AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Background

Acute myocardial infarction is rare in childhood and adolescence. Although adults acquire coronary artery disease from lifelong deposition of atheroma and plaque, which causes coronary artery spasm and thrombosis, children usually have either an acute inflammatory condition of the coronary arteries or an anomalous origin of the left coronary artery. Intrauterine myocardial infarction also does occur, often in association with coronary artery stenosis.¹

Pathophysiology

Whatever the etiology, the final common pathway of acute myocardial infarction includes myocardial ischemia (resulting in hypoxia), release of inflammatory cytokines, and cell death. The terminal event is often a cardiac arrhythmia, either ventricular tachycardia deteriorating to ventricular fibrillation or extreme bradycardic arrest. The onset of the terminal event is heralded by a loss of peripheral circulation and consciousness and by cardiovascular collapse and cardiac arrest.

Frequency

United States

According to the Centers for Disease Control and Prevention (CDC), annual mortality rates in the United States from all causes in the pediatric population range from 22 deaths per 100,000 population in children aged 5-14 years to 756 deaths per 100,000 population in infants younger than 1 year. (Compare this to 90 deaths per 100,000 in persons aged 15-24 y and 2,538 deaths 100,000 in individuals aged 65-74 y.² )

The CDC also reports that the mortality rate from acute myocardial infarction is 0.2 deaths per 100,000 population in persons aged 15-24 years and fewer than 0.2 deaths per 100,000 in infants younger than 1 year. (Compare this to 1.4 deaths per 100,000 population in persons aged 25-34 y and 262 deaths per 100,000 population in individuals aged 65-74 y.²)

One study used data from the Nationwide Inpatient Sample (NIS) from 1998-2001 to determine the incidence and outcomes of adolescent acute myocardial infarction and revealed an incidence of 157 cases per year, or 6.6 events per 1 million patient-years.³ Within the subset of adolescents with acute myocardial infarction, the incidence was higher in individuals aged 16-18 years than in individuals aged 13-15 years.

Mortality/Morbidity

Acute myocardial infarction affects a small subset of children at risk for sudden cardiac death. Sudden cardiac death is defined as any natural death from cardiac causes that occurs from minutes to 24 hours after onset of symptoms.⁴

• The early mortality rate can be high, depending on the cause, the speed of diagnosis, and the availability of therapeutic interventions.
• Unlike adult myocardial infarction secondary to ischemic and atherogenic disease, children with myocardial infarction who survive are less likely to have significant prolonged illness or disability.
• Some data suggest the hospital survival for acute myocardial infarction in adolescents is excellent (mortality rate is 0.8%).³

Sex

One study from the NIS suggests a significant male preponderance in adolescent acute myocardial infarction (80%).³

Age

The etiology of myocardial infarction determines the age of incidence.

• Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) may occur as unexplained sudden death in a neonate.
• Coronary artery ostial stenosis may occur after repair of a dextro-transposition of the great arteries (D-TGA) in the neonatal period. In childhood, infarction may occur years after arterial switch due to kinking of the coronary arteries, possibly in association with aortic root dilation.
• Thrombotic coronary artery occlusion from Kawasaki disease may occur in early childhood.
• Sudden death from an aberrantly coursing left main coronary artery with its origin at the right sinus of Valsalva may occur in athletes who are exercising.
• Coronary insufficiency may develop in patients with Marfan syndrome, Takayasu arteritis, or cystic medial necrosis with aortic root dilatation, aneurysm formation, and dissection into the coronary artery.
• Although very rarely, traumatic myocardial infarction can occur in patients at any age but is more likely to occur in ambulatory patients.
• Accelerated atherosclerosis is known to occur in orthotopic cardiac transplant recipients on immunosuppressive therapy and can occur in early adolescence.
• Coronary artery spasm as a cause of acute typical chest pain with associated cardiac enzyme elevation has been increasingly recognized in adolescents with otherwise normal coronary arteries.⁵
• The incidence of substance abuse and smoking are higher in adolescents with acute myocardial infarction than in adolescents admitted to the hospital for other conditions.³

CLINICAL

Section 3 of 10  

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• Clinical
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History

Patients who experience myocardial infarction in whom sudden death does not occur may present with a prodrome that can include any of the following features:

• Chest pain (angina)
• Palpitation
• Dyspnea
• Evidence of poor cardiac output
• Weakness
• Dizziness
• Mental confusion
• Irritability
• Orthostasis
• Presyncope
• Syncope

Physical

Examination findings vary, depending on the degree of disability and duration of ischemia.

• Altered level of consciousness
• • Lethargy
  • Unconsciousness
  • Irritability
• Pulse abnormalities
• • Tachycardia
  • Bradycardia
  • Dysrhythmia
• Respiratory embarrassment
• • Apnea
  • Bradypnea
  • Tachypnea
  • Hyperpnea
  • Nasal flaring
  • Grunting
  • Head bobbing
  • Retractions (supraclavicular, intercostal, subcostal)
  • Paradoxic respirations
  • Rales
  • Rubs
  • Rhonchi
  • Consolidation
• Cardiac examination abnormalities
• • Hyperdynamic precordium
  • Broad cardiac impulse
  • Displaced apical beat
  • S₃
  • S₄
  • Holosystolic murmur at the apex (mitral insufficiency)
  • Holosystolic murmur at the left lower sternal border (tricuspid insufficiency)
  • Loud pulmonic closure sound (P₂, pulmonary hypertension)
  • Diastolic murmur of aortic/pulmonary insufficiency
  • Diastolic rumble of increased tricuspid/mitral flow
• Hypotension and signs of low cardiac output
• • Cool skin
  • Prolonged capillary refill time (CRFT)
  • Diaphoresis
  • Poor turgor
  • Peripheral cyanosis
• Signs of cor pulmonale (right heart failure)
• • Jugular vein distention
  • Hepatosplenomegaly
  • Hepatojugular reflux
  • Ascites
  • Peripheral edema

Causes

Two leading causes of acute myocardial infarction in children are anomalous left coronary artery from the pulmonary artery (ALCAPA) and Kawasaki disease.

• ALCAPA
• • Infants with ALCAPA develop irritability with dyspnea, tachycardia, diaphoresis, and vomiting while feeding. Irritability is secondary to anginal pain caused by a coronary artery steal phenomenon to the anomalous origin of the left coronary artery. The flow in this vessel, which has its distribution over the left ventricular myocardium, is retrograde to the main pulmonary artery.
  • The diagnosis of ALCAPA is suspected in irritable anxious infants presenting with pain while feeding (a modified stress test). Electrocardiography (ECG) demonstrates classic findings of deep Q waves, peaked T waves, and/or ST segment changes consistent with ischemia, injury, or infarction. Confirmation of the anomaly may be obtained using high-quality 2-dimensional and Doppler echocardiography or cardiac catheterization with angiography. A high degree of suspicion must predominate to make this diagnosis.
• Kawasaki disease
• • Kawasaki disease is an acquired disease of unknown etiology, and it can affect all cardiac tissues (pericardium, endocardium, myocardium, valvular, conductive). The pathogenetic mechanism is attributable to a high degree of immune activation. Since the introduction of intravenous gammaglobulin to standard therapy for Kawasaki disease, the incidence of acute myocardial infarction due to Kawasaki disease has decreased.
  • Coronary artery involvement occurs in 15-25% of children with Kawasaki disease within 1-3 weeks of onset. In patients with untreated Kawasaki disease, sudden death has resulted from acute myocardial infarction caused by ruptured coronary artery aneurysms or thromboses.
  • Detrimental changes in arterial wall hemodynamics are present and persist after acute Kawasaki disease which may predispose to long-term cardiovascular events.
• Other conditions: Other, often rarer, conditions that predispose children to acute myocardial infarction have been described, as follows:
• • Coronary artery ostial stenosis or coronary artery kinking: These may present after arterial switch repair of dextro-transposition of the great arteries (D-TGA) in the neonatal period or may develop years later, possibly related to aortic root dilation. These may also occur status post Ross procedure for aortic valve disease. 
  • Other abnormalities of coronary structure or course: Left main coronary artery atresia is a rare anomaly that can masquerade as dilated cardiomyopathy. Coronary ostial stenoses can be seen in patients with Williams syndrome, most commonly accompanying supravalvar aortic stenosis, but can rarely occur in isolation. Infarction can present in utero in these cases.¹
  • Sudden death: Sudden death due to an aberrantly coursing left main coronary artery with its origin at the right sinus of Valsalva may present in athletes who are exercising.
  • Coronary insufficiency: This may develop in patients with Marfan syndrome, Takayasu arteritis, or cystic medial necrosis with aortic root dilatation, aneurysm formation, and dissection into the coronary artery.
  • Traumatic myocardial infarction: Although very rare, traumatic myocardial infarction can occur in patients of any age but is more likely to occur in ambulatory and adolescent patients.
  • Atherosclerosis: Accelerated coronary artery atherosclerosis is known to occur in orthotopic cardiac transplant recipients on immunosuppressive therapy.
  • Familial homozygous hypercholesterolemia
  • Cocaine intoxication
  • Accelerated coronary atherosclerosis due to juvenile diabetic dyslipidemia or nephrotic syndrome
  • Accelerated coronary vascular disease associated with chronic kidney disease and renal failure⁶  
  • Accelerated atherogenesis after treatment for childhood cancer
  • Inflammatory conditions including viral and eosinophilic myocarditis and systemic lupus erythematosus (SLE): Dyslipidemia frequently occurs in children with SLE and is often underrecognized and undertreated.⁷  
  • Sickle cell disease
  • Prothrombotic defects (such as protein C deficiency and prothrombin gene mutations), especially in conjunction with other coronary anomalies⁸
  • Coronary artery spasm in adolescents
  • Complications of dilated or ischemic cardiomyopathy
  • D-TGA
  • • For patients undergoing the Jatene arterial switch procedure, the presence of an intramural coronary artery course in patients with D-TGA may prohibit arterial repair.
    • Hypothetically, manipulation of the intramural coronary artery may cause damage and resultant inflammation, kinking, thrombosis, and myocardial ischemia or infarction (see Transposition of the Great Arteries).
  • Tetralogy of Fallot
  • • Surgical repair of pulmonary outflow obstruction often involves patching of the right ventricular outflow tract and resecting of the obstructing right ventricular muscle. An estimated 2-9% of patients with tetralogy of Fallot have coronary arterial anomalies, possibly affecting the timing of or approach to surgical repair.
    • The most common anomaly (4% of patients) is the origin of the left anterior descending (LAD) coronary artery from the right coronary artery (RCA), which then courses across the pulmonary outflow tract. Inadvertent transection of this vessel yields disastrous consequences. Frequently, the conus branch of the RCA is large and supplies a significant portion of right ventricular infundibular muscle.
    • Surgical techniques to avoid transection include limited incisions, varied tunneling techniques, and, perhaps, conduit placement. Cardiologists must predefine these abnormalities by noninvasive or invasive study (see Tetralogy of Fallot with Pulmonary Atresia).
  • Pulmonary atresia with an intact ventricular septum
  • • Primitive embryonic sinusoidal connections to coronary vasculature (most commonly affected is the RCA, then the LAD system, and, less frequently, the distal extent of the circumflex [Cx] coronary artery) may demonstrate severe intimal thickening, occlusion, or interruption.
    • In most patients, endocardial fibroelastosis, myocardial fibrosis, and acute myocardial infarction are observed (see Pulmonary Atresia with Intact Ventricular Septum).

DIFFERENTIALS

Section 4 of 10  

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WORKUP

Section 5 of 10  

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Lab Studies

The following studies are indicated in pediatric patients with myocardial infarction:

• Testing of cardiac enzymes is the criterion standard for identification of myocardial cell death by measuring the following levels:
• • Serum glutamic-oxaloacetic transaminase (SGOT)
  • Lactate dehydrogenase (LDH) and isoenzymes
  • Creatine kinase (CK)
  • CK-MB isoforms
  • Troponin I and troponin T
• Levels of acute-phase reactants are elevated in the early stages of Kawasaki disease.
• • WBC
  • C-reactive protein
  • Erythrocyte sedimentation rate (ESR)
  • Thrombocytosis
  • a₁-Antitrypsin (A1AT)

Evaluation for heritable forms of thrombophilia, such as prothrombin G20210 and C677T MTHFR gene mutations, and protein C deficiencies should be considered in young patients with myocardial ischemia.⁸

Imaging Studies

• Chest radiography: This is indicated to reveal cardiomegaly, with or without pulmonary venous congestion.
• Echocardiography
• • Two-dimensional echocardiography may be used to identify the following:
  • • The abnormal origin of the left coronary artery from the main pulmonary artery
    • Chamber enlargement
    • Systolic and diastolic dysfunction
    • Coronary artery ectasia or aneurysm
    • A flail mitral valve leaflet and ruptured papillary muscle
    • Segmental wall motion abnormality
    • Mural or intraventricular thrombi
  • In experienced hands, color-flow Doppler mapping can have the following uses:
  • • Can be diagnostic for anomalous left coronary artery from the pulmonary artery (ALCAPA), demonstrating retrograde flow from the anomalous left coronary into the pulmonary trunk
    • Demonstrates direction of coronary artery flow
    • Quantifies mitral insufficiency
    • In conjunction with spectral Doppler, quantifies pulmonary hypertension
  • Tissue Doppler imaging (TDI): TDI is an echocardiographic technique that can noninvasively evaluate myocardial contraction and relaxation. Data suggest that TDI may have a role in early detection of graft failure due to coronary vasculopathy in orthotopic transplant recipients.⁹
• CT and MRI
• • Multislice CT angiography has been shown to be useful in identifying coronary ostial or arterial stenoses in pediatric patients following the arterial switch operation for dextro-transposition of the great arteries (D-TGA).
  • MRI can reveal coronary origins, anatomy and coronary artery abnormalities, and infarction in patients with Kawasaki disease.
  • Cardiac MRI has been used to determine myocardial viability and prognosis in a case of in utero myocardial infarction.¹⁰ 
• Myocardial perfusion imaging: This may be useful in evaluating myocardial ischemia and infarction in various disease states.

Other Tests

• Classic electrocardiography (ECG) findings for diagnosing ischemia/infarction in adults have been described as follows:
• • Deep Q waves in a completed transmural infarct over the involved areas
  • Peaked T waves hyperacutely
  • ST elevation in the acute phase
  • ST depression when ischemia is present or in the latter stages of acute injury
  • Various dysrhythmias and ectopy secondary to ischemia and irritable myocardium or conductive tissue
• An anterolateral infarct is demonstrated with abnormal deep (>3 mm) and wide (>30 ms) q waves in leads I, aVL, V₅, and V₆, with absent q waves in leads II, III, and aVF.
• The QRS axis is typically normal, although in some patients, a left superior axis is observed.
• ST-segment changes diagnostic of transmural infarction in adults may be seen in pediatric patients in the absence of coronary occlusion.¹¹ Additional criteria for diagnosing pediatric ischemia have been described:¹²
• • Wide Q waves (>35ms) with or without Q-wave notching
  • ST-segment elevation (>2mm)
  • Prolonged QTc (>440ms) with accompanying Q-wave abnormalities 
• Exercise myocardial perfusion stress testing has been shown to be safe and useful in assessing myocardial perfusion and for risk stratification in children with Kawasaki disease.¹³

Procedures

• Angiographic evaluation of the coronary artery system should be urgently performed but with caution because of the inherent instability of the diseased myocardium.
• • Definitive diagnosis of an anomalous left coronary artery from the pulmonary artery is made.
  • Aortography demonstrates an enlarged right coronary artery (RCA) system with collateralization to the left coronary artery and reflux of contrast into the pulmonary arterial system (ALCAPA).
  • Coronary aneurysm, ectasia, or both is frequently identified in patients with Kawasaki disease.
• Hemodynamic (oximetric) measurements may demonstrate the following:
• • Decreased systemic venous oxygen content is consistent with low cardiac output.
  • A small left-to-right shunt may be demonstrated by oximetry in the main pulmonary artery if ALCAPA is the diagnosis.
  • Elevated left atrial pressures are secondary to reduced left ventricular compliance, significant mitral valve insufficiency, or both.
• Successful percutaneous transluminal coronary angioplasty for proximal coronary stenoses following the arterial switch procedure has been reported in a small number of patients with apparent excellent results 3-5 years later.
• Postcatheterization effects that require precautions include hemorrhage, vascular disruption after balloon dilation, pain, nausea and vomiting, and arterial or venous obstruction from thrombosis or spasm.
• Possible complications include rupture of blood vessel, tachyarrhythmias, bradyarrhythmias, and vascular occlusion.
• The use of cardiac catheterization and percutaneous coronary interventions appears to be less in adolescents with acute myocardial infarction (29%) than in adults (40-50%) with acute myocardial infarction in review of the NIS. This may be due to a higher incidence of coronary vasospasm and subendocardial acute myocardial infarction in adolescents.³ 

TREATMENT

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Medical Care

Medical care for a disease or condition that predisposes children to acute myocardial infarction can be found in Anomalous Left Coronary Artery from the Pulmonary Artery and Kawasaki Disease. The primary treatment in patients with anomalous left coronary artery from the pulmonary artery (ALCAPA) is surgical. Surgical revascularization may also be necessary in patients with Kawasaki disease who develop significant coronary stenoses or occlusion.

• Intensive and acute care of the infant with symptoms of coronary artery ischemia or injury is initially directed at reducing myocardial oxygen demands while administering oxygen, fluids, or blood products and endotracheal intubation and correction of acid-base status and paralysis to reduce the work of breathing.
• Treatment of congestive heart failure (CHF) includes carefully administering diuretics, afterload reduction medications, and inotropic drugs.
• Aggressive afterload reduction may be deleterious in patients with ALCAPA. Right coronary artery (RCA) perfusion may be reduced during aggressive afterload reduction, leading to decreased left coronary blood flow.
• Conversely, inotropic support may increase myocardial oxygen consumption significantly, which, in the presence of reduced myocardial blood flow, may worsen ischemia.
• Spontaneous resolution of CHF symptoms is rare. Surgical revascularization is usually necessary in the event of acute myocardial infarction.
• Percutaneous transluminal coronary angioplasty for proximal coronary stenoses following the arterial switch procedure for dextro-transposition of the great arteries (D-TGA) has been reported.

Surgical Care

Once the patient is stabilized, surgical revascularization is performed to create a patent coronary arterial distribution. For more information, see Anomalous Coronary Artery from the Pulmonary Artery: Surgical Perspective.

• Oral administration of digitalis, diuretics, and afterload reduction medications improves cardiac output and reduces preoperative symptoms in patients with CHF. These techniques are frequently used until left ventricular systolic and diastolic functions improve and mitral insufficiency stabilizes.
• Cardiac dysrhythmia secondary to preoperative myocardial ischemia or infarction is likely. Monitor continuously in the immediate postoperative period.
• In a recent review of NIS data, only 2% of adolescents with acute myocardial infarction underwent coronary artery bypass graft surgery, compared with 12-24% of adults with acute myocardial infarction. The higher incidence of subendocardial acute myocardial infarction and coronary vasospasm (possibly related to substance abuse) in adolescents may at least partially account for this difference.³

Consultations

• Consultation with an adult interventional cardiologist is indicated because of the wealth of information they have regarding proper imaging planes and anatomic variations of the coronary arteries.
• A nuclear medicine radiologist or cardiologist may help quantify approximate myocardial injury and recovery potential.
• Pediatric and adult cardiovascular surgeons may collaborate to effect optimal surgical repair.

Diet

No specific restrictions are usually necessary.

• Postoperative patients may require increased caloric density if failure to thrive is a preoperative morbidity.
• Patients with residual CHF may require salt and/or fluid restriction.

Activity

Restrictions are directly related to the severity of the left ventricular dysfunction and postoperative mitral valve insufficiency.

• In patients able to participate in exercise or competitive sports or in patients with residual postoperative hemodynamic problems, consider recommending avoidance of significant isometric activities.
• Exercise stress testing (eg, ECG, echocardiogram) is advised for assessment of myocardial response to exercise, preparticipation screening, and ongoing monitoring of conditioning effect.

MEDICATION

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Drug Category: Inotropic agents

These agents are used to enhance cardiac contractility as an adjunct to treating congestive heart failure (CHF).

Drug Category: Antiplatelet agents

These agents are used for reduction of platelet adhesiveness in thrombotic disease and as anti-inflammatory agents for immune-mediated or noninfectious inflammatory conditions.

Drug Category: Afterload reduction

These agents are used for systemic afterload reduction following myocardial infarction with depressed left ventricular function.

FOLLOW-UP

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Further Inpatient Care

• The severity of myocardial infarction symptoms at presentation determines whether the patient is admitted to an ICU for aggressive medical management of congestive heart failure (CHF) before surgical revascularization.
• Initial postoperative treatment is usually performed in a pediatric ICU until the patient is extubated and no longer requires intravenous inotropic support or antiarrhythmics.
• Following surgical revascularization, postoperative care includes the use of inotropes, diuretics, and afterload reduction medication to improve cardiac output and eliminate the preoperative symptoms of CHF.
• Monitor patients continuously during the immediate postoperative period because, although unusual, cardiac dysrhythmia secondary to preoperative myocardial ischemia or infarction is a risk.

Further Outpatient Care

• The clinical status of the patient, in relation to residual CHF symptoms, determines the frequency of postoperative outpatient follow-up visits.
• Most patients do not require frequent cardiac evaluations following surgical revascularization once ventricular function and mitral valve insufficiency have dramatically improved.
• For patients with Kawasaki disease, long-term follow-up is recommended, even in cases without evidence of obvious coronary dilatation or aneurysms. Dipyridamole stress scintigraphy may be useful in long-term follow-up and risk stratification in patients with Kawasaki disease.
• Patients on coronary vasodilators for coronary artery spasm require long-term follow-up.⁵

In/Out Patient Meds

• Short-term use of oral digoxin, diuretics, and ACE inhibitors is common following surgical revascularization.
• Long-term antiplatelet therapy with aspirin may be needed in conditions predisposed to coronary thrombosis, such as Kawasaki disease with significant aneurysm formation. In patients with giant aneurysms, additional anticoagulation with dipyridamole or warfarin may be recommended. A small retrospective study suggested that combination therapy with warfarin and aspirin was associated with a decreased risk of myocardial infarction in patients with giant aneurysms due to Kawasaki disease.¹⁴
• Coronary spasm is generally treated with nitrates or calcium channel blockade.

Complications

• Complications are rare. The need for future valve surgery depends on the occurrence of hemodynamic complications (eg, residual mitral valve insufficiency precipitated by permanent damage of the mitral valve architecture) following surgery.
• Late complications related to coronary artery insufficiency are more likely to occur if revascularization was accomplished via any of the following:
• • Surgical ligation
  • Bypass grafts, which may become occluded or stenotic
  • Intrapulmonary tunnel technique, which may cause supravalvar pulmonary stenosis or, less commonly, obstruction of the surgically created aortopulmonary window
• Although unlikely, growth of the coronary anastomosis may be inadequate if surgical reimplantation of the left coronary artery is performed. This occurrence is similar to the rare reports of late coronary artery problems following the arterial switch procedure for transposition of the great vessels, which also requires direct coronary transfer and reimplantation.

Prognosis

• Early diagnosis using echocardiography with color-flow mapping and improvements in surgical techniques (eg, myocardial preservation) dramatically improve the prognosis.

Patient Education

• All patients should undergo formal exercise stress testing at an appropriate age to aid in determining an appropriate exercise program.
• Long-term physical restrictions, including restrictions of participation in competitive sports, depend on whether myocardial ischemia is evident at rest or during exercise.
• No dietary restrictions are necessary following successful surgical revascularization with subsequent clinical improvement.
• For excellent patient education resources, see eMedicine's Heart Center and Cholesterol Center. Also, visit eMedicine's patient education articles Chest Pain, Coronary Heart Disease, Heart Attack, and Tetralogy of Fallot.

MULTIMEDIA

Section 9 of 10  

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Media file 1:  Electrocardiogram in an infant with anomalous origin of the left coronary artery from the pulmonary artery, demonstrating pathologic q waves in leads I and aVL and diffuse ST-T wave changes consistent with an anterolateral infarction.
	View Full Size Image
Media type:  ECG

REFERENCES

Section 10 of 10

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• Differentials
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• Follow-up
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24. Esterly JR, Oppenheimer EH. Some aspects of cardiac pathology in infancy and childhood. IV. Myocardial and coronary lesions in cardiac malformations. Pediatrics. Jun 1967;39(6):896-903. [Medline].
25. Fukuda T, Ishibashi M, Shinohara T, et al. Follow-up assessment of the collateral circulation in patients with Kawasaki disease who underwent dipyridamole stress technetium-99m tetrofosmin scintigraphy. Pediatr Cardiol. Sep-Oct 2005;26(5):558-64. [Medline].
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Article Last Updated: Oct 8, 2008