Atrial Septal Defect
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Atrial septal defect (ASD) is one of the more commonly recognized congenital cardiac anomalies presenting in adulthood. ASD is characterized by a defect in the interatrial septum allowing pulmonary venous return from the left atrium to pass directly to the right atrium. Depending on the size of the defect, size of the shunt, and associated anomalies, this can result in a spectrum of disease ranging from no significant cardiac sequelae to right-sided volume overload, pulmonary arterial hypertension, and even atrial arrhythmias.
With the routine use of echocardiography, the detection and, therefore, the incidence of ASD is increased compared to earlier incidence studies using catheterization, surgery, or autopsy for diagnosis. [1] The subtle physical examination findings and often minimal symptoms during the first 2-3 decades of life contribute to a delay in diagnosis until adulthood, the majority (more than 70%) of which is detected by the fifth decade of life. However, earlier intervention of most types of ASD is recommended.
The magnitude of the left-to-right shunt across the atrial septal defect (ASD) depends on the defect size, the relative compliance of the ventricles, and the relative resistance in both the pulmonary and systemic circulation. With small ASD, left atrial pressure may exceed right atrial pressure by several millimeters of mercury, whereas with large ASD, mean atrial pressures are nearly identical. Shunting across the interatrial septum is usually left-to-right and occurs predominantly in late ventricular systole and early diastole. Likely some augmentation occurs during atrial contraction. Note, however, that a transient and small right-to-left shunt can occur, especially during respiratory periods of decreasing intrathoracic pressure, even in the absence of pulmonary arterial hypertension.
The chronic left-to-right shunt results in increased pulmonary blood flow and diastolic overload of the right ventricle. Resistance in the pulmonary vascular bed is commonly normal in children with ASD, and the volume load is usually well tolerated even though pulmonary blood flow may be more than 2 times systemic blood flow. Altered ventricular compliance with age can result in an increased left-to-right shunt contributing to symptoms. The chronic significant left-to-right shunt can alter the pulmonary vascular resistance leading to pulmonary arterial hypertension, even reversal of shunt and Eisenmenger syndrome.
Because of an increase in plasma volume during pregnancy, shunt volume can increase, leading to symptoms. Pulmonary artery pressure usually remains normal.
Atrial septal defect (ASD) is a congenital cardiac disorder caused by the spontaneous malformation of the interatrial septum. Note the following types of ASD:
Ostium secundum ASD: This type of ASD results from incomplete adhesion between the flap valve associated with the foramen ovale and the septum secundum after birth. The patent foramen ovale usually results from abnormal resorption of the septum primum during the formation of the foramen secundum. Resorption in abnormal locations causes a fenestrated or netlike septum primum. Excessive resorption of the septum primum results in a short septum primum that does not close the foramen ovale. An abnormally large foramen ovale can occur as a result of defective development of the septum secundum. The normal septum primum does not close this type of abnormal foramen ovale at birth. A combination of excessive resorption of the septum primum and a large foramen ovale produces a large ostium secundum ASD.
Ostium primum ASD: These defects are caused by incomplete fusion of septum primum with the endocardial cushion. The defect lies immediately adjacent to the atrioventricular (AV) valves, either of which may be deformed and incompetent. In most cases, only the anterior or septal leaflet of the mitral valve is displaced, and it is commonly cleft. The tricuspid valve is usually not involved.
Sinus venosus ASD: Abnormal fusion between the embryologic sinus venosus and the atrium causes these defects. In most cases, the defect lies superior in the atrial septum near the entry of superior vena cava. Often there is associated anomalous drainage of the right superior pulmonary vein. The relatively uncommon inferior type is associated with partial anomalous drainage of the right inferior pulmonary vein. Anomalous drainage can be into the right atrium, the superior vena cava, or the inferior vena cava.
Coronary sinus ASD: The coronary sinus defect is characterized by unroofed coronary sinus and persistent left superior vena cava that drains into the left atrium. A dilated coronary sinus often suggests this defect. This can result is desaturation due to right-to-left shunt into the left atrium. The diagnosis can be made by injecting contrast agent into left upper extremity; coronary sinus opacification precedes right atrial opacification.
ASD may occur on a familial basis. Holt-Oram syndrome characterized by an autosomal dominant pattern of inheritance and deformities of the upper limbs (most often, absent or hypoplastic radii) has been attributed to a single gene defect in TBX5. [2] The penetrance is nearly 100% for Holt-Oram syndrome. Approximately 40% of Holt-Oram cases are due to new mutations.
Ellis van Creveld syndrome is an autosomal recessive disorder associated with skeletal dysplasia characterized by short limbs, short ribs, postaxial polydactyly, dysplastic nails and teeth, and a common atrium, occurring in 60% of affected individuals. [3]
Mutations in the cardiac transcription factor NKX2.5 have been attributed to the syndrome familial ASD associated with progressive atrioventricular block. [4, 5, 6] This syndrome is an autosomal dominant trait with a high degree of penetrance but no associated skeletal abnormalities.
Variants in the GATA4 gene have also been implicated in ASD. [5, 7] More recently, a novel mutation at the methylation position of GATA4 (c.A899C, p.K300T) has been reported in association with ASD. [7]
Wang et al reported that downregulation of the following genes in ASD may affect heart atrial septum formation, cardiomyocyte proliferation, and cardiac muscle development [5] :
The investigators noted that dysregulation of these genes during heart septum morphogenesis may lead to cell cycle as the dominant pathway among downregulated genes, with the potential for the decreased expression of the proteins included in the cell cycle then disturbing cardiomyocyte growth and differentiation during atrial septum formation. [5]
The three major types of atrial septal defect (ASD) account for 10% of all congenital heart disease and as much as 20-40% of congenital heart disease presenting in adulthood. The most common types of ASD include the following:
Ostium secundum: The most common type of ASD accounting for 75% of all ASD cases, representing approximately 7% of all congenital cardiac defects and 30-40% of all congenital heart disease in patients older than 40 years.
Ostium primum: The second most common type of ASD accounts for 15-20% of all ASDs. Primum ASD is a form of atrioventricular septal defect and is commonly associated with mitral valve abnormalities.
Sinus venosus: The least common of the three, sinus venosus (SV) ASD is seen in 5-10% of all ASDs. The defect is located along the superior aspect of the atrial septum. Anomalous connection of the right-sided pulmonary veins is common and should be expected. Alternate imaging is generally required.
ASD occurs with a female-to-male ratio of approximately 2:1.
Patients with ASD can be asymptomatic through infancy and childhood, though the timing of clinical presentation depends on the degree of left-to-right shunt. Symptoms become more common with advancing age. By age 40 years, 90% of untreated patients have symptoms of exertional dyspnea, fatigue, palpitation, sustained arrhythmia, or even evidence of heart failure.
Constantinescu T, Magda SL, Niculescu R, et al. New echocardiographic techniques in pulmonary arterial hypertension vs. right heart catheterization – a pilot study. Maedica (Buchar). 2013 Jun. 8(2):116-23. [Medline]. [Full Text].
Li QY, Newbury-Ecob RA, Terrett JA, et al. Holt-Oram syndrome is caused by mutations in TBX5, a member of the Brachyury (T) gene family. Nat Genet. 1997 Jan. 15(1):21-9. [Medline].
Ruiz-Perez VL, Ide SE, Strom TM, et al. Mutations in a new gene in Ellis-van Creveld syndrome and Weyers acrodental dysostosis. Nat Genet. 2000 Mar. 24(3):283-6. [Medline].
Benson DW, Silberbach GM, Kavanaugh-McHugh A, et al. Mutations in the cardiac transcription factor NKX2.5 affect diverse cardiac developmental pathways. J Clin Invest. 1999 Dec. 104(11):1567-73. [Medline]. [Full Text].
Wang W, Niu Z, Wang Y, et al. Comparative transcriptome analysis of atrial septal defect identifies dysregulated genes during heart septum morphogenesis. Gene. 2016 Jan 10. 575(2 pt 1):303-12. [Medline].
Cao Y, Wang J, Wei C, et al. Genetic variations of NKX2-5 in sporadic atrial septal defect and ventricular septal defect in Chinese Yunnan population. Gene. 2016 Jan 1. 575(1):29-33. [Medline].
Chen J, Qi B, Zhao J, Liu W, Duan R, Zhang M. A novel mutation of GATA4 (K300T) associated with familial atrial septal defect. Gene. 2016 Jan 10. 575(2 pt 2):473-7. [Medline].
Tsai SK, Hsiung MC, Wei J, et al. Transesophageal echocardiography for incremental value of Amplatezer cribriform septal occluder for percutaneous transcatheter closure of complex septal defects: Case series. J Chin Med Assoc. 2017 Apr 25. [Medline].
[Guideline] Warnes CA, Williams RG, Bashore TM, et al. ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to develop guidelines for the management of adults with congenital heart disease). Circulation. 2008 Dec 2. 118(23):2395-451. [Medline].
Putra ST, Djer MM, Idris NS, Samion H, Sastroasmoro S. Transcatheter closure of atrial septal defects in a center with limited resources: outcomes and short term follow-up. Iran J Pediatr. 2015 Dec. 25(6):e3906. [Medline].
Kutty S, Hazeem AA, Brown K, et al. Long-term (5- to 20-year) outcomes after transcatheter or surgical treatment of hemodynamically significant isolated secundum atrial septal defect. Am J Cardiol. 2012 May 1. 109(9):1348-52. [Medline].
Ostermayer SH, Srivastava S, Doucette JT, et al. Malattached septum primum and deficient septal rim predict unsuccessful transcatheter closure of atrial communications. Catheter Cardiovasc Interv. 2015 Dec 1. 86(7):1195-203. [Medline].
Nishida H, Nakatsuka D, Kawano Y, Hiraiwa N, Takanashi S, Tabata M. Outcomes of totally endoscopic atrial septal defect closure using a glutaraldehyde-treated autologous pericardial patch. Circ J. 2017 Apr 25. 81 (5):689-93. [Medline].
Kaya Y, Yurtdas M, Ceylan Y, et al. [Percutaneous closure of secundum atrial septal defects in pediatric and adult patients: short- and mid-term follow-up results] [Turkish]. Turk Kardiyol Dern Ars. 2013 Dec. 41(8):705-13. [Medline].
Humenberger M, Rosenhek R, Gabriel H, et al. Benefit of atrial septal defect closure in adults: impact of age. Eur Heart J. 2011 Mar. 32(5):553-60. [Medline].
Salehian O, Horlick E, Schwerzmann M, et al. Improvements in cardiac form and function after transcatheter closure of secundum atrial septal defects. J Am Coll Cardiol. 2005 Feb 15. 45(4):499-504. [Medline].
Di Salvo G, Drago M, Pacileo G, et al. Atrial function after surgical and percutaneous closure of atrial septal defect: a strain rate imaging study. J Am Soc Echocardiogr. 2005 Sep. 18(9):930-3. [Medline].
Wang JK, Chiu SN, Lin MT, Chen CA, Lu CW, Wu MH. Mid-to-long-term follow-up results of transcatheter closure of atrial septal defect in patients older than 40 years. Heart Vessels. 2017 Apr. 32 (4):467-3. [Medline].
Krumsdorf U, Ostermayer S, Billinger K, et al. Incidence and clinical course of thrombus formation on atrial septal defect and patient foramen ovale closure devices in 1,000 consecutive patients. J Am Coll Cardiol. 2004 Jan 21. 43(2):302-9. [Medline].
Brandt RR, Neumann T, Neuzner J, Rau M, Faude I, Hamm CW. Transcatheter closure of atrial septal defect and patent foramen ovale in adult patients using the Amplatzer occlusion device: no evidence for thrombus deposition with antiplatelet agents. J Am Soc Echocardiogr. 2002 Oct. 15(10 pt 1):1094-8. [Medline].
Divekar A, Gaamangwe T, Shaikh N, Raabe M, Ducas J. Cardiac perforation after device closure of atrial septal defects with the Amplatzer septal occluder. J Am Coll Cardiol. 2005 Apr 19. 45(8):1213-8. [Medline].
Amin Z, Hijazi ZM, Bass JL, Cheatham JP, Hellenbrand WE, Kleinman CS. Erosion of Amplatzer septal occluder device after closure of secundum atrial septal defects: review of registry of complications and recommendations to minimize future risk. Catheter Cardiovasc Interv. 2004 Dec. 63(4):496-502. [Medline].
Tarnok A, Bocsi J, Osmancik P, Hausler HJ, Schneider P, Dahnert I. Cardiac troponin I release after transcatheter atrial septal defect closure depends on occluder size but not on patient’s age. Heart. 2005 Feb. 91(2):219-22. [Medline].
Egred M, Andron M, Albouaini K, Alahmar A, Grainger R, Morrison WL. Percutaneous closure of patent foramen ovale and atrial septal defect: procedure outcome and medium-term follow-up. J Interv Cardiol. 2007 Oct. 20(5):395-401. [Medline].
Fischer G, Stieh J, Uebing A, Hoffmann U, Morf G, Kramer HH. Experience with transcatheter closure of secundum atrial septal defects using the Amplatzer septal occluder: a single centre study in 236 consecutive patients. Heart. 2003 Feb. 89(2):199-204. [Medline].
Goldberg JF. Long-term follow-up of “simple” lesions-atrial septal defect, ventricular septal defect, and coarctation of the aorta. Congenit Heart Dis. 2015 Sep. 10(5):466-74. [Medline].
Anzai H, Child J, Natterson B, et al. Incidence of thrombus formation on the CardioSEAL and the Amplatzer interatrial closure devices. Am J Cardiol. 2004 Feb 15. 93(4):426-31. [Medline].
Argenziano M, Oz MC, DeRose JJ Jr, et al. Totally endoscopic atrial septal defect repair with robotic assistance. Heart Surg Forum. 2002. 5(3):294-300. [Medline]. [Full Text].
Bartel T, Konorza T, Arjumand J, et al. Intracardiac echocardiography is superior to conventional monitoring for guiding device closure of interatrial communications. Circulation. 2003 Feb 18. 107(6):795-7. [Medline].
Bartel T, Konorza T, Neudorf U, et al. Intracardiac echocardiography: an ideal guiding tool for device closure of interatrial communications. Eur J Echocardiogr. 2005 Mar. 6(2):92-6. [Medline].
Bedford DE. The anatomical types of atrial septal defect. Their incidence and clinical diagnosis. Am J Cardiol. 1960 Sep. 6:568-74. [Medline].
Benson DW, Sharkey A, Fatkin D, et al. Reduced penetrance, variable expressivity, and genetic heterogeneity of familial atrial septal defects. Circulation. 1998 May 26. 97(20):2043-8. [Medline].
Besterman E. Atrial septal defect with pulmonary hypertension. Br Heart J. 1961 Sep. 23(5):587-98. [Medline].
Bialkowski J, Karwot B, Szkutnik M, Banaszak P, Kusa J, Skalski J. Closure of atrial septal defects in children: surgery versus Amplatzer device implantation. Tex Heart Inst J. 2004. 31(3):220-3. [Medline]. [Full Text].
Braunwald E. Atrial septal defect. In: Braunwald E, ed. Heart Disease: A Text of Cardiovascular Medicine. 4th ed. Philadelphia, Pa: WB Saunders; 1992. 906-8.
Carlsson E. Anatomic diagnosis of atrial septal defects. Am J Roentgenol Radium Ther Nucl Med. 1961 Jun. 85:1063-70. [Medline].
Cherian G, Uthaman CB, Durairaj M, et al. Pulmonary hypertension in isolated secundum atrial septal defect: high frequency in young patients. Am Heart J. 1983 Jun. 105(6):952-7. [Medline].
Chessa M, Carminati M, Butera G, et al. Early and late complications associated with transcatheter occlusion of secundum atrial septal defect. J Am Coll Cardiol. 2002 Mar 20. 39(6):1061-5. [Medline].
Goldman L, Braunwald E. Primary Cardiology. Philadelphia, Pa: WB Saunders; 1998. 394-411.
Holmvang G, Palacios IF, Vlahakes GJ, et al. Imaging and sizing of atrial septal defects by magnetic resonance. Circulation. 1995 Dec 15. 92(12):3473-80. [Medline].
Humenberger M, Rosenhek R, Gabriel H, et al. Benefit of atrial septal defect closure in adults: impact of age. Eur Heart J. 2011 Mar. 32(5):553-60. [Medline].
Isselbacher KJ, Braunwald E, Wilson JD. Atrial septal defect. In: Isselbacher KJ, ed. Harrison’s Principles of Internal Medicine. 13th ed. New York, NY: McGraw-Hill; 1994. 1041.
Attenhofer Jost CH, Connolly HM, Danielson GK, et al. Sinus venosus atrial septal defect: long-term postoperative outcome for 115 patients. Circulation. 2005 Sep 27. 112(13):1953-8. [Medline].
Kirklin JW, Barratt-Boyes BG. Cardiac Surgery. London, England: Churchill Livingstone; 1986. 463-97.
Konstantinides S, Geibel A, Olschewski M, et al. A comparison of surgical and medical therapy for atrial septal defect in adults. N Engl J Med. 1995 Aug 24. 333(8):469-73. [Medline].
Kronzon I, Tunick PA, Freedberg RS, et al. Transesophageal echocardiography is superior to transthoracic echocardiography in the diagnosis of sinus venosus atrial septal defect. J Am Coll Cardiol. 1991 Feb. 17(2):537-42. [Medline].
Latson LA. Per-catheter ASD closure. Pediatr Cardiol. 1998 Jan-Feb. 19(1):86-93; discussion 94. [Medline].
Marelli AJ, Moodie DS, Topol EJ. Adult congenital heart disease. Textbook of Cardiovascular Medicine. Philadelphia, Pa: Lippincott-Raven; 1998. 775-9.
Masura J, Gavora P, Podnar T. Long-term outcome of transcatheter secundum-type atrial septal defect closure using Amplatzer septal occluders. J Am Coll Cardiol. 2005 Feb 15. 45(4):505-7.
Moore KL, Persaud TVN. Before We Are Born: Essentials of Embryology and Birth Defects. Philadelphia, Pa: WB Saunders Co; 1998. 774-7.
Murphy JG, Gersh BJ, Mair DD, et al. Long-term outcome in patients undergoing surgical repair of tetralogy of Fallot. N Engl J Med. 1993 Aug 26. 329(9):593-9. [Medline].
O’Laughlin MP. Catheter closure of secundum atrial septal defects. Tex Heart Inst J. 1997. 24(4):287-92. [Medline]. [Full Text].
Piechaud JF. Closing down: transcatheter closure of intracardiac defects and vessel embolisations. Heart. 2004 Dec. 90(12):1505-10. [Medline].
Rao PS. Catheter closure of atrial septal defects. J Invasive Cardiol. 2003 Jul. 15(7):398-400. [Medline].
Ruge H, Wildhirt SM, Libera P, Vogt M, Holper K, Lange R. Images in cardiovascular medicine. Left atrial thrombus on atrial septal defect closure device as a source of cerebral emboli 3 years after implantation. Circulation. 2005 Sep 6. 112(10):e130-1. [Medline].
Sealy WC, Farmer JC, Young Jr WG, et al. Atrial dysrhythmia and atrial secundum defects. J Thorac Cardiovasc Surg. 1969 Feb. 57(2):245-50. [Medline].
Seward JB, Khandheria BK, Edwards WD, et al. Biplanar transesophageal echocardiography: anatomic correlations, image orientation, and clinical applications. Mayo Clin Proc. 1990 Sep. 65(9):1193-213. [Medline].
Staniloae CS, El-Khally Z, Ibrahim R, et al. Percutaneous closure of secundum atrial septal defect in adults a single center experience with the amplatzer septal occluder. J Invasive Cardiol. 2003 Jul. 15(7):393-7. [Medline].
Stark J. Secundum atrial septal defect. Surgery for Congenital Heart Defects. New York, NY: Grune & Stratton; 1983.
Tardif JC, Schwartz SL, Vannan MA, et al. Clinical usefulness of multiplane transesophageal echocardiography: comparison to biplanar imaging. Am Heart J. 1994 Jul. 128(1):156-66. [Medline].
Thuny F, Di Salvo G, Belliard O, et al. Risk of embolism and death in infective endocarditis: prognostic value of echocardiography: a prospective multicenter study. Circulation. 2005 Jul 5. 112(1):69-75. [Medline].
Tonni G, Ferrari B, Defelice C, Centini G. Neonatal porencephaly in very low birth weight infants: ultrasound timing of asphyxial injury and neurodevelopmental outcome at two years of age. J Matern Fetal Neonatal Med. 2005 Dec. 18(6):361-5. [Medline].
Vick GW 3rd, Murphy DJ Jr, Ludomirsky A, et al. Pulmonary venous and systemic ventricular inflow obstruction in patients with congenital heart disease: detection by combined two-dimensional and Doppler echocardiography. J Am Coll Cardiol. 1987 Mar. 9(3):580-7. [Medline].
Warnes CA. The adult with congenital heart disease: born to be bad?. J Am Coll Cardiol. 2005 Jul 5. 46(1):1-8. [Medline].
Webb G, Gatzoulis MA. Atrial septal defects in the adult: recent progress and overview. Circulation. 2006 Oct 10. 114(15):1645-53. [Medline].
Weyman AE, Wann LS, Caldwell RL, et al. Negative contrast echocardiography: a new method for detecting left-to- right shunts. Circulation. 1979 Mar. 59(3):498-505. [Medline].
Zanchetta M, Onorato E, Rigatelli G, et al. Intracardiac echocardiography-guided transcatheter closure of secundum atrial septal defect: a new efficient device selection method. J Am Coll Cardiol. 2003 Nov 5. 42(9):1677-82. [Medline].
Thanopoulos BD, Biasco L, Dardas P, et al. Catheter closure of atrial septal defects using the Cocoon septal occluder: preliminary results of a European multicenter study. Int J Cardiol. 2014 Dec 15. 177 (2):418-22. [Medline].
Assaidi A, Sumian M, Mauri L, et al. Transcatheter closure of complex atrial septal defects is efficient under intracardiac echocardiographic guidance. Arch Cardiovasc Dis. 2014 Dec. 107 (12):646-53. [Medline].
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