(Circulation. 2001;103:2376.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Mortality Associated With Congenital Heart Defects in the United States
Trends and Racial Disparities, 1979–1997
From the National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention, Atlanta, Ga.
Correspondence to Roumiana S. Boneva, MD, PhD, National Center for Infectious Disease, Centers for Disease Control and Prevention (CDC), Mailstop G-19, 1600 Clifton Rd, Atlanta, GA 30333. E-mail rboneva{at}cdc.gov
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Abstract |
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Background—Surgical series and some population-based studies have documented a decrease in mortality from heart defects. Recent population-based data for the United States are lacking, however. We examined population-based data for patterns, time trends, and racial differences of mortality from heart defects for the United States from 1979 through 1997.
Methods and Results—We examined the multiple-cause mortality files compiled by the National Center for Health Statistics of the CDC from all death certificates filed in the United States. From these data, we derived death rates (deaths per 100 000 population) by the decedent’s age, race, year of death, and heart defect type. We also analyzed age at death as an indirect indicator of survival. From 1979 through 1997, mortality from heart defects (all ages) declined 39%, from 2.5 to 1.5 per 100 000 population; among infants, the decline was 39%, or 2.7% per year. In 1995 to 1997, heart defects contributed to 5822 deaths per year. Of these deaths, 51% were among infants and 7% among children 1 to 4 years old. Mortality was on average 19% higher among blacks than among whites; this gap does not appear to be closing. Age at death increased for most heart defects, although less among blacks than among whites.
Conclusions—Mortality from heart defects is declining in the United States, although it remains a major cause of death in infancy and childhood. Age at death is increasing, suggesting that more affected persons are living to adolescence and adulthood. The racial discrepancies should be investigated to identify opportunities for prevention.
Key Words: heart defects, congenital • vital statistics • race • mortality
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Congenital heart defects (CHDs) are diagnosed in
1 in 100 to 150
newborns.1 2 3
The global impact of CHDs on mortality in the United States in
recent years, however, is unclear. Surgical series on specific CHDs
from selected tertiary
centers4 5 6 7 8
have documented improvements in survival for children with CHDs. Such
studies, however, lack data on persons who did not undergo or did not
survive to surgery. The extent to which findings from selected medical
centers can be generalized to the entire US population is unclear.
Researchers have used a variety of other sources, including death
certificates, to evaluate the contribution of CHDs to
mortality9 in the US
population. No data after 1988 are available, however. We present trends and patterns of mortality from CHDs in the United States for 1979 to 1997. We studied death certificates to determine (1) the extent to which CHDs contributed to mortality at different ages and how that changed over time, (2) which heart defects contributed most to mortality, and (3) whether patterns of mortality differed between races.
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Methods |
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Since 1968, the National Center for Health Statistics has annually compiled data from all death certificates filed in the United States and has made these data available on its Multiple-Cause Mortality Files. These files include demographic and geographic information on the decedent, International Classification of Disease (ICD) codes for the underlying cause of death, and up to 20 conditions listed (after 1979) on the death certificate. The ICD, Ninth Revision (ICD-9), was implemented in 1978. Details on these files and the quality assurance of the data have been published.10
From these multiple-cause mortality files, we determined the number of deaths for which a CHD was noted in the death certificate for 1979 to 1997. We identified records that contained ICD-9 codes 745.0 to 747.4 in the fields for underlying or contributing causes of death. The selected range of codes includes congenital anomalies of the heart and great vessels and excludes anomalies of the peripheral circulatory system. We defined as deaths associated with a CHD the records that had any mention of such codes as a cause of death, and as deaths due to a CHD the subset for which 1 such code was listed as the underlying cause of death.
We calculated the age-specific annual death rates as the
number of deaths per 100 000 population. We used 1970, 1980, and 1990
national census data to calculate intercensal population by age, sex,
and racial groups to estimate the appropriate denominators by such
groups. For infant mortality, we used the number of births as
denominator. We examined the age-specific death rates for the following
groups: <1 year (infants), 1 to 4 years, 5 to 9 years, and then on in
5-year increments up to age 64 years, and 1 group for persons age 
65
years. We examined 3 racial/ethnic groups: whites, blacks, and others.
We studied the following specific groups of heart defects: outflow
tract defects (ICD-9-CM codes 745.0 to 745.2), including common truncus
arteriosus (745.0), transposition of the great arteries (745.1), and
tetralogy of Fallot (745.2); septal defects (745.4 to 745.9, with the
exclusion of 745.0 to 745.2), including ventricular
(745.4), atrial (745.5), and atrioventricular septal
defects (AV canal) (745.6); patent ductus arteriosus (747.0);
coarctation of the aorta (747.1); aortic valve anomalies (746.3 to
746.4); pulmonary valve anomalies (746.0); hypoplastic left
heart syndrome (HLHS) (746.7); and single ventricle (745.3). We
excluded cases of patent ductus arteriosus among infants <37
gestational weeks or weighing <2500 g.
We calculated rates for each year and for 3-year intervals. We computed the average annual percentage change in death rates over the study period as the yearly percent change that, compounded over the total period, would generate the total change. We evaluated time trends using the Cochran-Armitage test11 12 implemented in SAS statistical software (SAS Corp).
Death rates included only deaths for which a CHD was the underlying cause of death. We calculated age at death as an indirect estimate of the survival of persons with CHDs, and for that purpose, we used records with any mention of a CHD (ICD-9 codes 745.0 to 747.4). Age-at-death estimates were truncated at age group 65 to 70 years.
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Results |
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Impact of Heart Defects on Mortality
The multiple-cause mortality files for all ages for 1979 to 1997 contain records for
40.6 million deaths. We
identified 124 832 deaths (0.31%) associated with a CHD. In 76% of
these deaths (94 249, or 0.23% of all), the CHD was the underlying
cause, ie, the death was due to a CHD. Mortality due to a CHD was
highest among infants and children, then declined rapidly and
was stable for persons 15 to 65 years old
(Figure 1
). The mortality due to CHDs was on average 24%
higher among males than among females
(Figure 1, note the logarithmic scale;
Table 1).
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From 1979 through 1997, mortality due to CHDs declined
39.4%, from 2.54 to 1.54 per 100 000, or 1.9% per year
(Figure 2). Deaths associated with CHDs declined from an
annual average of 7169 in 1979 to 1981 to an annual average of 5822 in
1995 to 1997. Approximately half of all deaths associated with or due
to a CHD occurred in infancy. In 1995 to 1997, 1 in 10 infant deaths
(9.8%) were associated with a CHD, and 1 in 13 infant deaths (7.4%)
were due to a CHD (data not shown).
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Mortality from CHDs decreased in nearly all age groups, but
particularly among children <5 years old
(Table 1
). For example, the number of deaths among infants
in 1995 to 1997 was half that recorded in 1979 to 1981. Among
infants, mortality due to CHDs declined gradually, an average 2.7% per
year (38.7% total), during the study period
(Table 1). Among children 1 to 4 years old, the decline was
even greater, 4.5% per year (56.9% total). Mortality was higher among
boys than among girls in both age groups
(Table 1).
Specific Types of Heart Defects
A specific type of heart anomaly was recorded in
>60% of infant deaths due to CHDs
(Table 1).
Mortality varied by type of defect, and for several defects it changed
over time. HLHS was associated with the highest mortality among
infants, 15 per 100 000, remaining high despite a slight decrease
over the study period. Among children age 1 to 4 years, mortality from
HLHS increased (Table 1). Other major
causes of death were outflow tract defects, defects of septal closure,
and coarctation of the aorta. The mortality from most of these defects
declined gradually during the study period (Figure 3). These trends among children age 1 to
4 years were generally similar to those among infants, but mortality
was much lower (Table 1).
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Survival: Trends in Median Age at
Death
The age at death from CHDs increased over the study
period for most defects
(Table 2). The increase in age at death was usually more
notable for the 75th percentile than for the median (50th percentile).
We presented data on several major defects: transposition of
the great arteries and tetralogy of Fallot (as examples of serious and
relatively common cyanotic heart defects), ventricular
septal defects (common defects with usually good prognosis), atrial
septal defects (defects with good survival throughout the study
period), pulmonary and aortic valve anomalies (common defects
with variable prognosis), and HLHS (defect with high mortality).
For most anomalies, with the exception of HLHS, the median age at death
increased considerably, as did the 75th percentile. The median age at
death for all CHDs combined increased by months and the 75th percentile
by years. For ventricular septal defects, the median age at
death increased by 28 years and the 75th percentile by 20 years
(Table 2).
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Racial Disparities
Mortality from CHDs was higher and declined more slowly
among blacks than among whites
(Table 1). In 1995 to 1997, for example, infant mortality
was 19% higher among blacks than among whites (68.4 and 55.5 per
100 000, respectively) and declined more slowly (by 2.1% versus 2.7%
per year, respectively). Such disparity occurred for most types of
heart defects and throughout the study period
(Figure 4).
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In general, the increase in average age at death was more
pronounced among whites than among blacks
(Table 2). These differences did not seem to decrease. For a
number of defects (eg, transposition of the great arteries, tetralogy
of Fallot, ventricular septal defects), blacks died at a
younger age (often approximately half the age of
whites).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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These national, population-based data show that mortality from CHDs declined
40% from 1979 through 1997. Most of
the decline occurred in children <5 years old. This age group,
however, still experiences the highest mortality from CHDs. Mortality
declined for many heart defects, although not equally. For some
defects, such as patent ductus arteriosus and coarctation of the aorta,
the marked mortality decrease in the early part of the study seems to
have leveled off during the last decade. Infant mortality from HLHS has
not decreased much since the mid-1980s. The average age at death from
this defect almost doubled, however, from 0.4 to 0.7 years, suggesting
improved short-term survival. Not only are people dying at a slower rate from CHDs, but deaths also tend to occur progressively later. Although the median age at death is only an indirect indicator of survival, its increase suggests that, overall, survival has improved for people with a CHD. Such improvements, however, did not seem to accrue equally among whites and blacks. Outcomes among blacks appeared generally worse than among whites, regardless of outcome measure (mortality or age at death) and type of heart defect. Moreover, the gap is not closing. The higher death rates among blacks cannot be explained by higher prevalence, because the prevalence of CHDs may actually be lower than among whites.2 13 The causes of these disparities are unknown but could be related to access to health care, rate of complications, or differences in severity of the lesions.
Death rates tended to be higher among boys, particularly during infancy. This can be partially explained by the higher proportion of boys among infants born with serious CHDs such as HLHS, transposition of the great arteries, pulmonary atresia, tricuspid atresia, coarctation of the aorta, and aortic stenosis.14 15
The interpretation of our findings must incorporate the limitations and strengths of the study design and analysis. Although many efforts have been made to improve the quality of data on death certificates, the completeness and accuracy of information are still not ideal. Miscoding and misclassification leading to substantial underreporting16 or overreporting17 have been shown for some diseases. Death certificates may not be a reliable data source for diseases that have a low case-fatality rate18 or for which survival is very long.19 This is not usually the case for CHDs, however. A British study found substantial underreporting of congenital anomalies in stillbirth and neonatal death certificates.20 Underreporting of heart anomalies was also suggested in a US study, particularly when the affected child died soon after birth.2 21 We are unable to estimate the degree of overreporting and underreporting in our data. Nevertheless, time trends and racial comparisons should still be valid, provided that the sensitivity of the system remained the same.
Ideally, to study trends in mortality and survival, the population at risk (persons born with a heart defect) should be identified and followed up over time. Using death certificates instead could lead to spurious results if prevalence or case-fatality ratio varies over time. Decreasing prevalence of CHDs at birth could theoretically account for part of the decrease in mortality. Data from the United States are consistent with an increase, however, rather than a decrease, in reported prevalence of CHDs.3 22 23 Thus, decrease in mortality and increase in age at death are mutually consistent and suggest a real increase in survival.
The major strength of the study was the opportunity to assess national trends. The use of death certificates, which record nearly all deaths, enabled us to assess the impact of CHDs on essentially the entire population, including individuals who do not undergo surgery and thus are not reported in surgical series.
The decline in mortality in this study is not explained by a decrease in number of births, which did not occur, or a decrease in birth rates, which declined only slightly, from 15.6/1000 in 1979 to 14.5/1000 in 1997,24 and which is already incorporated into the computation of infant death rates.
Our findings are consistent with population-based data from the United States and other countries that suggest a significant survival among persons with CHDs.1 25 Reduced mortality probably results from improved diagnostic abilities, enhanced surgical techniques, and advances in intensive care over the past 2 decades. Pregnancy termination is unlikely to have contributed in determining overall trends in heart defect mortality, because the proportion of prenatally diagnosed CHDs still appears to be small in the United States.26 Two further points emerge from these data. First, our findings on racial disparities in mortality suggest that some deaths from CHDs could be preventable. Finding the causes of these disparities will be a crucial step to improve outcomes. Second, the increasing survival of infants and children with CHDs into adolescence and adulthood underscores the need for the healthcare community to prepare for the challenging and often complex needs of adults with CHDs.27 28 For those who reach adulthood, reproductive counseling and carefully tailored pregnancy management may help reduce pregnancy complications and improve pregnancy outcomes. A concerted effort of cardiologists and other specialists is needed to successfully face these challenges and further decrease the burden of congenital heart disease.
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Acknowledgments |
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We thank Michael Atkinson for assisting with statistical programming.
Received August 16, 2000; revision received February 23, 2001; accepted March 3, 2001.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Meberg A, Otterstad JE, Froland G, et al. Outcome of congenital heart defects: a population-based study. Acta Paediatr. 2000;89:1344–1351.[Medline] [Order article via Infotrieve]
2.
Ferencz C, Rubin
JD, McCarter RJ, et al. Congenital heart disease: prevalence at
livebirth. The Baltimore-Washington Infant Study
Am J Epidemiol. 1985;121:31–36.
3. Botto LD, Correa A, Erickson JD. Racial and temporal variations in the prevalence of heart defects. Pediatrics. 2001;107:E32.
4.
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;329:593–599.
5. Moller JH, Anderson RC. 1,000 consecutive children with a cardiac malformation with 26- to 37-year follow-up. Am J Cardiol. 1992;70:661–667.[Medline] [Order article via Infotrieve]
6.
Walsh EP,
Rockenmacher S, Keane JF, et al. Late results in patients with
tetralogy of Fallot repaired during infancy.
Circulation. 1988;77:1062–1067.
7.
Wernovsky G, Mayer
JE Jr, Jonas RA, et al. Factors influencing early and late outcome of
the arterial switch operation for transposition of the
great arteries. J Thorac Cardiovasc
Surg. 1995;109:289–301; discussion
301–302.
8. Cetta F, Feldt RH, O’Leary PW, et al. Improved early morbidity and mortality after Fontan operation: the Mayo Clinic experience, 1987 to 1992. J Am Coll Cardiol. 1996;28:480–486.[Abstract]
9. Gillum RF. Epidemiology of congenital heart disease in the United States. Am Heart J. 1994;127:919–927.[Medline] [Order article via Infotrieve]
10.
Israel RA,
Rosenberg HM, Curtin LR. Analytical potential for multiple
cause-of-death data. Am J
Epidemiol. 1986;124:161–179.
11. Cochran WG. Some methods for strengthening the common chi-square tests. Biometrics. 1954;10:417–454.
12. Armitage P. Test for linear trend in proportions and frequencies. Biometrics. 1955;11:375–386.
13.
Correa-Villasenor
A, McCarter R, Downing J, et al. White-black differences in
cardiovascular malformations in infancy and
socioeconomic factors. The Baltimore-Washington Infant Study Group.
Am J Epidemiol. 1991;134:393–402.
14. Samanek M. Boy:girl ratio in children born with different forms of cardiac malformation: a population-based study. Pediatr Cardiol. 1994;15:53–57.[Medline] [Order article via Infotrieve]
15. Francannet C, Lancaster PA, Pradat P, et al. The epidemiology of three serious cardiac defects: a joint study between five centres. Eur J Epidemiol. 1993;9:607–616.[Medline] [Order article via Infotrieve]
16.
Messite J,
Stellman SD. Accuracy of death certificate completion: the need for
formalized physician training.
JAMA. 1996;275:794–796.
17.
Lloyd-Jones DM,
Martin DO, Larson MG, et al. Accuracy of death certificates for coding
coronary heart disease as the cause of death.
Ann Intern Med. 1998;129:1020–1026.
18.
Kuller LH. The
use of existing databases in morbidity and mortality studies.
Am J Publ Health. 1995;85:1198–1200.
19. Zumwalt RE, Ritter MR. Incorrect death certification: an invitation to obfuscation. Postgrad Med. 1987;81:245–247, 250, 253–254.
20. Duley LM. A validation of underlying cause of death, as recorded by clinicians on stillbirth and neonatal death certificates. Br J Obstet Gynaecol. 1986;93:1233–1235.[Medline] [Order article via Infotrieve]
21. Ferencz C. On the birth prevalence of congenital heart disease. J Am Coll Cardiol. 1990;16:1701–1702.[Medline] [Order article via Infotrieve]
22. Wilson PD, Correa-Villasenor A, Loffredo CA, et al. Temporal trends in prevalence of cardiovascular malformations in Maryland and the District of Columbia, 1981–1988. The Baltimore- Washington Infant Study Group. Epidemiology. 1993;4:259–265.[Medline] [Order article via Infotrieve]
23. Lin AE, Herring AH, Amstutz KS, et al. Cardiovascular malformations: changes in prevalence and birth status, 1972–1990. Am J Med Genet. 1999;84:102–110.[Medline] [Order article via Infotrieve]
24. Ventura SJ, Martin JA, Curtin SC, et al. Births: final data for 1998. National Vital Statistics Reports. 2000;48:1–100.
25.
Morris CD,
Menashe VD. 25-year mortality after surgical repair of congenital heart
defect in childhood: a population-based cohort study.
JAMA. 1991;266:3447–3452.
26. Montana E, Khoury MJ, Cragan JD, et al. Trends and outcomes after prenatal diagnosis of congenital cardiac malformations by fetal echocardiography in a well defined birth population, Atlanta, Georgia, 1990–1994. J Am Coll Cardiol. 1996;28:1805–1809.[Abstract]
27. Perloff JK. Medical center experiences. J Am Coll Cardiol. 1991;18:315–318.[Medline] [Order article via Infotrieve]
28. Somerville J. Near misses and disasters in the treatment of grown-up congenital heart patients. J R Soc Med. 1997;90:124–127. [Medline] [Order article via Infotrieve]
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K. Dimopoulos, D. O. Okonko, G.-P. Diller, C. S. Broberg, T. V. Salukhe, S. V. Babu-Narayan, W. Li, A. Uebing, S. Bayne, R. Wensel, et al. Abnormal Ventilatory Response to Exercise in Adults With Congenital Heart Disease Relates to Cyanosis and Predicts Survival Circulation, June 20, 2006; 113(24): 2796 - 2802. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. G. Berry, C. G. Cowley, C. J. Hoff, and R. Srivastava In-Hospital Mortality for Children With Hypoplastic Left Heart Syndrome After Stage I Surgical Palliation: Teaching Versus Nonteaching Hospitals Pediatrics, April 1, 2006; 117(4): 1307 - 1313. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Thom, N. Haase, W. Rosamond, V. J. Howard, J. Rumsfeld, T. Manolio, Z.-J. Zheng, K. Flegal, C. O'Donnell, S. Kittner, et al. Heart Disease and Stroke Statistics--2006 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee Circulation, February 14, 2006; 113(6): e85 - e151. [Full Text] [PDF]
|
|
|
|
|
|
J. T. Baldwin, H. S. Borovetz, B. W. Duncan, M. J. Gartner, R. K. Jarvik, W. J. Weiss, and T. R. Hoke The National Heart, Lung, and Blood Institute Pediatric Circulatory Support Program Circulation, January 3, 2006; 113(1): 147 - 155. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. A. Boyle and J. F. Cordero Birth Defects and Disabilities: A Public Health Issue for the 21st Century Am J Public Health, November 1, 2005; 95(11): 1884 - 1886. [Full Text] [PDF]
|
|
|
|
 |
|
 L. B Bailey and R. J Berry Folic acid supplementation and the occurrence of congenital heart defects, orofacial clefts, multiple births, and miscarriage Am. J. Clinical Nutrition, May 1, 2005; 81(5): 1213S - 1217S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Moons, K. Van Deyk, W. Budts, and S. De Geest Caliber of Quality-of-Life Assessments in Congenital Heart Disease: A Plea for More Conceptual and Methodological Rigor Arch Pediatr Adolesc Med, November 1, 2004; 158(11): 1062 - 1069. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Connor, R. R. Arons, M. Figueroa, and K. M. Gebbie Clinical Outcomes and Secondary Diagnoses for Infants Born With Hypoplastic Left Heart Syndrome Pediatrics, August 1, 2004; 114(2): e160 - e165. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. E. Lipshultz, L. A. Sleeper, J. A. Towbin, A. M. Lowe, E. J. Orav, G. F. Cox, P. R. Lurie, K. L. McCoy, M. A. McDonald, J. E. Messere, et al. The Incidence of Pediatric Cardiomyopathy in Two Regions of the United States N. Engl. J. Med., April 24, 2003; 348(17): 1647 - 1655. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Strauss and J. E. Lock Pediatric Cardiomyopathy -- A Long Way to Go N. Engl. J. Med., April 24, 2003; 348(17): 1703 - 1705. [Full Text] [PDF]
|
|
|
|
|
|
C. L. Webb, K. J. Jenkins, P. P. Karpawich, A. F. Bolger, R. M. Donner, H. D. Allen, R. J. Barst, and and the Congenital Cardiac Defects Committee of th Collaborative Care for Adults With Congenital Heart Disease Circulation, May 14, 2002; 105(19): 2318 - 2323. [Full Text] [PDF]
|
|
|
|
|
|
J. K Triedman Arrhythmias in adults with congenital heart disease Heart, April 1, 2002; 87(4): 383 - 389. [Full Text] [PDF]
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