed in the blood after myocardial necrosis. CK is released by the myocardium but is not specific. The CK-MB fraction is more specific for myocardial origin. The troponin complex is a heteromeric complex that plays a role in skeletal and cardiac muscle contraction. Cardiac troponin I is expressed only in myocardium. It is both more sensitive and specific than CK or CK-MB. It is present within 3 to 6 hours after the onset of ischemia and may persist for 5 to 8 days. Detection of the troponin complex was used in the last 8 patients in our series when it was commercially available.
As has been shown by Hirsch et al25 and Soldin et al,26 CK values and troponin I levels are valid indicators of myocardial injury even in the pediatric population from neonates to adolescents and, thereby, were used in our series to diagnose myocardial necrosis. All of our patients had abnormal cardiac enzyme levels with elevated absolute blood levels. All of the patients exhibited a single peak enzyme level that receded without additional peak. There were no cases of multiple peaks such as might be seen with myocarditis or stuttering infarction.
Pericarditis and congenital cardiac anomalies were ruled out by the echocardiogram. Drug abuse was excluded by history and drug screen. Hyperlipidemia and early atherosclerosis were ruled out as causes by a lipid profile and normal coronary angiograms.
There were no dysrhythmias that required acute treatment, and the 3 patients with nonsustained ventricular tachycardia were hemodynamically stable. No palpitations or dysrhythmias were observed on long-term follow-up.
Heart catheterization and coronary angiography excluded atherosclerotic and thrombotic processes and, thus, also suggested a vasoactive mechanism. Ergonovine-like medications that provoke coronary vasospasm were not used because of their contraindication in acute myocardial infarction because of the risk of extending the size of the infarction. All 3 of the patients with echocardiographic segmental motion abnormality remained stable hemodynamically and did not require inotropic support.
All of the patients in this series responded to nitroglycerin initially and, therefore, were treated later with calcium channel blockade long-term, with no recurrence of anginal pain in follow-up. Diltiazem was chosen because of its effectiveness in coronary spasm, favorable adverse-effect profile, and benefit in non–Q wave myocardial infarction.27 The necessary duration of therapy with calcium channel blockers is unknown.
Thrombolytic medications were not used in our series because of the lack of evidence for coronary thrombosis. This is in contrast to myocardial infarction in the adult in whom the myocardial infarction mechanism usually involves coronary thrombus on a ruptured coronary arterial plaque; vessel reperfusion is accomplished by lysing the clot. It is of interest that the Young Adult Myocardial Infarction and Ischemic Stroke Study, which examined the role of paradoxical emboli and thrombophilia in young adult myocardial infarction in patients 16 to 30 years old, also did not find evidence for coronary clots and thrombophilia as a risk factor in this patient population.28 Desai et al4 also did not recommend thrombolytic therapy in the 4 adolescents in their series with presumed myocardial infarction because of coronary vasospasm. Long-term follow-up of these patients is necessary, because recurrence of chest pain could occur, and changes in the treatment may be required.
One of the patients in this series was treated with methylphenidate. Methylphenidate was started years before the acute infarct and continued since that time with no recurrent anginal pain and a negative exercise stress test result. It seems, therefore, unlikely that the methylphenidate therapy played a causative role in the infarction. Amphetamines and other stimulants are suspected as a possible causative factor in coronary ischemia and infarction29–33 and should be ruled out as an etiologic element in patients presenting with myocardial injury. No history of over-the-counter drug use or abuse was obtained in our series.
No precipitating event could be identified as a cause for coronary spasm and, furthermore, it is unclear at this time which adolescents are at risk to develop coronary spasm and myocardial infarction. Currently, therefore, preventative measures cannot be given. Additional research would be required to identify such markers.
The implications of acute myocardial infarction in otherwise healthy adolescents for future cardiac events, activities, and lifestyle, as well as for long-term treatment, are as of yet unknown. Therefore, it is important to identify and establish long-term follow-up into the adult years.
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CONCLUSIONS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSREFERENCES |
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Although myocardial ischemia and infarction are uncommon in the pediatric population, particularly in children with normal coronary anatomy, acute typical chest pain in the adolescent presenting to the emergency department cannot be presumed noncardiac. Such patients need a protocol workup and even hospital admission if myocardial enzyme levels are abnormal for additional workup, dysrhythmia monitoring, possible coronary angiography, and treatment. A positive response to nitroglycerin by these patients suggests coronary artery spasm and would indicate a likely benefit of chronic treatment with nitrates or calcium channel blockade. Thrombolytic treatment is unwarranted in adolescents with myocardial infarction because of a different mechanism of myocardial infarction than that which occurs in the adult patient with coronary atherosclerosis. Long-term follow-up of these patients is necessary.
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FOOTNOTES |
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Accepted Mar 14, 2007.
Address correspondence to John R. Lane, MD, Akron Children's Hospital, One Perkins Square, Akron, OH 44308. E-mail: jlane{at}chmca.org
The authors have indicated they have no financial relationships relevant to this article to disclose.
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PEDIATRICS (ISSN 1098-4275). ©2007 by the American Academy of Pediatrics
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