Myocardial Infarction in Childhood Clinical Presentation

  • Author: Louis I Bezold, MD; Chief Editor: Stuart Berger, MD   more...
 
Updated: Dec 5, 2011
 

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
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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
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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.[6]
    • 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 failure[7]
    • 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.[8]
    • Sickle cell disease
    • Prothrombotic defects (such as protein C deficiency and prothrombin gene mutations), especially in conjunction with other coronary anomalies[9]
    • 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).
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Contributor Information and Disclosures
Author

Louis I Bezold, MD  Associate Professor and Vice Chair of Inpatient Services, Department of Pediatrics, University of Kentucky College of Medicine; Chief, Division of Pediatric Cardiology, Medical Director, Kentucky Children's Hospital

Louis I Bezold, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Society of Echocardiography, and Society of Pediatric Echocardiography

Disclosure: Nothing to disclose.

Coauthor(s)

Kurt Pflieger, MD, FAAP  Active Staff, Department of Pediatrics, Lake Pointe Medical Center

Kurt Pflieger, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Jeffrey Allen Towbin, MD, MSc, FAAP, FACC, FAHA  Professor, Departments of Pediatrics (Cardiology), Cardiovascular Sciences, and Molecular and Human Genetics, Baylor College of Medicine; Chief of Pediatric Cardiology, Foundation Chair in Pediatric Cardiac Research, Texas Children's Hospital

Jeffrey Allen Towbin, MD, MSc, FAAP, FACC, FAHA is a member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American College of Cardiology, American College of Sports Medicine, American Heart Association, American Medical Association, American Society of Human Genetics, Cardiac Electrophysiology Society, New York Academy of Sciences, Society for Pediatric Research, Texas Medical Association, and Texas Pediatric Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Julian M Stewart, MD, PhD  Associate Chairman of Pediatrics, Director, Center for Hypotension, Westchester Medical Center; Professor of Pediatrics and Physiology, New York Medical College

Julian M Stewart, MD, PhD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Gilbert Z Herzberg, MD  Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center

Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD  Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

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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.
 
 
 
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