eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiothoracic Surgery
Ebstein Malformation, Surgical Treatment
Updated: Apr 23, 2009
Introduction
Ebstein malformation is a rare congenital cardiac defect. The primary pathologic finding is abnormal development of the tricuspid valve marked by a downward displacement of the septal and posterior leaflets into the cavity of the right ventricle. This defect is characterized by remarkable morphologic variability and a broad spectrum of clinical presentations. Consequently, diagnosis may be made in symptomatic newborn infants, young adults, or middle-aged adults, depending on the severity of the defect and clinical manifestations.
Anatomical features of Ebstein malformation. Note the atrialized portion of the right ventricle and displacement of the tricuspid valve.
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History of the Procedure
In 1866, Wilhelm Ebstein, a young physician in Breslau, Poland, reported findings from a postmortem examination performed 2 years earlier.1 The patient was a 19-year-old laborer who presented with dyspnea and palpitations and was noted to be profoundly cyanotic. In his report, Ebstein described in great detail the morphology and clinical correlations of the congenital cardiac malformation that bears his name. His report provided a strong basis for the subsequent development of surgical techniques for the treatment of this anomaly 100 years later.2
Early surgical attempts to treat Ebstein malformation using palliative shunts resulted in extremely high mortality rates.3 In 1958, Hunter and Lillihei described a technique of surgical repair that involved plication of the atrialized right ventricle, closure of the atrial septal defect, and tricuspid valve annuloplasty.4 In 1964, Hardy reported the first successful repair of Ebstein malformation using this technique.5
During the 1960s, most attempts to repair the tricuspid valve were unsuccessful, and prosthetic valve replacement became the preferred approach. In 1962, Christian Barnard described the first successful tricuspid valve replacement in a patient with Ebstein malformation using a mechanical valve.6 In the early 1970s, interest once again focused on tricuspid valve repair with a successful technique described by Danielson and colleagues at the Mayo Clinic.7 Several modifications of tricuspid valve repair have been described recently, and early results have been successful.8,9,10,11
Problem
Ebstein malformation is defined by a downward displacement of the annular attachments of the septal and posterior leaflets of the tricuspid valve into the inlet portion of the right ventricle. This downward displacement of the leaflets reduces the distal chamber of the right ventricle, leaving part of the ventricle above the valve as an extension of the right atrium. The entire wall of the right ventricle, both above and below the tricuspid valve, is often thin, dilated, and dysfunctional. In most patients, annular dilatation and malformation of the leaflets result in moderate-to-severe insufficiency of the tricuspid valve. Most patients have an atrial septal defect or a patent foramen ovale, which allows predominant right-to-left shunting at the atrial level. A high incidence of atrial and ventricular arrhythmia, including an association with Wolff-Parkinson-White syndrome, occurs in these patients.
Frequency
Ebstein malformation accounts for less than 1% of all congenital heart disease.12 Geographical variation in the prevalence of this defect, inside or outside the United States, has not been documented. Although no increase in prevalence has been documented, an improvement in diagnostic techniques has led to earlier diagnosis. The malformation occurs in both sexes with equal frequency.
Etiology
The exact embryologic cause of Ebstein malformation is unknown. The tricuspid valve leaflets form by a process of delamination of the inner layers of the inlet portion of the right ventricle.13 Evidence suggests that the anterior leaflet forms earlier in development than the septal and posterior leaflets. In Ebstein malformation, the insertions of the septal and posterior leaflets are displaced to the junction of the inlet and trabecular portions of the right ventricle, indicating abnormal delamination.14 The insertion of the anterior leaflet is at the level of the true annulus. The right ventricle endocardium is often thickened and fibrotic, suggesting that formation of the valve leaflets was interrupted prior to completion of the delamination process. The tricuspid valve is usually incompetent, but it may also be stenotic or even imperforate. In addition, both the atrialized right ventricular wall and the functional right ventricular wall may be abnormally thin and fibrotic.
The observed morphologic variability indicates the complexity of this defect's origin during embryologic development. Interestingly, exposure of the fetus to lithium carbonate during the first trimester has been linked to the development of Ebstein malformation.15 Although no specific genetic inheritance pattern has been documented, a familial association has been reported.3
Pathophysiology
In most patients, the tricuspid valve is incompetent with some degree of functional impairment of the right ventricle. The atrialized right ventricle paradoxically moves with right atrial and right ventricular contractions. The net effect is reduced forward blood flow through the right ventricle and pulmonary arteries. The impaired filling of the functional right ventricle and the incompetence of the tricuspid valve both result in systemic venous hypertension.
The right atrium and the atrialized right ventricle become dilated, often to extreme proportions. In most patients, right-to-left shunting occurs across a defect in the atrial septum and results in cyanosis. The presence of pulmonary hypertension in neonates increases this atrial shunting and can lead to profound cyanosis in newborn infants. In some neonates, right ventricular outflow tract obstruction and pulmonary stenosis or atresia may result in a completely ductal-dependent pulmonary circulation. Both atrial arrhythmias and ventricular arrhythmias may contribute to impaired right ventricular function.
Although the primary pathology involves the right ventricle, patients with Ebstein malformation may also demonstrate abnormal left ventricular geometry and function.16 The severity of left ventricular dysfunction is associated with the degree of displacement of the tricuspid valve, the size and dysfunction of the right ventricle, and the severity of paradoxical motion of the interventricular septum.
Presentation
Clinical presentation widely varies. Patients presenting with Ebstein malformation range from neonates who are severely ill to adults who are mildly symptomatic. Some patients may be completely asymptomatic with a murmur detected during a physical examination, or they may have abnormal findings on an electrocardiogram (ECG) or a chest radiograph.17 Presenting symptoms are directly related to the severity of tricuspid valve incompetence, the presence or absence of an atrial septal defect, the degree of right and left ventricular dysfunction, and the presence of arrhythmia and associated cardiac defects.
Beyond the neonatal period, most patients present with dyspnea, fatigue, and some degree of cyanosis. In most patients, exercise tolerance is markedly compromised and maximum oxygen uptake during exercise is less than half of predicted.18 Despite these findings, growth and development are usually normal. The most common clinical presentations by age are as follows: cyanosis in neonates, heart failure in infants, incidental murmurs in older children, and arrhythmia and exercise intolerance in adolescents and adults.
Paroxysmal supraventricular arrhythmia occurs in 25-40% of patients; this condition is most often found in teenagers or young adults.3,12 Ventricular arrhythmia is also common, and Wolff-Parkinson-White syndrome has been diagnosed in 10-18% of patients.3,12 . Sudden death due to ventricular arrhythmia may occur in as many as 5-7% of patients12 Patients with atrial or ventricular arrhythmia may present with episodes of syncope, near syncope, or recurrent palpitation. Likewise, patients with mild manifestations present as late as the third or fourth decade of life with complaints of palpitation or mild exercise intolerance. While some patients may reach advanced age without serious clinical manifestations, most eventually develop significant symptoms. The most common causes of death are congestive heart failure, severe hypoxia, and cardiac arrhythmia.19,20
Upon physical examination, jugular venous distension and a prominent v wave in the jugular pulse may indicate severe tricuspid regurgitation. Heart sounds are usually soft, and the first and second heart sounds are widely split. A systolic murmur of tricuspid regurgitation may be heard along the left sternal border, but this may also be due to right ventricular outflow tract obstruction. The liver may be palpably enlarged, but ascites and peripheral edema are rare. Evidence of significant cyanosis may be seen in the extremities.
Indications
Indications for surgical intervention in patients with Ebstein malformation include the following:
- Functional New York Heart Association (NYHA) class III or class IV symptoms
- Significant or progressive cyanosis
- Decline in exercise tolerance
- Significant decrease in growth curve
- Severe cardiomegaly (cardiothoracic ratio >0.65)
- Associated cardiac anomalies, including right ventricular outflow tract obstruction
- Refractory atrial or ventricular arrhythmia
- History of paradoxical embolus
Relevant Anatomy
The characteristic finding of Ebstein malformation is a downward displacement of the attachments of the septal and posterior leaflets of the tricuspid valve below the true tricuspid annulus. These valve leaflets are often hypoplastic and adherent to the endocardial surface of the right ventricle. The commissure between these 2 leaflets is usually the point of maximal displacement. The anterior leaflet is typically larger than normal and sail-like in appearance. The anterior leaflet may be thin and fenestrated, and it may also adhere to the endocardial surface of the right ventricle.
The individual valve leaflets may be larger or smaller than expected. The chordae tendineae and papillary muscles are often abnormal in their number, development, and location. In rare instances, the anterior leaflet may attach to the apical region of the right ventricle and obstruct blood flow through the right ventricular outflow tract. Additionally, the tricuspid annulus is usually enlarged to 2-4 times the normal size.
Anatomical features of Ebstein malformation are presented in Media file 1.
Anatomical features of Ebstein malformation. Note the atrialized portion of the right ventricle and displacement of the tricuspid valve.
The displacement of the septal and posterior leaflets of the tricuspid valve into the right ventricle leaves a portion of the right ventricular wall between the leaflet attachments and the true annulus in continuity with the right atria. This atrialized right ventricle is usually very thin and dilated with a decrease in the actual number of myocardial fibers. The functional right ventricle below the valve may also be thin and dilated with decreased contractile function.21
The anatomy of the conduction system is normal; the atrioventricular node is located at the apex of the triangle of Koch, and the sinoatrial node is located at the junction of the superior vena cava and the right atrium. The location of the bundle of His is normal, but abnormalities of the right bundle branch have been described.21,22 Accessory atrioventricular connections are present in as many as 20% of patients and are associated with Wolff-Parkinson-White syndrome.23,24,25
The right atrium is enlarged and may reach enormous size. An atrial septal defect is usually present and ranges from a patent foramen ovale to a large secundum defect. The coronary arteries are normal in distribution, and the right coronary artery is often displaced by the enlarged right atrium and atrialized right ventricle. Associated cardiac anomalies include pulmonary stenosis or atresia, ventricular septal defect, patent ductus arteriosus, tetralogy of Fallot, and coarctation of the aorta.3,20 In patients with Wolff-Parkinson-White syndrome, accessory pathways are typically the atrioventricular type and are localized to the right ventricular free wall or to the posterior interventricular septum (bundles of Kent).26
Ebstein malformation of the left atrioventricular valve occurs in up to 75% of patients with L-transposition of the great arteries or corrected transposition of the great arteries.27 In these patients, displacement of the septal and posterior leaflets is similar to that in right-sided lesions, but the anterior leaflet is usually smaller.14 In addition, the wall of the functional right ventricle is rarely thin and dilated, and the wall of the atrialized right ventricle is also less thin and dilated. Left-sided accessory pathways have been described only in those patients with Ebstein malformation of the left-sided atrioventricular valve.
Contraindications
Patients with Ebstein malformation and biventricular failure should not undergo attempted repair of the defect, and they should be considered candidates for orthotopic heart transplantation. Neonates with Ebstein malformation are controversial because some patients with severe defects may not be considered candidates for surgery (except possibly for heart transplantation).
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References
Ebstein W. Ueber einen sehr seltenen Fall von Insufficienz der Valvula Tricuspidalis bedingt durch eine angeborene hochgradige Missbildung derselben. Arch Anat Physiol. 1866;33:238.
van Son JA, Konstantinov IE, Zimmermann V. Wilhelm Ebstein and Ebstein's malformation. Eur J Cardiothorac Surg. Nov 2001;20(5):1082-5. [Medline].
Watson H. Natural history of Ebstein's anomaly of tricuspid valve in childhood and adolescence. An international co-operative study of 505 cases. Br Heart J. May 1974;36(5):417-27. [Medline].
Hunter SW, Lillehei CW. Ebstein's malformation of the tricuspid valve; study of a case together with suggestion of a new form of surgical therapy. Dis Chest. Mar 1958;33(3):297-304. [Medline].
Hardy KL, May IA, Webster CA, Kimball KG. Ebstein's anomaly: A functional concept and successful definitive repair. J Thorac Cardiovasc Surg. Dec 1964;48:927-40. [Medline].
Barnard CN, Schrire V. Surgical correction of Ebstein's malformation with prosthetic tricuspid valve. Surgery. Aug 1963;54:302-8. [Medline].
Danielson GK, Maloney JD, Devloo RA. Surgical repair of Ebstein's anomaly. Mayo Clin Proc. Mar 1979;54(3):185-92. [Medline].
Carpentier A, Chauvaud S, Mace L, et al. A new reconstructive operation for Ebstein's anomaly of the tricuspid valve. J Thorac Cardiovasc Surg. Jul 1988;96(1):92-101. [Medline].
Hetzer R, Nagdyman N, Ewert P, et al. A modified repair technique for tricuspid incompetence in Ebstein's anomaly. J Thorac Cardiovasc Surg. Apr 1998;115(4):857-68. [Medline].
Quaegebeur JM, Sreeram N, Fraser AG, et al. Surgery for Ebstein's anomaly: the clinical and echocardiographic evaluation of a new technique. J Am Coll Cardiol. Mar 1 1991;17(3):722-8. [Medline].
Starnes VA, Pitlick PT, Bernstein D, Griffin ML, Choy M, Shumway NE. Ebstein's anomaly appearing in the neonate. A new surgical approach. J Thorac Cardiovasc Surg. Jun 1991;101(6):1082-7. [Medline].
Hong YM, Moller JH. Ebstein's anomaly: a long-term study of survival. Am Heart J. May 1993;125(5 Pt 1):1419-24. [Medline].
Netter FH, Van Mierop LH. Embryology. In: Yonkman FF, ed. The Ciba Collection of Medical Illustrations. Vol 5. Summit, NJ: Ciba Pharmaceutical Co; 1969:125.
Anderson KR, Danielson GK, McGoon DC, Lie JT. Ebstein's anomaly of the left-sided tricuspid valve: pathological anatomy of the valvular malformation. Circulation. Sep 1978;58(3 Pt 2):I87-91. [Medline].
Zalzstein E, Koren G, Einarson T, Freedom RM. A case-control study on the association between first trimester exposure to lithium and Ebstein's anomaly. Am J Cardiol. Mar 15 1990;65(11):817-8. [Medline].
Benson LN, Child JS, Schwaiger M, Perloff JK, Schelbert HR. Left ventricular geometry and function in adults with Ebstein's anomaly of the tricuspid valve. Circulation. Feb 1987;75(2):353-9. [Medline].
Ghosh S, Avari JN, Rhee EK, Woodard PK, Rudy Y. Noninvasive electrocardiographic imaging (ECGI) of epicardial activation before and after catheter ablation of the accessory pathway in a patient with Ebstein anomaly. Heart Rhythm. Jun 2008;5(6):857-60. [Medline].
Barber G, Danielson GK, Heise CT, Driscoll DJ. Cardiorespiratory response to exercise in Ebstein's anomaly. Am J Cardiol. Sep 15 1985;56(8):509-14. [Medline].
Giuliani ER, Fuster V, Brandenburg RO, Mair DD. Ebstein's anomaly: the clinical features and natural history of Ebstein's anomaly of the tricuspid valve. Mayo Clin Proc. Mar 1979;54(3):163-73. [Medline].
Kumar AE, Fyler DC, Miettinen OS, Nadas AS. Ebstein's anomaly. Clinical profile and natural history. Am J Cardiol. Jul 1971;28(1):84-95. [Medline].
Anderson KR, Lie JT. The right ventricular myocardium in Ebstein's anomaly: a morphometric histopathologic study. Mayo Clin Proc. Mar 1979;54(3):181-4. [Medline].
Lev M, Liberthson RR, Joseph RH, et al. The pathologic anatomy of Ebstein's disease. Arch Pathol. Oct 1970;90(4):334-43. [Medline].
Danielson GK, Driscoll DJ, Mair DD, Warnes CA, Oliver WC Jr. Operative treatment of Ebstein's anomaly. J Thorac Cardiovasc Surg. Nov 1992;104(5):1195-202. [Medline].
Oh JK, Holmes DR Jr, Hayes DL, Porter CB, Danielson GK. Cardiac arrhythmias in patients with surgical repair of Ebstein's anomaly. J Am Coll Cardiol. Dec 1985;6(6):1351-7. [Medline].
Gentles TL, Calder AL, Clarkson PM, Neutze JM. Predictors of long-term survival with Ebstein's anomaly of the tricuspid valve. Am J Cardiol. Feb 1 1992;69(4):377-81. [Medline].
Smith WM, Gallagher JJ, Kerr CR, et al. The electrophysiologic basis and management of symptomatic recurrent tachycardia in patients with Ebstein's anomaly of the tricuspid valve. Am J Cardiol. Apr 1 1982;49(5):1223-34. [Medline].
Allwork SP, Bentall HH, Becker AE, et al. Congenitally corrected transposition of the great arteries: morphologic study of 32 cases. Am J Cardiol. Dec 1976;38(7):910-23. [Medline].
Shiina A, Seward JB, Edwards WD, Hagler DJ, Tajik AJ. Two-dimensional echocardiographic spectrum of Ebstein's anomaly: detailed anatomic assessment. J Am Coll Cardiol. Feb 1984;3(2 Pt 1):356-70. [Medline].
Celermajer DS, Dodd SM, Greenwald SE, Wyse RK, Deanfield JE. Morbid anatomy in neonates with Ebstein's anomaly of the tricuspid valve: pathophysiologic and clinical implications. J Am Coll Cardiol. Apr 1992;19(5):1049-53. [Medline].
Patel V, Nanda NC, Rajdev S, et al. Live/real time three-dimensional transthoracic echocardiographic assessment of Ebstein's anomaly. Echocardiography. Nov 2005;22(10):847-54. [Medline].
Link KM, Herrera MA, D'Souza VJ, Formanek AG. MR imaging of Ebstein anomaly: results in four cases. AJR Am J Roentgenol. Feb 1988;150(2):363-7. [Medline].
Ivy D, Loehr J, Schaffer M. Usefulness of prolonged prostaglandin infusion in neonates with Ebstein's anomaly. Am J Cardiol. Dec 1 1993;72(17):1327-9. [Medline].
Chauvaud S, Berrebi A, d'Attellis N, Mousseaux E, Hernigou A, Carpentier A. Ebstein's anomaly: repair based on functional analysis. Eur J Cardiothorac Surg. Apr 2003;23(4):525-31. [Medline].
Wu Q, Huang Z. A new procedure for Ebstein's anomaly. Ann Thorac Surg. Feb 2004;77(2):470-6; discussion 476. [Medline].
Nakata T, Fujimoto Y, Hirose K, Tosaka Y, Ide Y, Sakamoto K. Norwood procedure combined with the Starnes procedure. Ann Thorac Surg. Oct 2008;86(4):1378-80. [Medline].
Kotoulas C, Jones RP, Turkie W, Hasan R. Edge-to-edge repair of tricuspid valve in a corrected transposition of the great vessels. Hellenic J Cardiol. Nov-Dec 2008;49(6):434-6. [Medline].
Barbara DW, Edwards WD, Connolly HM, Dearani JA. Surgical pathology of 104 tricuspid valves (2000-2005) with classic right-sided Ebstein's malformation. Cardiovasc Pathol. May-Jun 2008;17(3):166-71. [Medline].
Sanfelippo PM, Giuliani ER, Danielson GK, et al. Tricuspid valve prosthetic replacement. Early and late results with the Starr-Edwards prosthesis. J Thorac Cardiovasc Surg. Mar 1976;71(3):441-5. [Medline].
Brown ML, Dearani JA, Danielson GK, et al. Comparison of the outcome of porcine bioprosthetic versus mechanical prosthetic replacement of the tricuspid valve in the Ebstein anomaly. Am J Cardiol. Feb 15 2009;103(4):555-61. [Medline].
Kiziltan HT, Theodoro DA, Warnes CA, O'Leary PW, Anderson BJ, Danielson GK. Late results of bioprosthetic tricuspid valve replacement in Ebstein's anomaly. Ann Thorac Surg. Nov 1998;66(5):1539-45. [Medline].
Tanaka M, Ohata T, Fukuda S, Kigawa I, Yamashita Y, Wanibuchi Y. Tricuspid valve supra-annular implantation in adult patients with Ebstein's anomaly. Ann Thorac Surg. Feb 2001;71(2):582-6. [Medline].
Milgalter E, Laks H. Use of a pericardial patch to bridge the conduction tissue during tricuspid valve replacement. Ann Thorac Surg. Dec 1991;52(6):1337-9. [Medline].
Glenn WW, Browne M, Whittemore R. Circulatory bypass of the right side of the heart: Cavo-pulmonary artery shunt–Indications and results (report of a collected series of 537 cases). In: Cassels DE, ed. The heart and circulation in newborn and infant. New York, NY: Grune & Stratton; 1966:345.
Marianeschi SM, McElhinney DB, Reddy VM, Silverman NH, Hanley FL. Alternative approach to the repair of Ebstein's malformation: intracardiac repair with ventricular unloading. Ann Thorac Surg. Nov 1998;66(5):1546-50. [Medline].
Mayer JE Jr, Perry S, O'Brien P, et al. Orthotopic heart transplantation for complex congenital heart disease. J Thorac Cardiovasc Surg. Mar 1990;99(3):484-91; discussion 491-2. [Medline].
Weyand M, Kececioglu D, Kehl HG, et al. Neonatal mechanical bridging to total orthotopic heart transplantation. Ann Thorac Surg. Aug 1998;66(2):519-22. [Medline].
Celermajer DS, Bull C, Till JA, et al. Ebstein's anomaly: presentation and outcome from fetus to adult. J Am Coll Cardiol. Jan 1994;23(1):170-6. [Medline].
Yetman AT, Freedom RM, McCrindle BW. Outcome in cyanotic neonates with Ebstein's anomaly. Am J Cardiol. Mar 15 1998;81(6):749-54. [Medline].
Brown ML, Dearani JA, Danielson GK, Cetta F, Connolly HM, Warnes CA, et al. The outcomes of operations for 539 patients with Ebstein anomaly. J Thorac Cardiovasc Surg. May 2008;135(5):1120-36, 1136.e1-7. [Medline].
Danielson GK. Ebstein's anomaly: Historical aspects and current management. AHA Cardiothoracic and Vascular Newsletter. 2000.
Brown ML, Dearani JA, Danielson GK, Cetta F, Connolly HM, Warnes CA, et al. Functional status after operation for Ebstein anomaly: the Mayo Clinic experience. J Am Coll Cardiol. Aug 5 2008;52(6):460-6. [Medline].
Chen JM, Mosca RS, Altmann K, et al. Early and medium-term results for repair of Ebstein anomaly. J Thorac Cardiovasc Surg. 2004;127 (4):990-8. [Medline].
McElhinney DB, Salvin JW, Colan SD, et al. Improving outcomes in fetuses and neonates with congenital displacement (Ebstein's malformation) or dysplasia of the tricuspid valve. Am J Cardiol. Aug 15 2005;96(4):582-6. [Medline].
Knott-Craig CJ, Overholt ED, Ward KE, Ringewald JM, Baker SS, Razook JD. Repair of Ebstein's anomaly in the symptomatic neonate: an evolution of technique with 7-year follow-up. Ann Thorac Surg. Jun 2002;73(6):1786-92; discussion 1792-3. [Medline].
Boston US, Dearani JA, O'Leary PW, Driscoll DJ, Danielson GK. Tricuspid valve repair for Ebstein's anomaly in young children: a 30-year experience. Ann Thorac Surg. Feb 2006;81(2):690-5; discussion 695-6. [Medline].
Spitaels SE. Ebstein's anomaly of the tricuspid valve complexities and strategies. Cardiol Clin. Aug 2002;20(3):431-9, vii. [Medline].
Watanabe M, Harada Y, Takeuchi T, Satomi G, Yasukouchi S. Modified Starnes operation for neonatal Ebstein's anomaly. Ann Thorac Surg. Sep 2002;74(3):916-7. [Medline].
Further Reading
- Relevant clinical guidelines include the following:
- American College of Radiology appropriateness criteria for suspected congenital heart disease in the adult
- American College of Cardiology and American Heart Association 2006 guidelines for the management of patients with valvular heart disease
- Guidelines on the diagnosis and management of pericardial diseases from the task force on the diagnosis and management of pericardial diseases of the European Society of Cardiology
- A recent clinical trial is found at Congenital Heart Disease Research Registry.
- Related eMedicine topics include the following:
Keywords
Ebstein malformation, Ebstein's malformation, Ebstein's disease, Ebstein's anomaly, Ebstein disease, Ebstein anomaly, congenital cardiac defect, congenital heart defect, congenital cardiac malformation, congenital heart disease, tricuspid valve, tricuspid valve abnormality, tricuspid valve repair, Wolff-Parkinson-White syndrome, atrial septal defect, patent foramen ovale, ventricular arrhythmia, treatment, diagnosis, ventricular septal defect, VSD, patent ductus arteriosus, tetralogy of Fallot, coarctation of the aorta, L-transposition of the great arteries, metabolic acidosis, congestive heart failure, CHF, exercise intolerance
