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A study of congenital cardiac disease in a neonatal population. The validity of echocardiography undertaken by a neonatologist

A study of congenital cardiac disease in a neonatal population – the validity of echocardiography undertaken by a neonatologist
Authors: Gregory R. Samson; Suresh R. Kumar


Source : Cardiology in the Young, December 2004, vol. 14, no. 6, pp. 585-593(9)


Publisher: Greenwich Medical Media

Abstract:

Objectives: To estimate the incidence of, and profile the spread of, congenital cardiac defects, and to assess the accuracy of the echocardiographic diagnosis as performed by a neonatologist. Design: Hospital-based study. Methods: All neonates meeting our criterions, specifically those with a persistent murmur 48 hours after birth, underwent an echocardiographic examination to exclude an underlying congenital cardiac defect. All scans performed by the neonatologist were videotaped and reviewed by a paediatric cardiologist. We assessed concordane according to inter-rater agreement. Results: Out of 11,085 live births, there were 83 infants with a congenital cardiac defect, giving an incidence of 7.49 per 1000 live births, with 95% confidence interval from 5.88 to 9.09. Of the infants with a murmur persisting at or greater than 48 hours after birth, who had a median age of 4.5 days, 75% had a congenital heart defect, with ventricular septal defect being the commonest, encountered in 56.7% of cases. Concordance between the neonatologist and the cardiologist was good, with Cohen’s Kappa coefficient being calculated at 0.68, and 95% confidence interval from 0.51 to 0.85. Conclusion: The incidence of congenital cardiac malformations as determined in our hospital-based study in the United Arab Emirates is similar to that described in the Gulf region and worldwide. A persistent murmur at or greater than 48 hours after birth is strongly suggestive of an underlying congenital cardiac malformation. Our experience shows that a neonatologist appropriately trained in echocardiography can perform as well as a paediatric cardiologist. Where specialist resources are limited, this allows for early diagnosis, earlier referral if necessary, and early institution of appropriate therapy.

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Prenatal diagnosis of tetralogy of Fallot associated with a fistula from left coronary artery to the left atrium

Prenatal diagnosis of tetralogy of Fallot associated with
a fistula from the left coronary artery to the left atrium
Mohammed D. Khan, Sivasankaran Sivasubramonian, John M. Simpson
Department of Congenital Heart Disease, Guy’s Hospital, London, UK

Abstract

In a fetus at 20 weeks gestation, we found a large fistula from the left coronary artery to the left
atrium in association with tetralogy of Fallot. Postnatally, the therapeutic issues were complex because of prematurity, low birth weight, decreased flow of blood to the lungs, and volume overload of the left ventricle because of the huge fistula. At three months, the baby underwent repair of tetralogy of Fallot, with surgical ligation of the fistula, but the baby died postoperatively.
Keywords: Echocardiography; fetal heart; prematurity

Cardiol Young 2003; 13: 194–196

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Inherited Arrhythmias: Long QT Syndrome

The Challenge
Long QT syndrome (LQTS) is a disorder of cardiac repolarization. It is characterized by a prolongation of the QT interval, and a predisposition to ventricular tachyarrhythmias, which are associated with syncope, arrhythmic events, and sudden cardiac death (SCD). In recent years, there have been significant advances in understanding the genetic basis of the syndrome. Newer genetic forms of LQTS have been identified, too, plus a laboratory test has become available to help in the diagnosis of the syndrome. As knowledge of LQTS continues to expand, clinical applications of this growing body of information need further study

LQTS usually presents with cardiac events in childhood, adolescence, or early adulthood. The syndrome runs in families; thus, when SCD (or an aborted sudden death) has occurred in one family member, electrocardiograms of other family members is advisable, and could lead to multiple presymptomatic (pre-syncope) diagnoses.

Numerous genetic loci of long QT syndrome have been identified, with the initial LQTS types labeled LQT1 through LQT6; most are potassium channel mutations. More recently, newer complex forms of long QT have been identified, notably the LQT7 type, which is associated with Andersen Syndrome (AS). In addition to a prolonged QT interval with ventricular arrhythmias, this rare variant of hereditary-familial LQTS is characterized by periodic paralysis and abnormalities in physical development (e.g., micrognathia, clinodactyly). Long QT has been identified in 71% of all gene carriers of AS, and some researchers have proposed that AS be considered a subtype of LQTS.1

Another newly identified gene has been associated with Timothy Syndrome, another complicated disorder characterized by long QT. Timothy Syndrome is also a rare condition with multiorgan dysfunction, including lethal arrhythmias, autism, and syndactyly (webbing of fingers and toes).2 The syndrome’s genetic mutations interfere with the calcium channels that regulate cardiac activity.

Using genetic testing, along with knowledge of the patient’s personal and family history, some patients may be considered for an implantable cardioverter defibrillator (ICD). However, there is limited long-term clinical experience with the ICDs in this setting. Available data are encouraging. In one trial, patients who were cardiac arrest survivors or had recurrent syncope were followed for a mean of 8 years. LQTS patients with an ICD had a 1.3% death rate compared with 16% in controls who did not receive an implant.3

Even with a careful personal and family history, plus meticulous inspection with a 12-lead electrocardiogram, there are still numerous challenges facing the clinician trying to unmask this potentially silent killer. Once diagnosed, risk stratification is necessary given the profound heterogeneity of this syndrome, but it can be exceedingly difficult. The effort is important, however, considering that some patients may be destined for asymptomatic longevity while others will be walking time bombs waiting for the right trigger to detonate. (Triggers may be related to physical activity or emotional distress, or may even be auditory in nature.) The greatest challenge may be to discern which of these divergent outcomes is most likely in a given patient and the appropriate therapy to reduce this risk, which may be greatly influenced by the specific genotype of LQTS.

According to Jeffrey A. Towbin, MD, FACC, individuals who have had an aborted SCD should be strongly considered for an ICD. The need for an ICD also should be evaluated in families where long QT syndrome has been associated with sudden death in multiple family members. It’s still not clear which other patients might benefit from ICD placement. “Research is ongoing,” he said, “and over the next few years, I think there will be more stringent criteria available so that clinicians can make wise decisions about ICD use.”

Until then, clinicians may be able to answer some important questions about individual patients with a new genetic test for LQTS. Genaissance Pharmaceuticals (New Haven, CT) has intellectual property rights relating to the five genes that have been identified as explaining the majority of familial LQTS and Brugada Syndrome. (Like LQTS, Brugada Syndrome is caused by abnormalities in cardiac ion channels and can result in abnormal electrical activity in the heart, particularly ventricular fibrillation.) Genaissance Pharmaceuticals started offering the new test at its CLIA laboratory in 2004.

While the test is expensive, Dr. Towbin said, “The cost decreases dramatically when you test other family members after identifying the gene mutation in the index case. Once you have a presymptomatic diagnosis, it can be life saving over the long term.” One possible benefit of the new genetic test: more specific information regarding genotype and a better assessment of individual patient risk may lead to fewer ICDs used in this population.

Source

Guidelines
Gregoratos G, Abrams J, Epstein AE, et al. ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices—summary article:
a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). J Am Coll Cardiol 2002;40:1703-19.

References

  • Tristani-Firouzi M, Jensen JL, Donaldson MR, et al. Functional and clinical characterization of KCNJ2 mutations associated with LQT7 (Andersen syndrome) J Clin Invest 2002;110:381-388.
  • Splawski I, Timothy KW, Sharpe LM, et al. Ca(V)1.2 calcium channel dysfunction causes a multisystem disorder including arrhythmia and autism Cell 2004;119:19-31.
  • Zareba W, Moss AJ, Daubert JP, et al. Implantable cardioverter defibrillator in high-risk long QT syndrome patients J Cardiovasc Electrophysiol 2003;14:337-41.
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Fetal EChocardiography centers in USA

Fetal Echocardiography North American Centers

  • Institut of Biochemistry and Biophysics
    University of Pennsylvania
    Rm. C-501 Richards Bldg. Philadelphia, PA 19104-6089 U.S.A.
    Phone (215) 898-6396 Fax (215)898-4215
    Responsible : Krzysztof Wroblewski
    Phone (215)898-6396 fax (215)898-4215
  • Dept of Pediatric Cardiology, Babies Hospital
    Columbia Presbyterian Medical Center
    W 168th St – New York – NY 10032 – USA
    Responsible : Lindsey D. Allan Dr
    Phone ++ 212-305-6542 fax 212-305-4429
  • Clinical Care Center for Congenital Heart Disease
    Doernbecher Children’s Hospital
    Oregon Health Sciences University
    3181 SW Sam Jackson Park Road – Portland 97201 – U.S.A.
    Phone ++ (503) 494-8650 fax > (503) 494-
    Responsible : Mary Jo Rice, M.D.* & David J. Sahn, M.D **.
    *Mary Jo Rice, M.D. is Director of the Pediatric Echocardiolgraphy Lab and does major of the fetal echocardiograms.
    **David J. Sahn, M.D. is the Director of the Clinical Care Center of Congenital Heart Disease.
    Internet URL : http://www.ohsu.edu/
  • Pediatric Cardiology – University of California, San Diego
    200 West Arbor Drive-8445 San Diego 92103-8445 – USA
    Responsible Mark Sklansky, M.D.
    Phone (619) 543-2927 fax (619) 543-5994
    Internet URL http://Tanya.ucsd.edu
    State-of-the-Art Fetal Cardiology Center.
    Multidisciplinary group includes Pediatric Cardiology, Obstetrics & Gynecology,
    Perinatology, Genetics, Neonatology, Radiology, Pediatric Cardiothoracic Surgery.
    Gated Three-Dimensional Fetal Echocardiography:
    We are the only institution in this country currently performing
    this technique.
  • Cardiology – Clinica Buena Salud Los Angeles
    1832 W. 7th Street, Los Angeles . CA 90057
    Responsible Imperiale Bloise
    Phone ++ 310 3798811 fax ++ 310 7980286
  • Maternal-Fetal Medicine, Ob/Gyn – Childrens Hospital of Buffalo (SUNY @ Buffalo)
    219 Bryant Street – Buffalo, New York – 14222 – USA
    Responsible : Bruce D. Rodgers, M.D. – Director
    Phone ++ 716-878-7861
    For Appointments, call 716-878-7861-Location is a tertiary perinatal center.Team approach to management including in-house pediatric cardiology, neonatology, pediatric cardiothoracic surgery,
    pediatric surgery, level IV NICU, and genetics.
    Cordocentesis, intraumbilical drug administration and umbilical transfusion available.
  • The Heart Center – Children’s Hospital of New Jersey at Newark Beth Israel
    201 Lyon’s Ave – Newark – 07112 – United States
    Phone ++ 973 926 3511 fax ++ 973 923 0639
    Responsible : Judith A. Becker M.D.
    Internet : www.sbhcs.net/hospitals/saint_barnabas/mservices/index.html
    Notice : We are an up-and-coming pediatric Cardiac program with all services at this campus:? infant and pediatric heart surgery, interventional catheterization, echo,
    fetal echo, and transesophageal echo, ECMO, Nitric oxide therapy, a 50 bed NICU, and a high risk Obstetrics program.
  • Center for Maternal and Child Health, Division of Pediatric Cardiology
    University of North Carolina at Chapel Hill
    311 Burnett-Womack, CB #7220 – Chapel Hill, NC – 27599-7220 -USA
    telephon 919-966-4601 fax 919-966-6894
    Internet http://www.med.unc.edu/
    Responsible ; John Cotton, MD
    Director, Pediatric Echocardiography Laboratory

 


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Fetal coronary fistula

Prenatal diagnosis and perinatal management of left coronary
artery to right atrium fistula

G. MIELKE*, L. SIEVERDING†, T. BORTH-BRUNS†, K. EICHHORN‡, D. WALLWIENER* and
U. GEMBRUCH§

Departments of *Obstetrics and Gynecology and †Pediatric Cardiology, University of Tuebingen, ‡Medical Practice, Weimar and §Department of
Obstetrics and Gynecology, University of Luebeck, Germany

KEYWORDS: Coil embolization, Coronary artery fistula, Echocardiography, Fetal circulation, Fetal heart, Prenatal diagnosis
Ultrasound Obstet Gynecol 2002; 19: 612–615

ABSTRACT
Serious complications due to coronary artery fistulae have
been described. Most authors recommend early intervention
at the time of diagnosis. We present a case of a fistula
originating from a dilated left coronary artery and draining
into the right atrium, which was diagnosed prenatally by
color Doppler echocardiography. During pregnancy, the
echocardiographic findings remained unchanged, and there
were no signs of heart failure. After birth, the fistula was
confirmed by angiography. Additionally, a persistent left
superior vena cava draining into the coronary sinus and
a very small ventricular septal defect were detected. The
fistula was closed successfully by transcatheter coil embolization.
At 17 months old the child was in good clinical
condition. Prenatal diagnosis of coronary artery fistulae
may be possible and may improve perinatal management and
outcome.

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CONGENITAL CORONARY ARTERY FISTULAS

ANZ J. Surg. 2004; 74: 350–355

CONGENITAL CORONARY ARTERY FISTULAS: CLINICAL
CONSIDERATIONS AND SURGICAL TREATMENT
GOU-JIENGHONG,* CHIH-YUANLIN,* CHUNG-YILEE,* SHIN-HURNLOH,† HOU-SHENGYANG,*KUANG-YILIU,* YI-TINGTSAI*AND CHIEN-SUNGTSAI*
*Division of Cardiovascular Surgery, Department of Surgery, and † Department of Pharmacology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, China

Background:
Coronary artery fistulas are uncommon abnormalities that can cause significant cardiac morbidity. Indications for operation vary, particularly, for asymptomatic patients. Early surgical correction is indicated because of the high incidence of late symptoms and complications.

Methods:
From January 1981 to December 2001, all 15 patients who underwent surgical management of congenital coronary artery fistulas at the Tri-Service General Hospital, Taipei, Taiwan, China were included in the present retrospective study.

Results:
Twelve patients were symptomatic at the time of the diagnosis. Coronary artery fistulas involved the right coronary artery in five patients, left coronary artery in nine, and both the right and the left coronary arteries in one. Coronary artery fistula drained into the right ventricle in seven patients, right atrium in three, pulmonary artery in two, left ventricle in one, left atrium in two, and
coronary venous sinus in one. The value of pulmonary blood flow/systemic blood flow ranged from 0.98 to 2.1. Six patients had associated cardiac anomalies. All patients received surgical correction. Nine patients received cardiopulmonary bypass during operation. There was zero operative mortality and operative morbidity was low. All patients had a stable condition and were asymptomatic during a mean postoperative follow-up of 13.3 years.

Conclusions:
Early surgical treatment for coronary artery fistulas is safe and effective. The risk of operative correction appears to be considerably less than the potential for development of serious and potentially fatal complications, even in asymptomatic patients.

Key words: coronary artery fistula.
Abbreviations : Qp/Qs, pulmonary blood flow/systemic blood flow; TEE, transesophageal echocardiography.

REFERENCES

  • 1. Roberts WC. Major anomalies of coronary arterial origin seen in
    adulthood. Am. Heart J. 1986; 111: 941–63.
  • 2. Yamanaka O, Hobbs RE. Coronary artery anomalies in 125 595
    patients undergoing coronary angiography. Cathet. Cardiovasc.
    Diagn. 1990; 21: 28–40.
  • 3. Vavurunakis M, Bush CA, Boudoulas H. Coronary artery fistula
    in adult: incidence, angiographic characteristic, natural history.
    Cathet. Cardiovasc. Diagn. 1995; 35: 116–20.
  • 4. Sapin P, Frantz E, Jain A, Nichols TC, Dehmer GJ. Coronary
    artery fistula: an abnormality affecting all age group. Medicine
    1990; 69: 101–13.
  • 5. Liotta D, Hallman GL, Hall RJ, Cooley DA. Surgical treatment
    of congenital coronary artery fistula. Surgery 1971; 70: 856–64.
  • 6. Krause W. Ueber den Ursprung einer access orischen a: coronaria
    cordis aus der a. pulmonalis. Z. Rat. Med. 1865; 24: 225–7.
  • 7. Biorck G, Crafoord C. Arteriovenous aneurysm on pulmonary
    artery simulating patent ductus arteriosus Botalli. Thorax 1947;
    2: 65–8.
  • 8. Rittenhouse EA, Doty DB, Ehrenhaft JL. Congenital coronary
    artery-cardiac chamber fistula. Ann. Thorac Surg. 1975; 20: 468–85.
  • 9. Fernandes ED, Kadivar H, Hallman GL, Reul GJ, Ott DA,
    Cooley DA. Congenital malformation of the coronary arteries:
    the Texas Heart Institute experience. Ann. Thorac. Surg. 1992;
    54: 732–40.

  • 10. Liberthson RR, Sagar K, Berkoben JP, Weintraub RM, Levine
    FH. Congenital coronary arteriovenous fistula. Report of 13
    patients, review of the literature, and delineation of management.
    Circulation 1979; 59: 849–54.

  • 11. Lowe JE, Oldham HN, Sabiston DC. Surgical management of
    congenital coronary artery fistula. Ann. Surg. 1981; 194: 373–80.

  • 12. Falaschi G, Ott DA, Cooley DA.Urrutia-S CO, Surgical management
    of 56 patients with congenital coronary artery fistulas. Ann.
    Thorac. Surg. 1983; 35: 300–7.

  • 13. Shyam Sunder KR, Balakrishnan KG, Tharaha JA et al. Coronary
    artery fistula in children and adult: a review of 25 cases
    with long term observations. Int. J. Cardiol. 1997; 58: 47–53.

  • 14. Cottier C, Kiowski W, von Betrab R, Pfisterer M, Burkart F.
    Multiple coronary arteriocameral fistulas as a cause of myocardial
    ischemia. Am. Heart J. 1988; 115: 181–4.

  • 15. Reitz BA, Harrison LH, Michaelis LL. Experimental coronary
    artery fistula. J. Thor. Cardiovasc. Surg. 1975; 69: 279–82.

  • 16. Davis JT, Allen HD, Wheller JJ et al. Coronary artery fistula in
    the pediatric age group: a 19-year institutional experience. Ann.
    Thorac. Surg. 1994; 58: 760–3.

  • 17. Boger AJJC, Quaegebeur JM, Huysmans HA. Early and late
    results of surgical treatment of congenital coronary artery fistula.
    Thorax 1987; 42: 396–40.

  • 18. Phillips WS, Cooley DA. Successful repair of a massive coronary
    arteriovenous fistula in a 68-year-old man. Ann. Thorac.
    Surg. 1996; 61: 984–6.

  • 19. Misumi T, Nishikawa K, Yasudo M, Suzuki T, Kumamaru H.
    Rupture of an aneurysm of coronary arteriovenous fistula. Ann.
    Thorac. Surg. 2001; 71: 2026–7.

  • 20. Katoh T, Zempo N, Minami Y et al. Coronary arteriovenous
    fistulas with giant aneurysm: two case reports. Cardiovasc. Surg.
    1999; 7: 470–2.

  • 21. Shimaya K, Suzuki Y, Inoue Y. Right coronary artery fistula
    with associated arteriovenous fistula. Int. J. Cardiol. 1997; 58:
    192–4.

  • 22. Bauer HH, Allmendinger PD, Flaherty J, Owlia D, Rossi MA,
    Chen CG. Congenital coronary arteriovenous fistula: spontaneous
    rupture and cardiac tamponade. Ann. Thorac. Surg. 1996;
    62: 1521–3.

  • 23. Shirai K, Ogawa M, Kawaguchi H, Kawano T, Nakashima Y,
    Arakawa K. Acute myocardial infarction due to thrombus formation
    in congenital coronary fistula. Eur. Heart J. 1994; 15:
    577–9.

  • 24. Moro-Serrano C, Martinez J, Madrid AH et al. Ventricular
    tachycardia in a patient with congential coronary arteriovenous
    fistula. Am. Heart J. 1992; 124: 503–5.

  • 25. Cheung LC, Au WK, Cheung HC, Chiu SW, Lee WT. Coronary
    artery fistula: long-term results of surgical correction. Ann.
    Thorac. Surg. 2001; 71: 190–5.

  • 26. Stevenson JG, Sorensen GK, Stamm SJ, McCloskey JP, Hall
    DG, Tittenhouse EA. Intraoperative transesophageal echocardiography
    of coronary artery fistulas. Ann. Thorac. Surg. 1994; 57:
    1217–21.

  • 27. Kim Hyun IL, Koshiji T, Okomoto M, Arai Y, Masumoto H.
    Surgical repair of coronary arteriovenous fistula: a simple and
    useful approach to identify the fistulous communication. Eur. J.
    Cardiothorac. Surg. 2001; 20: 850–2.

  • 28. deNef JJE, Varghese PJ, Losekoot G. Congenital coronary fistula.
    Analysis of 17 cases. Br. Heart J. 1971; 33: 857–62.

  • 29. Effler DB, Sheldon WC, Turner JJ, Groves LK. Coronary arteriovenous
    fistulas: diagnosis and surgical management. Report of
    fifteen cases. Surgery 1967; 61: 41–50.

  • 30. Mavroudis C, Backer CL, Rocchini AP, Muster AJ, Gevitz M.
    Coronary artery fistulas in infants and children. A surgical
    review and discussion of coil embolization. Ann. Thorac. Surg.
    1997; 63: 1235–42.

  • 31. Armsby LR, Keane JF, Sherwood MC, Forbess JM, Perry SB,
    Lock JE. Management of coronary artery fistulae: patient selection
    and results of transcatheter closure. J. Am. Coll. Cardiol.
    2002; 39: 1026–32.

  • 32. Reidy JF, Anjos RT, Qureshi SA, Baker EJ, Tynan MJ. Transcatheter
    embolization in the treatment of coronary artery fistulas.
    J. Am. Coll. Cardiol. 1991; 18: 187–92.

  • 33. Perry SB, Rome J, Keane JF, Baim DS, Lock JE. Transcatheter
    closure of coronary artery fistula. J. Am. Coll. Cardiol. 1992; 20:
    205–9.

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Twin-twin transfusion syndrome

General Obstetrics and Gynecology: Obstetrics
Prenatal cardiovascular manifestations in the twin-to-twin transfusion syndrome recipients and the impact of therapeutic amnioreduction

Catherine Barrea, MD – a-, Fawaz Alkazaleh, MD -b-, Greg Ryan, MB -b-, Brian W. McCrindle, MD -a-, Anita Roberts, BSc -a-, Jean-Luc Bigras, MD -a-, Jon Barrett, MD -c-, Gareth P. Seaward, MB -b- , Jeffrey F. Smallhorn, MB, BS -a-, Lisa K. Hornberger, MD -a*.

Abstract

Objective
We evaluated the cardiovascular pathologic condition in the recipient twin in twin-to-twin transfusion syndrome and the influence of amnioreduction.

Study design Fetal echocardiograms and medical records of 54 pregnancies that were complicated by twin-to-twin transfusion syndrome were reviewed. Recipient twin right and left ventricular wall thickness, diameters, systolic and diastolic function, valve regurgitation, and structural cardiac defects were assessed at examination and after amnioreduction.

Results At examination (n=28 pregnancies), cardiomegaly because of right ventricular and/or left ventricular hypertrophy was observed in 58% of recipient twins, and biventricular hypertrophy was observed in 33% of recipient twins, without ventricular dilation. Biventricular diastolic dysfunction was present in two thirds of recipient twins, and right ventricular systolic dysfunction and significant atrioventricular valve regurgitation was observed in one third of recipient twins. Serial assessment (n=21 pregnancies) revealed progressive biventricular hypertrophy and right ventricular systolic and biventricular diastolic dysfunction in most recipient twins. Steeper progression of hypertrophy, diastolic dysfunction, and structural or functional right ventricular outflow disease (20% incidence) were associated with an increased perinatal mortality rate.

Conclusion In twin-to-twin transfusion syndrome, the recipient twin has progressive biventricular hypertrophy with predominant right ventricular systolic and biventricular diastolic dysfunction. Despite amnioreduction, the cardiovascular disease persists and even progresses in many recipient twins.

Publishing and Reprint Information

aDepartment of Pediatrics, Division of Cardiology, Fetal Cardiac Program, The Hospital for Sick Children
bDivision of Maternal-Fetal Medicine, Mount Sinai Hospital
cWomen’s College Hospital, University of Toronto, Ontario, Canada
Supported in part by The Physician’s Services Incorporated Foundation, grant no. 78390 and by the Foundation “Saint Luc,” Cliniques Universitaires Saint Luc, Catholic University of Louvain, Brussels, Belgium.
*Reprint requests: Lisa K. Hornberger, MD, UCSF Medical Center, Fetal Cardiovascular Program, Pediatric Echocardiography Laboratory, 505 Parnassus Ave, Room M-306, San Francisco, CA 94143.
Email address: lhornberger@pedcard.ucsf.edu (Lisa K. Hornberger)



The American Journal of Obstetrics and Gynecology
March 2005 • Volume 192 • Number 3

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Interventional Cardiology

Transcatheter Atrial Septal Defect Closure With
the Amplatzer Septal Occluder: Five-Year Follow-Up
Guan Yew, MD, and Nigel J. Wilson* MBChB

We report 5-year follow-up data of patients following atrial septal defect (ASD) closure with the Amplatzer septal occluder (ASO). Patients completed a questionnaire related to symptoms pre- and post-ASO implantation.

Complete transthoracic echocardiography
was used to assess residual atrial septal defect, right ventricular volume overload, and degree of mitral regurgitation. Mean follow-up duration was 4.8 6 0.6 years (range, 5.7–3.0 years). Complete closure was observed in all patients. Right ventricular volume overload, present in all patients prior to ASD closure, had resolved in 82% of patients.
No mitral valve sequelae were found; 75% of patients were symptomatic or felt much improved compared to their preclosure symptoms. New onset of migraine-type headaches was encountered in two patients, one for 12 months and one patient persisted with intermittent migrainous episode.

In conclusion, we report 100% closure rate of ASD with ASO device, with return of right ventricular size to normal in the majority of
patients. New onset of migraine headaches after ASO implantation can persist more than a few months.

Catheter Cardiovasc Interv 2005;64:193–196. ‘ 2005 Wiley-Liss, Inc.

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