eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Cardiac Tumors: Treatment & Medication

Author: Edwin Rodriguez-Cruz, MD, Assistant Professor, Department of Pediatrics, San Juan Bautista Medical School and Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Pediatrics, Hospital El Maestro and San Juan Bautista Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Cardiology, Cardiovascular Center of Puerto Rico and the Caribbean and Veterans Affairs Hospital and Medical Center of Puerto Rico
Coauthor(s): Rosa M Cintrón-Maldonado, MD, Clinical Instructor of Pediatrics, Department of Pediatrics, San Juan Bautista Medical Center; Robert D Ross, MD, Co-Director of Pediatric Cardiology Fellowship Program, Department of Pediatrics, Division of Pediatric Cardiology, Professor, Children's Hospital of Michigan and Wayne State University
Contributor Information and Disclosures

Updated: Nov 10, 2008

Treatment

Medical Care

Most childhood cardiac tumors are benign, with no treatment necessary unless the tumor severely obstructs blood flow or causes intractable arrhythmias. Most only require close follow-up care.

New data have addressed the use of serum creatine kinase-myocardial band (CK-MB) fraction levels in evaluating ventricular function. Greater ventricular dysfunction correlated with higher CK-MB levels.

Nonetheless, examine the patient extensively and expeditiously because finding a tumor is a stressful situation for both patient and family. By reaching a prompt and precise diagnosis, the physician can proceed with the best treatment approach.

The mode of treatment varies and cannot be easily simplified because the kind of tumor (benign vs malignant, infiltrative vs localized) dictates therapy. Location and extent of the tumor, as well as symptoms, are clinical variables that direct treatment. Observation is sufficient when the mass is small and does not interfere with vascular hemodynamics. However, the clinician must be aggressive when the tumor is causing hemodynamic problems. In occasions, electrical problems may also arise due to the location requiring resection and/or implantation of a pacemaker if atrioventricular block occurs.

Surgical Care

Many advocate excision of the mass as soon as it is found; however, most childhood tumors are benign and do not require resection. Nevertheless, if a tumor is causing severe obstruction or intractable arrhythmias and has been rendered resectable, perform surgery as soon as possible.

  • Excision and biopsy: If excision is required, perform it as extensively and completely as possible. Certain tumors recur even after complete excision. An extensive resection carries its own risks since, occasionally, removal of papillary muscles, valves, chordae tendineae, and conduction tissue are necessary.
  • Heart transplantation is an option for unresectable benign masses causing hemodynamic compromise. Transplantations have been performed with variable results for primary malignant cardiac tumors in children and adults without evidence of metastases.

Consultations

Consult a cardiologist, thoracic and cardiovascular surgeon, pathologist, radiologist, and hematologist/oncologist.

Diet

No dietary restrictions are needed. Occasionally, certain restrictions such as low-sodium diet for congestive heart failure (CHF) are required.

Activity

Advise no restrictions unless clinical condition merits otherwise.

Medication

Focus medical treatment of a patient with a cardiac neoplasm on symptoms and possible complications resulting from primary disease. Two of the more common complications of patients with heart tumors are development of arrhythmias and congestive heart failure (CHF).

CHF management includes diuretics and afterload reduction. Severe cases with hemodynamic compromise may require intravenous inotropes, afterload reduction, vasodilators, and anticoagulation. Arrhythmias vary; thus, specific antiarrhythmics should be chosen.

Cardiac glycosides

These agents may improve left ventricular function by inhibiting the Na+/K+ -ATPase activity that results in increased myocardial contraction. This leads to sodium accumulation within the myocyte that stimulates the sodium calcium exchange pump. Increased intracellular calcium increases the force of contraction while producing antiarrhythmic effects on cardiac muscle.


Digoxin (Lanoxin)

Cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system.

Adult

0.125-0.375 mg/d PO

Pediatric

Total digitalizing dose (TDD):
Note: TDD administered within 24 h
Premature infants: 0.02 mg/kg PO divided q8h
Full-term infants: 0.03 mg/kg PO divided q8h
1-24 months: 0.04-0.05 mg/kg PO divided q8h
>2 years: 0.03-0.04 mg/kg PO divided q8h
Maintenance dose:
Infants: 6-8 mcg/kg/d PO
2-5 years: 10-15 mcg/kg/d PO
5-10 years: 7-10 mcg/kg/d PO
>10 years: 3-5 mcg/kg/d PO
<10 years: Divided bid dosing is recommended

Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, PO amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil
Medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, PO colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid

Documented hypersensitivity; beriberi heart disease, idiopathic hypertrophic subaortic stenosis, constrictive pericarditis, and carotid sinus syndrome

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

TDD may need to be lowered based on drug concentrations obtained; adjust dose for patients with decreased renal function; dosing must be individualized/titrated and serum levels followed; it is arrhythmogenic and interacts with several drugs used commonly to treat arrhythmias; use cautiously in patients with outflow tract obstructions
Hypokalemia may reduce positive inotropic effect of digitalis; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis; adjust dose in renal impairment; highly toxic (overdoses can be fatal)

Diuretic agents

Hypoperfusion of kidneys causes retention of sodium and water, producing peripheral and pulmonary edema. Diuretics decrease intravascular volume overload. They promote excretion of water and electrolytes by the kidneys and are used to treat heart failure or hepatic, renal, or pulmonary disease when sodium and water retention has resulted in edema or ascites. Pay special attention to patients with a combination of CHF and outflow obstruction because a decrement in cardiac output caused by a decrease in cardiac preload produced by diuretics may further compromise patients' conditions.


Furosemide (Lasix)

Loop diuretic that increases excretion of water by interfering with chloride-binding cotransport system, which in turn inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. DOC in pediatric patients.

Adult

1 mg/kg/dose PO/IV/IM; titrate to effect

Pediatric

0.5-2 mg/kg/dose PO/IV/IM up to tid

Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide (hearing loss of varying degrees may occur); anticoagulant activity of warfarin may be enhanced when taken concurrently with this medication; increased plasma lithium levels and toxicity are possible when taken concurrently with this medication

Documented hypersensitivity; hepatic coma, anuria, and state of severe electrolyte depletion

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause profound diuresis and electrolyte loss; metabolic alkalosis is a common complication; should not be given in the same IV line with inamrinone since it may cause precipitation of the compounds; may cause renal stones, especially in premature newborns; coadministration of chlorothiazide may decrease the hypercalciuria


Chlorothiazide (Diuril)

Thiazide diuretic. If given with furosemide, may decrease the hypercalciuria produced by furosemide.

Adult

0.5-2 g/d PO or 100-500 mg/d IV

Pediatric

PO:
<6 months: 20-40 mg/kg/d PO divided bid
>6 months: 20 mg/kg/d PO divided bid
IV:
<6 months: 2-8 mg/kg/d IV divided bid
>6 months: 4 mg/kg/d IV divided bid

Thiazides may decrease effects of anticoagulants, antigout agents, and sulfonylureas; thiazides may increase toxicity of allopurinol, anesthetics, antineoplastics, calcium salts, loop diuretics, lithium, diazoxide, digitalis, amphotericin B, and nondepolarizing muscle relaxants

Documented hypersensitivity; anuria or renal decompensation

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Safety of IV use in children has not been established; may produce electrolyte imbalance; should not be given SC or IM


Spironolactone (Aldactone)

Potassium-sparing diuretic. Competes with aldosterone for receptor sites in distal renal tubules, increasing water excretion while retaining potassium and hydrogen ions.

Adult

6.25-25 mg/d PO

Pediatric

2-3 mg/kg/d PO divided bid/tid

May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity of spironolactone; concomitant use with indomethacin or ACE inhibitors may cause hyperkalemia

Documented hypersensitivity; anuria, renal failure, or hyperkalemia

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Can cause electrolyte imbalance, especially hyperkalemia; caution in renal and hepatic impairment

Angiotensin converting enzyme inhibitors

ACE inhibitors are beneficial in all stages of chronic heart failure. Pharmacologic effects result in a decrease in systemic vascular resistance, reducing blood pressure, preload, and afterload. Dyspnea and exercise tolerance are improved. Blood pressure is determined by cardiac output and systemic resistance. When systemic resistance is decreased with afterload reduction, myocardial shortening and stroke volume improve; thus, cardiac output can be maintained at a lower heart rate with lower myocardial oxygen demand. ACE inhibitors decrease production of angiotensin II, a potent vasoconstrictor. As with the diuretics, pay special attention when administering to patients with outflow tract obstruction, since afterload is decreased.


Captopril (Capoten)

Used to reduce afterload. Prevents conversion of Angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Adult

6.25-12.5 mg PO tid; not to exceed 150 mg tid

Pediatric

<6 months: 0.05-0.5 mg/kg/dose PO up to tid
>6 months: 0.5-2 mg/kg/dose PO up to tid
Test dose: 0.1 mg/kg/dose PO

NSAIDs may reduce hypotensive effects of captopril; may increase digoxin, lithium, and allopurinol levels; rifampin decreases captopril levels; probenecid may increase captopril levels; the hypotensive effects of ACE inhibitors may be enhanced when given concurrently with diuretics

Documented hypersensitivity; renal impairment

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Dose should be titrated to the patient's tolerance and to effect; dose should be adjusted in patients with renal impairment; may cause idiosyncratic hypotension after first dose in children; test dose should be given and blood pressure monitored frequently after the dose

Adrenergic agonist agents (inotropes)

These agents improve the hemodynamic status by increasing myocardial contractility and heart rate, resulting in increased cardiac output. They also increase peripheral resistance by causing vasoconstriction. Increased cardiac output and increased peripheral resistance lead to increased blood pressure.


Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effect is dependent on the dose. Lower doses predominantly stimulate dopaminergic receptors that, in turn, produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation are produced by higher doses.
After initiating therapy, increase dose by 1-4 mcg/kg/min q10-30min until optimal response is obtained. More than 50% of patients are satisfactorily maintained on doses <20 mcg/kg/min.

Adult

2-20 mcg/kg/min IV

Pediatric

Administer as in adults

Phenytoin, alpha-adrenergic and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects

Documented hypersensitivity; pheochromocytoma or ventricular fibrillation; subaortic stenosis

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hypovolemia should be treated before infusion; extravasation should be treated promptly with SC administration of phentolamine (Regitine); administration through a central vein is recommended; do not use the umbilical artery for infusion; if >20 mcg/kg/min are required, consider a different agent (epinephrine, dobutamine)


Dobutamine (Dobutrex)

Stimulates beta1-adrenergic receptors. Has less alpha1 stimulation than dopamine, producing less increase in systemic vascular resistance.

Adult

2-15 mcg/kg/min IV

Pediatric

Administer as in adults

Beta-adrenergic blockers antagonize effects of dobutamine; general anesthetics may increase toxicity

Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis and atrial fibrillation or flutter

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hypovolemia should be treated before infusion; administration through a central vein is recommended; do not use umbilical artery for infusion; may decrease CVP and wedge pressure

Cyclic adenosine monophosphate (cAMP) phosphodiesterase inhibitors

Inotropic effect occurs by inhibiting cAMP phosphodiesterase that increases cellular levels of cAMP. It does not affect the sodium-potassium pump like digitalis. Vasodilatory activity is related to direct relaxation effect on vascular smooth muscle.


Inamrinone - formerly amrinone (Inocor)

Produces vasodilation and increases inotropic state. More likely to cause tachycardia than dobutamine; may exacerbate myocardial ischemia.

Adult

0.75 mg/kg IV bolus slowly over 2-3 min; maintenance infusion is 5-10 mcg/kg/min; not to exceed a cumulative dose of 10 mg/kg/d
Adjust dose according to patient response

Pediatric

Administer as in adults

Coadministration with diuretics may result in hypovolemia and a decrease in filling pressure; cardiac glycosides have additive effects on inamrinone; inamrinone precipitates in presence of furosemide

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May aggravate outflow tract obstructions; should not be diluted in glucose-containing solutions; discontinue therapy if symptoms of liver toxicity develop; correct hypokalemic states before giving therapy


Milrinone (Primacor)

Bipyridine positive inotrope and vasodilator with little chronotropic activity. Different in mode of action from both digitalis glycosides and catecholamines.

Adult

50 mcg/kg IV loading dose over 10 min, followed by continuous infusion at 0.375-0.75 mcg/kg/min

Pediatric

Administer as in adults

Milrinone precipitates in presence of furosemide

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor fluids, electrolyte changes, and renal function during therapy; excessive diuresis may increase potassium loss and predispose digitalized patients to arrhythmias; important to correct hypokalemia with potassium supplementation prior to treatment; patients showing excessive decreases in blood pressure should have infusion rates slowed or stopped; previous vigorous diuretic therapy has caused significant decreases in cardiac filling pressure (cautiously administer milrinone and monitor blood pressure, heart rate, and clinical symptomatology)

Antiarrhythmic agents

These agents alter the electrophysiologic mechanisms responsible for arrhythmia.


Procainamide (Procan, Procanbid)

Class I-A antiarrhythmic used for PVCs. Increases refractory period of the atria and ventricles. Myocardiac excitability is reduced by an increase in the threshold for excitation and by inhibition of ectopic pacemaker activity.

Adult

Loading dose: 17 mg/kg IV infused over 1 h; followed by 1-6 mg/min IV
PO maintenance dose: 2-4 g/d PO in divided doses

Pediatric

17 mg/kg IV infused over 1 h; followed by 20-80 mcg/kg/min IV
PO maintenance dose: 15-50 mg/kg PO in divided doses

Can expect increased levels of procainamide metabolite NAPA in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim, and quinidine; procainamide may increase effect of skeletal muscle relaxants, quinidine and lidocaine, and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may increase bioavailability; when taken concurrently with sparfloxacin, may increase risk of cardiotoxicity

Documented hypersensitivity; complete heart block or second-degree or third-degree heart block, if a pacemaker is not in place; torsade de pointes; systemic lupus erythematosus

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause QRS widening and ventricular arrhythmias; continuously monitor during first administration; blood dyscrasias have been reported during the administration of this medication; monitor blood levels; lower the dose when administering to patients with renal dysfunction


Lidocaine (Dilocaine, Xylocaine)

Class IB antiarrhythmic that increases the electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue. Could be used IV/ET/IO.

Adult

1-1.5 mg/kg IV infused over 2-3 min; may repeat doses of 0.5-0.75 mg/kg q5-10min; not to exceed a cumulative dose of 3 mg/kg; followed by 2-4 mg/min IV

Pediatric

1-1.5 mg/kg IV infused over 2-3 min; may repeat doses of 0.5-0.75 mg/kg q5-10min; not to exceed a cumulative dose of 3 mg/kg; followed by 20-40 mcg/kg/min IV

Coadministration with cimetidine or beta-blockers increases toxicity of lidocaine; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine

Documented hypersensitivity; Adams-Stokes syndrome/attacks and Wolff-Parkinson-White syndrome; severe sinoatrial, AV, or intraventricular block if artificial pacemaker not in place

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Use a solution without preservatives; caution in heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory depression, and bradycardia; may increase risk of CNS and cardiac adverse effects in elderly patients; high plasma concentrations can cause seizures, heart block, and AV conduction abnormalities


Propranolol (Inderal, Betachron E-R)

Class II antiarrhythmic, nonselective, beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions. May be used to treat supraventricular as well as ventricular tachyarrhythmias.

Adult

1 mg/dose IV, may repeat q5min; not to exceed a cumulative dose of 5 mg
Maintenance dose: 40-320 mg/d PO in divided doses

Pediatric

0.01-0.1 mg/kg/dose IV infused over 10-15 min, may repeat q6-8h; not to exceed a cumulative dose of 1 mg for infants or 3 mg for children
Maintenance dose: 0.5-4 mg/kg/d PO divided q6-8h

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol

Documented hypersensitivity; uncompensated CHF; bradycardia; cardiogenic shock; AV conduction abnormalities

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; slowly withdraw drug and closely monitor


Sotalol (Betapace)

Currently under investigation for use in children. It has class II (ie, beta-blocking effects) and class III action potential prolongation properties. Less negative inotropic effect than class II antiarrhythmics.

Adult

80 mg PO bid, may increase dose gradually q2-3d to 240-320 mg/d; not to exceed 320 mg/d

Pediatric

Not established

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity of sotalol may increase when administered concurrently with other drugs that prolong the QT interval (eg, sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, phenothiazines, cisapride, dofetilide)

Documented hypersensitivity; asthma; severe sinus bradycardia; second- or third-degree AV block

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Medication should be initiated in hospital under monitored conditions; beta-adrenergic blockade may decrease signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; slowly withdraw drug and closely monitor patient; caution in hypokalemia, peripheral vascular disease, hypomagnesemia, and CHF


Verapamil (Calan, Isoptin)

Calcium channel blocker. Elicits negative inotropic effect. Can diminish PVCs associated with perfusion therapy and decrease the risk of ventricular fibrillation and ventricular tachycardia. By interrupting reentry at AV node, verapamil can restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardias (PSVT).

Adult

80-120 mg PO tid; not to exceed 480 mg/d

Pediatric

<2 years: Contraindicated
>2 years: 4-10 mg/kg/d PO divided tid; alternatively, 0.1-0.3 mg/kg IV over 3 min; not to exceed 5 mg/dose

Verapamil may increase carbamazepine, digoxin, and cyclosporine levels; coadministration with amiodarone can cause bradycardia and a decrease in cardiac output; when administered concurrently with beta-blockers, may increase cardiac depression; cimetidine may increase verapamil levels; verapamil may increase theophylline levels

Documented hypersensitivity; severe CHF, sick sinus syndrome or second- or third-degree AV block, and hypotension (<90 mm Hg systolic); age <2 years

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution if coadministered with a beta-blocker; may cause severe hypotension in children; hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued verapamil treatment); periodically monitor liver function

More on Cardiac Tumors

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Treatment & Medication: Cardiac Tumors
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Multimedia: Cardiac Tumors
References

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Further Reading

Keywords

cardiac tumors, cardiac neoplasm, heart tumors, heart neoplasm, neoplasm of the heart, rhabdomyoma, fibroma, myxoma, teratoma, sarcoma, angiosarcoma, cancer, cardiac mass, congenital heart failure, CHF, jugular venous distention, ascites, pericardial effusion, syncope, shortness of breath, vena cava syndrome, pulmonary embolism, restrictive cardiomyopathy, tuberous sclerosis, Carney syndrome, vascular tumors, hemangiomas, lymphangiomas, heart block, lipomas, papillary tumors, leiomyomas, mesotheliomas, fibroelastomas, fibroelastic papillomas, benign cystic tumors, rhabdomyosarcoma

Contributor Information and Disclosures

Author

Edwin Rodriguez-Cruz, MD, Assistant Professor, Department of Pediatrics, San Juan Bautista Medical School and Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Pediatrics, Hospital El Maestro and San Juan Bautista Medical Center; Consulting Interventional/Clinical Pediatric Cardiologist, Department of Cardiology, Cardiovascular Center of Puerto Rico and the Caribbean and Veterans Affairs Hospital and Medical Center of Puerto Rico
Edwin Rodriguez-Cruz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Medical Association, American Society of Echocardiography, Puerto Rico Medical Association, Society of Cardiac Angiography and Interventions, and Society of Pediatric Echocardiography
Disclosure: Nothing to disclose.

Coauthor(s)

Rosa M Cintrón-Maldonado, MD, Clinical Instructor of Pediatrics, Department of Pediatrics, San Juan Bautista Medical Center
Rosa M Cintrón-Maldonado, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Robert D Ross, MD, Co-Director of Pediatric Cardiology Fellowship Program, Department of Pediatrics, Division of Pediatric Cardiology, Professor, Children's Hospital of Michigan and Wayne State University
Robert D Ross, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, and Society of Pediatric Echocardiography
Disclosure: Nothing to disclose.

Medical Editor

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, Heart Rhythm Society, New York Academy of Sciences, Society for Pediatric Research, Texas Medical Association, and Texas Pediatric Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Ameeta Martin, MD, Clinical Associate Professor, Department of Pediatric Cardiology, University of Nebraska College of Medicine
Ameeta Martin, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.

CME Editor

Gilbert Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College
Gilbert Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Steven R Neish, MD, SM, Director of Pediatric Cardiology Fellowship Program, Associate Professor, Department of Pediatrics, Baylor College of Medicine
Steven R Neish, MD, SM is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Heart Association
Disclosure: Nothing to disclose.

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