Pediatric Valvar Aortic Stenosis Medication

  • Author: Howard S Weber, MD, FAAP, FACC, FSCAI; more...
 
Updated: Mar 29, 2011
 

Medication Summary

Treatment with prostaglandin E1 is necessary for neonates with critical aortic stenosis and low cardiac output. This agent establishes patency of the ductus arteriosus and can restore adequate systemic blood flow and the perfusion of vital organs.

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Prostaglandins

Class Summary

Prostaglandin E1 is used for the treatment of ductal-dependent, cyanotic congenital heart disease caused by decreased pulmonary blood flow. Patients with critical aortic stenosis and low cardiac output require resuscitation with prostaglandin E1. Establishing the patency of the ductus arteriosus can restore systemic blood flow and the perfusion of vital organs.

Alprostadil is a first-line palliative therapy to temporarily maintain patency of the ductus arteriosus before surgery. It produces vasodilation and increases cardiac output. Each 1 mL ampule contains 500 mcg/mL.

Alprostadil IV (Prostin VR Pediatric Injection)

 

This drug is effective in relaxing the smooth muscle of the ductus arteriosus. It is beneficial in infants with congenital defects that restrict pulmonary or systemic blood flow and who depend on a patent ductus arteriosus to get adequate oxygenation and lower body perfusion.

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Inotropic Agents

Class Summary

Inotropic drugs, such as dopamine, dobutamine, and epinephrine, are indicated in cases of reduced cardiac output in aortic stenosis.

Dopamine

 

Dopamine is a naturally occurring endogenous catecholamine that stimulates beta1 and alpha1 adrenergic and dopaminergic receptors in a dose-dependent fashion; it stimulates the release of norepinephrine.

Dobutamine

 

Dobutamine produces vasodilation and increases the inotropic state. At higher dosages, it may cause an increased heart rate, exacerbating myocardial ischemia.

Epinephrine (Adrenalin)

 

Epinephrine has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta2-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.

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Loop Diuretics

Class Summary

Loop diuretics such as intravenous furosemide may be used carefully in pediatric patients with reduced cardiac function and/or significant mitral valve insufficiency when associated with severe aortic valve stenosis. The benefit is to reduce pulmonary venous congestion secondary to elevated left atrial pressures.

Furosemide (Lasix)

 

Furosemide is a loop diuretic that increases excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. It increases renal blood flow without increasing the filtration rate. It increases potassium, sodium, calcium, and magnesium excretion.

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Contributor Information and Disclosures
Author

Howard S Weber, MD, FAAP, FACC, FSCAI  Professor, Assistant Chief, Section of Pediatric Cardiology, Penn State University School of Medicine; Director, Pediatric Catheterization Laboratory, Milton S Hershey Medical Center

Howard S Weber, MD, FAAP, FACC, FSCAI is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Coauthor(s)

Paul M Seib, MD  Associate Professor of Pediatrics, University of Arkansas for Medical Sciences; Medical Director, Cardiac Catheterization Laboratory, Co-Medical Director, Cardiovascular Intensive Care Unit, Arkansas Children's Hospital

Paul M Seib, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Arkansas Medical Society, International Society for Heart and Lung Transplantation, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Specialty Editor Board

Juan Carlos Alejos, MD  Clinical Professor, Department of Pediatrics, Division of Cardiology, University of California, Los Angeles, David Geffen School of Medicine

Juan Carlos Alejos, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Medical Association, and International Society for Heart and Lung Transplantation

Disclosure: Actelion Honoraria Speaking and teaching

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.

John W Moore, MD, MPH  Professor of Clinical Pediatrics, Section of Pediatric Cardiology, Department of Pediatrics, University of California San Diego School of Medicine; Director of Cardiology, Rady Children's Hospital

John W Moore, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

References
  1. Yetman AT, Rosenberg HC, Joubert GI. Progression of asymptomatic aortic stenosis identified in the neonatal period. Am J Cardiol. Mar 15 1995;75(8):636-7. [Medline].

  2. [Best Evidence] Ten Harkel AD, Berkhout M, Hop WC, Witsenburg M, Helbing WA. Congenital valvular aortic stenosis: limited progression during childhood. Arch Dis Child. Jul 2009;94(7):531-5. [Medline].

  3. Egito ES, Moore P, O'Sullivan J, Colan S, Perry SB, Lock JE, et al. Transvascular balloon dilation for neonatal critical aortic stenosis: early and midterm results. J Am Coll Cardiol. Feb 1997;29(2):442-7. [Medline].

  4. Magee AG, Nykanen D, McCrindle BW, Wax D, Freedom RM, Benson LN. Balloon dilation of severe aortic stenosis in the neonate: comparison of anterograde and retrograde catheter approaches. J Am Coll Cardiol. Oct 1997;30(4):1061-6. [Medline].

  5. Alekyan BG, Petrosyan YS, Coulson JD, Danilov YY, Vinokurov AV. Right subscapular artery catheterization for balloon valvuloplasty of critical aortic stenosis in infants. Am J Cardiol. Nov 15 1995;76(14):1049-52. [Medline].

  6. Fischer DR, Ettedgui JA, Park SC, Siewers RD, del Nido PJ. Carotid artery approach for balloon dilation of aortic valve stenosis in the neonate: a preliminary report. J Am Coll Cardiol. Jun 1990;15(7):1633-6. [Medline].

  7. Weber HS, Mart CR, Myers JL. Transcarotid balloon valvuloplasty for critical aortic valve stenosis at the bedside via continuous transesophageal echocardiographic guidance. Catheter Cardiovasc Interv. Jul 2000;50(3):326-9. [Medline].

  8. Turley K, Bove EL, Amato JJ, Iannettoni M, Yeh J, Cotroneo JV, et al. Neonatal aortic stenosis. J Thorac Cardiovasc Surg. Apr 1990;99(4):679-83; discussion 683-4. [Medline].

  9. McCrindle BW, Blackstone EH, Williams WG, Sittiwangkul R, Spray TL, Azakie A, et al. Are outcomes of surgical versus transcatheter balloon valvotomy equivalent in neonatal critical aortic stenosis?. Circulation. Sep 18 2001;104(12 Suppl 1):I152-8. [Medline].

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Valvular calcification of aortic stenosis seen with cardiac fluoroscopy during catheterization.
 
 
 
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