Supracristal Ventricular Septal Defect Medication

  • Author: Ira H Gessner, MD; Chief Editor: Stuart Berger, MD   more...
 
Updated: Nov 15, 2011
 

Medication Summary

For patients who develop aortic valve insufficiency, surgical closure of the ventricular septal defect (VSD) and repair of valve insufficiency is the preferred treatment. If surgical repair must be postponed, afterload reducers, such as angiotensin-converting enzyme (ACE) inhibitors or calcium channel blockers, have proved helpful in adults and children.[22] ACE inhibitors that may be employed include enalapril, lisinopril, and captopril. Nifedipine is an effective calcium channel blocker.

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Angiotensin Converting Enzyme (ACE) Inhibitors

Class Summary

These agents have proved beneficial in long-term therapy for aortic valve insufficiency. Positive effects include reductions in pulse pressure, regurgitant volume, left ventricular volume, and left ventricular mass (because of beneficial effects on ventricular remodeling).

Enalapril (Vasotec)

 

Enalapril is considered a reasonable first drug of choice in this group because of its increased dosing interval (q12-24h). A competitive ACE inhibitor, it reduces angiotensin II levels, decreasing aldosterone secretion. Enalapril is available in a liquid suspension.

Lisinopril (Prinivil, Zestril)

 

Lisinopril is considered a reasonable first drug of choice in this group because of its increased dosing interval (q12-24h). It prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Captopril

 

Captopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. For younger children or infants, this agent can be formulated as a suspension if it is stabilized with ascorbic acid to prevent hydrolysis. The dosing interval is 6-8 hours because of captopril's shorter half-life.

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Calcium Channel Blockers

Class Summary

Calcium channel blockers also have proved effective in reducing afterload and lowering pulse pressure and regurgitant volume. Prolonged, regular use may stabilize left ventricular volume, but the effect on left ventricular muscle mass is less pronounced than that of ACE inhibitors.

Nifedipine (Adalat, Procardia, Afeditab CR, Nifedical XL)

 

Nifedipine is a good first choice because of its primary action on peripheral resistance and its limited effect on cardiac function and heart rate.

Diltiazem (Cardizem, Dilacor XR, Diltzac, Matzim LA)

 

During depolarization, diltiazem inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

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Contributor Information and Disclosures
Author

Ira H Gessner, MD  Professor Emeritus, Pediatric Cardiology, University of Florida College of Medicine

Ira H Gessner, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Coauthor(s)

Edward J Bayne, MD  Assistant Professor, Division of Pediatric Cardiology, Emory University School of Medicine; Consulting Staff, Sibley Heart Center Cardiology, Children's Healthcare of Atlanta

Edward J Bayne, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Cardiology, American Heart Association, and American Society of Echocardiography

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.

Additional Contributors

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

Hugh D Allen, MD Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine

Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, and Western Society for Pediatric Research

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.

References
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Parasternal long-axis echocardiogram view showing supracristal ventricular septal defect (arrow) with buckling and prolapse (***) of the right coronary leaflet of the aortic valve.
Parasternal short-axis echocardiogram view with color Doppler showing proximity of ventricular septal defect jet to the aortic and pulmonic valves. The patient is an infant with neither aortic valve prolapse nor aortic insufficiency.
Subcostal "right ventricular inflow/outflow" view showing the close relationship between the aortic and pulmonic valves in the presence of supracristal ventricular septal defect. Turbulent shunt flow is shown directed into the main pulmonary artery. The patient is an infant with neither aortic valve prolapse nor insufficiency.
Transesophageal horizontal view of aortic root and right ventricle, showing sinus of Valsalva aneurysm leaking through a supracristal ventricular septal defect (VSD)(>
 
 
 
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