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Pediatric Cardiac Tumors Medication

  • Author: Edwin Rodriguez-Cruz, MD; Chief Editor: P Syamasundar Rao, MD  more...
 
Updated: Jan 04, 2016
 

Medication Summary

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.

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Cardiac glycosides

Class Summary

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.

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Diuretic agents

Class Summary

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.

Chlorothiazide (Diuril)

 

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

Spironolactone (Aldactone)

 

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

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Angiotensin converting enzyme inhibitors

Class Summary

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.

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Adrenergic agonist agents (inotropes)

Class Summary

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.

Dobutamine (Dobutrex)

 

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

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Cyclic adenosine monophosphate (cAMP) phosphodiesterase inhibitors

Class Summary

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

 

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

Milrinone (Primacor)

 

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

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Antiarrhythmic agents

Class Summary

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.

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.

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.

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.

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).

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Contributor Information and Disclosures
Author

Edwin Rodriguez-Cruz, MD Director, Section of Cardiology, Department of Pediatrics, San Jorge Children’s Hospital, Puerto Rico; Private Practice in Interventional Pediatric Cardiology and Internal Medicine, Centro Pedíatrico y Cardiovascular

Edwin Rodriguez-Cruz, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, American Society of Echocardiography, Society for Cardiovascular Angiography and Interventions, Society of Pediatric Echocardiography, American College of Physicians-American Society of Internal Medicine, American Medical Association, Puerto Rico Medical Association

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: St Jude's Medical Co.<br/>Received grant/research funds from NOVARTIS for investigator; Received consulting fee from St. Jude Medical Corp. for speaking and teaching.

Coauthor(s)

Robert D Ross, MD Director of Pediatric Cardiology Fellowship Program, Department of Pediatrics, Division of Pediatric Cardiology, Children's Hospital of Michigan; Professor of Pediatrics, Wayne State University School of Medicine

Robert D Ross, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Society of Pediatric Echocardiography

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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.

Chief Editor

P Syamasundar Rao, MD Professor of Pediatrics and Medicine, Division of Cardiology, Emeritus Chief of Pediatric Cardiology, University of Texas Medical School at Houston and Children's Memorial Hermann Hospital

P Syamasundar Rao, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, American College of Cardiology, American Heart Association, Society for Cardiovascular Angiography and Interventions, Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

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 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, New York Academy of Sciences, Society for Pediatric Research, Texas Medical Association, Texas Pediatric Society, Cardiac Electrophysiology Society

Disclosure: Nothing to disclose.

Acknowledgements

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.

References
  1. Tao TY, Yahyavi-Firouz-Abadi N, Singh GK, Bhalla S. Pediatric cardiac tumors: clinical and imaging features. Radiographics. 2014 Jul-Aug. 34 (4):1031-46. [Medline].

  2. Kutluk T, Demir HA, Buyukpamukcu M, et al. Cardiac rhabdomyomas in childhood: six cases from a single institution. Turk J Pediatr. 2013 Jan-Feb. 55(1):69-73. [Medline].

  3. Nield LE, Mendelson M, Ahmad N, Manlhiot C, Jaeggi ET, McCrindle BW. Clinical Review of Obstructive Primary Cardiac Tumors in Childhood. Congenit Heart Dis. 2013 Aug 21. [Medline].

  4. Lam KY, Dickens P, Chan AC. Tumors of the heart. A 20-year experience with a review of 12,485 consecutive autopsies. Arch Pathol Lab Med. 1993 Oct. 117(10):1027-31. [Medline].

  5. Miyake CY, Del Nido PJ, Alexander ME, Cecchin F, Berul CI, Triedman JK, et al. Cardiac tumors and associated arrhythmias in pediatric patients, with observations on surgical therapy for ventricular tachycardia. J Am Coll Cardiol. 2011 Oct 25. 58(18):1903-9. [Medline].

  6. Salpea P, Stratakis CA. Carney complex and McCune Albright syndrome: An overview of clinical manifestations and human molecular genetics. Mol Cell Endocrinol. 2013 Sep 5. [Medline].

  7. Kono T, Koide N, Hama Y, et al. Expression of vascular endothelial growth factor and angiogenesis in cardiac myxoma: a study of fifteen patients. J Thorac Cardiovasc Surg. 2000 Jan. 119(1):101-7. [Medline].

  8. Beroukhim RS, Prakash A, Buechel ER, Cava JR, Dorfman AL, Festa P, et al. Characterization of cardiac tumors in children by cardiovascular magnetic resonance imaging: a multicenter experience. J Am Coll Cardiol. 2011 Aug 30. 58(10):1044-54. [Medline].

  9. Grant FD, Treves ST. Nuclear medicine and molecular imaging of the pediatric chest: current practical imaging assessment. Radiol Clin North Am. 2011 Sep. 49(5):1025-51. [Medline].

  10. Amelia A, Mohd Nizam MB. Perinatal management of cardiac tumors: a case series. Med J Malaysia. 2013 Aug. 68(4):374-5. [Medline].

  11. Linnemeier L, Benneyworth BD, Turrentine M, Rodefeld M, Brown J. Pediatric cardiac tumors: a 45-year, single-institution review. World J Pediatr Congenit Heart Surg. 2015 Apr. 6 (2):215-9. [Medline].

  12. Butany J, Nair V, Naseemuddin A, et al. Cardiac tumours: diagnosis and management. Lancet Oncol. 2005 Apr. 6(4):219-28. [Medline].

  13. Dhillon G, Rodriguez-Cruz E, Kathawala M, Alqassem N. Primary cardiac myofibroblastic sarcoma, case report and review of diagnosis and treatment of cardiac tumors. Bol Asoc Med P R. 1998 Jul-Dec. 90(7-12):130-3. [Medline].

  14. Farooki ZQ, Ross RD, Paridon SM, et al. Spontaneous regression of cardiac rhabdomyoma. Am J Cardiol. 1991 Apr 15. 67(9):897-9. [Medline].

  15. Gaumann A, Strubel G, Bode-Lesniewska B, Schmidtmann I, Kriegsmann J, Kirkpatrick CJ. The role of tumor vascularisation in benign and malignant cardiovascular neoplasms: a comparison of cardiac myxoma and sarcomas of the pulmonary artery. Oncol Rep. 2008 Aug. 20(2):309-18. [Medline].

  16. Le Guyader A, Laskar M. Removal of left ventricular tumors by a transaortic transvalvular approach with the help of thoracoscopic instruments. J Thorac Cardiovasc Surg. 2008 Aug. 136(2):537-8. [Medline].

  17. Lopez M, Pinto A, Moreno V, Diaz M, Gonzalez Baron A. Primary cardiac osteosarcoma. Clin Transl Oncol. 2008 Aug. 10(8):515-6. [Medline].

  18. Ludomirsky A. Cardiac tumors. Bricker JT, Fisher DJ, eds. The Science and Practice of Pediatric Cardiology. 9th ed. Williams & Wilkins; 1998. Vol 2: 1885-93.

  19. Martinez Quesada M, Trujillo Berraquero F, Almendro Delia M, et al. [Cardiac hamartoma. Case report and literature review]. Rev Esp Cardiol. 2005 Apr. 58(4):450-2. [Medline].

  20. Marx GR. Cardiac Tumors. Emmanouilides GC, Gutgesell HP, Riemenschneider TA, Allen HD, eds. Moss and Adams Heart Disease in Infants, Children, and Adolescents: Including the Fetus and Young Adult. 5th ed. Baltimore, MD: Williams & Wilkins; 1995. Vol 2: 1773-86.

  21. McAllister HA, Fenoglio JJ Jr. Tumors of the cardiovascular system: atlas of tumor pathology, second series. Washington, DC: Armed Forces Institute of Pathology. 1978.

  22. Padalino MA, Basso C, Milanesi O, et al. Surgically treated primary cardiac tumors in early infancy and childhood. J Thorac Cardiovasc Surg. 2005 Jun. 129(6):1358-63. [Medline].

  23. Piazza N, Chughtai T, Toledano K, et al. Primary cardiac tumours: eighteen years of surgical experience on 21 patients. Can J Cardiol. 2004 Dec. 20(14):1443-8. [Medline].

  24. Rodriguez-Cruz E, Cintron-Maldonado RM, Bercu BA. Primary cardiac osteogenic sarcoma treated with heart transplantation. Bol Asoc Med PR. 1999. 91 (7-12):98-99. [Medline].

  25. Rodriguez-Cruz E, Cintron-Maldonado RM, Forbes TJ. Treatment of primary cardiac malignancies with orthotopic heart transplantation. Bol Asoc Med P R. 2000 Apr-Aug. 92(4-8):65-71. [Medline].

  26. Takach TJ, Reul GJ, Ott DA, Cooley DA. Primary cardiac tumors in infants and children: immediate and long-term operative results. Ann Thorac Surg. 1996 Aug. 62(2):559-64. [Medline].

  27. Tatli S, Lipton MJ. CT for intracardiac thrombi and tumors. Int J Cardiovasc Imaging. 2005 Feb. 21(1):115-31. [Medline].

  28. Tazelaar HD, Locke TJ, McGregor CG. Pathology of surgically excised primary cardiac tumors. Mayo Clin Proc. 1992 Oct. 67(10):957-65. [Medline].

  29. Wu XM, Hu CZ, Li N, et al. [Relationship of serum level of creatine kinase of MB type to cardiac function of patients with advanced tumors and its prognostic value]. Ai Zheng. 2005 Apr. 24(4):506-8.abs. [Medline].

 
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Echocardiographic parasternal long-axis view showing a large mass within the left ventricular cavity invading or connected to the anterior mitral valve leaflet. AO=Aorta, RV=Right ventricle, LA=Left atrium, Arrow=Left ventricular mass.
Echocardiographic subcostal view of a patient with a large mass within the left ventricular cavity invading or connected to the anterior mitral valve leaflet. Mass within the left ventricle fills most of the ventricular cavity. LA=Left atrium, RA=Right atrium, RV=Right ventricle, Arrow=Left ventricular mass.
Echocardiographic parasternal long-axis view demonstrating a rounded mass in the area of the right ventricular outflow tract. Mass was not causing any outflow obstruction. RV=Right ventricle, LV= Left ventricle, AO=Aorta, Arrow=Right ventricular mass.
Echocardiographic apical 5 chamber view of a 1 month old patient with several ventricular tumors filling the ventricular cavities in both sides. The patient was having seizures and diagnosed to have tuberous sclerosis. The tumor associated with this disease is rhabdomyoma (see text). RA= Right Atrium; Ao= Aorta; LA= Left Atrium; RV= Right Atrium; LV= Left Ventricle
Follow-up echocardiographic 4 chamber view from the same patient as shown in the image above. This echocardiogram was done 8 months after the previous view. Note that the tumors have changed in size and some of them have regressed totally, especially in the right ventricle. The arrows show the remaining areas of tumors seen in both ventricles.
 
 
 
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