Original Article
The Epidemiology of Childhood Cardiomyopathy in Australia
N Engl J Med 2003; 348:1639-1646April 24, 2003
- Abstract
Background
The incidence and age distribution of primary cardiomyopathy in children are not well defined. We undertook a population-based, retrospective cohort study in Australia to document the epidemiology of childhood cardiomyopathy.
Methods
We analyzed all cases of primary cardiomyopathy in children who presented between 1987 and 1996 and who were younger than 10 years of age. Children were recruited from multiple sources, and cases of cardiomyopathy were classified according to World Health Organization guidelines.
Results
Over the 10-year period, 314 new cases of primary cardiomyopathy were identified, for an annual incidence of 1.24 per 100,000 children younger than 10 years of age (95 percent confidence interval, 1.11 to 1.38). Dilated cardiomyopathy made up 58.6 percent of cases, hypertrophic cardiomyopathy 25.5 percent, restrictive cardiomyopathy 2.5 percent, and left ventricular noncompaction 9.2 percent of cases. The incidence of all types of cardiomyopathy except restrictive declined rapidly after infancy. In 11 cases (3.5 percent), sudden death was the first symptom. There was a male predominance among children with hypertrophic and unclassified cardiomyopathy. Indigenous children had a higher incidence of dilated cardiomyopathy than nonindigenous children (relative risk, 2.67; 95 percent confidence interval, 1.42 to 4.63) and a higher rate of death as the presenting symptom (16.7 percent vs. 2.6 percent, P=0.02). Lymphocytic myocarditis was present in 25 of 62 children with dilated cardiomyopathy (40.3 percent) who underwent cardiac histologic examination within two months after presentation.
Conclusions
Lymphocytic myocarditis and left ventricular noncompaction are important causes of childhood cardiomyopathy in Australia. The timing and severity of presentation in children with cardiomyopathy are related to the type of cardiomyopathy, as well as to genetic and ethnic factors.
Media in This Article
Figure 1
Echocardiogram Showing Characteristic Features of Left Ventricular Noncompaction Involving the Left Ventricular Free Wall, Apex, and Lower Interventricular Septum.Figure 2
Cumulative Frequency Distribution of Age at Presentation, According to the Type of Cardiomyopathy.Article Activity
- Article
The pediatric cardiomyopathies are an uncommon and heterogeneous group of disorders accounting for about half of all cardiac transplantations in children.1 Studies of childhood cardiomyopathy usually reflect the experience at a single institution2-5 or in a single region.6,7 A better understanding of the epidemiology, causes, and outcomes of childhood cardiomyopathy would facilitate planning and provision of medical services.
The centralization of Australian pediatric tertiary services provides an opportunity to examine the incidence and natural history of rare conditions. This report describes epidemiologic observations from a retrospective, population-based cohort study of all Australian children who presented with cardiomyopathy over a 10-year period.
Methods
Selection of Children
The National Australian Childhood Cardiomyopathy Study includes all children with primary cardiomyopathy who presented between January 1, 1987, and December 31, 1996, and were younger than 10 years of age at presentation. The patients were enrolled by three primary investigators during a series of site visits to all 9 Australian pediatric cardiology centers and 12 additional hospitals caring for children with heart disease. Patients were sought from all Australian adult cardiologists, rural pediatricians, and cardiac transplantation centers. Ethics-committee approval was obtained according to the requirements for each center. At each location, study candidates were recruited from multiple sources, including cardiology and medical-record data bases and echocardiography log books.
The exclusion criteria included congenital heart disease; arrhythmia-induced cardiac dysfunction; Kawasaki's disease; prior exposure to corticosteroids or anthracyclines; a progressive systemic, metabolic, or neuromuscular disease resulting in other severe organ involvement; cardiac dysfunction resulting from abnormalities in other organs; and maternal diabetes or prematurity for children who presented before four weeks of age. The available medical records of each enrolled patient were reviewed, and prospective follow-up was arranged for patients who had not been seen within the preceding 12 months. Death was considered to be the presenting symptom in patients with sudden or unexplained death and no prior symptoms. Australian law requires autopsies to be performed in cases of sudden or unexplained death, and these patients were identified from centralized records compiled by the Australian Bureau of Statistics, with the use of the same diagnostic codes used for hospital medical records.
Classification of Cases
A single observer assigned each patient to a diagnostic category according to the World Health Organization's classification of cardiomyopathy,8 after directly reviewing all available cardiac information. Dilated cardiomyopathy was defined by reduced left ventricular systolic function in the presence of symptoms or a family history of dilated cardiomyopathy, a left ventricular fractional shortening of 20 percent or less in the absence of regional wall-motion abnormalities on echocardiography in asymptomatic patients without a family history, or typical pathological features at autopsy (including lymphocytic myocarditis). Hypertrophic cardiomyopathy was defined by otherwise unexplained septal hypertrophy, left ventricular free-wall hypertrophy, or both (wall thickness more than 2 SD above the normal mean), or a right ventricular free-wall thickness exceeding 4 mm. Restrictive cardiomyopathy was defined by impaired diastolic filling with preserved systolic function and normal ventricular-wall thickness. Unclassified cardiomyopathy comprised all other cases, including those with left ventricular noncompaction.9 Diagnostic features of left ventricular noncompaction included involvement of more than 50 percent of the affected left ventricular segment, based on cardiac imaging or direct examination of the heart. Echocardiographic measurements were normalized according to body-surface area.10 An example of an echocardiogram from a patient with left ventricular noncompaction is shown in Figure 1Figure 1
Echocardiogram Showing Characteristic Features of Left Ventricular Noncompaction Involving the Left Ventricular Free Wall, Apex, and Lower Interventricular Septum.. Available cardiac histologic analyses from all sources were reviewed in a blinded fashion by a pediatric pathologist with cardiac expertise. Lymphocytic myocarditis was defined according to the Dallas criteria.11 A diagnosis of familial cardiomyopathy required at least one affected first- or second-degree relative.Statistical Analysis
Incidence rates were calculated with the use of the age-specific population at risk between 1987 and 1996.12-15 Ninety-five percent confidence intervals for incidence rates were calculated with the use of the Poisson distribution. Data were summarized as frequencies and percentages for categorical data and as medians for the age at presentation. Pearson's chi-square statistic or Fisher's exact test (when expected cell values were less than 5) was used to assess the association between two categorical variables. The Kruskal–Wallis rank-sum test (or the Mann–Whitney test for two groups) was used to compare the ages at presentation among the subgroups. Poisson regression was used to assess trends in the annual incidence of cardiomyopathy. Analyses were performed with the use of Stata software (version 6.0).16 All reported P values are two-sided.
Results
During the 10-year study period, there were 314 new cases of cardiomyopathy: 184 cases of dilated cardiomyopathy (58.6 percent), 80 cases of hypertrophic cardiomyopathy (25.5 percent), 42 cases of unclassified cardiomyopathy (13.4 percent), and 8 cases of restrictive cardiomyopathy (2.5 percent). Of 42 children with unclassified cardiomyopathy, 29 had left ventricular noncompaction (9.2 percent of all cases), 9 had cardiac hypertrophy with initially impaired systolic function, 2 had familial neonatal cardiomyopathy that caused death within hours after delivery, 1 had oncocytic cardiomyopathy, and 1 had left ventricular dysfunction associated with a congenital left ventricular diverticulum.
Incidence of Cardiomyopathy
Table 1Table 1
Annual Incidence of Each Type of Cardiomyopathy, According to the Age at Presentation. shows the annual incidence of each type of cardiomyopathy according to the age at presentation. The incidence of all types except restrictive cardiomyopathy declined markedly with age, with the highest annual incidence that of dilated cardiomyopathy before 12 months of age. There was little regional variation and no evidence of a change over time in the incidence of any type of cardiomyopathy (P=0.88).Presenting Symptoms
Death was the first manifestation of the disease (the presenting symptom) in 11 patients (3.5 percent), including 9 of 184 with dilated cardiomyopathy (4.9 percent), 2 of 42 with unclassified cardiomyopathy (4.8 percent), and none with hypertrophic or restrictive cardiomyopathy (P=0.15). Death as the presenting symptom was significantly more common among indigenous children (3 of 18, 16.7 percent) than among nonindigenous children (6 of 235, 2.6 percent) (P=0.02). There were 61 children whose ethnic origin was unknown, 2 of whom had death as the presenting symptom. Congestive heart failure was the presenting symptom in 165 of 184 children with dilated cardiomyopathy (89.7 percent), 6 of 80 with hypertrophic cardiomyopathy (7.5 percent), 4 of 8 with restrictive cardiomyopathy (50.0 percent), and 31 of 42 with unclassified cardiomyopathy (73.8 percent) (P<0.001).
Age at Presentation
Figure 2Figure 2
Cumulative Frequency Distribution of Age at Presentation, According to the Type of Cardiomyopathy. shows the cumulative frequency distribution of the age at presentation for each type of cardiomyopathy. The median age at presentation was 7.5 months among children with dilated cardiomyopathy, 5.7 months among those with hypertrophic cardiomyopathy, 3.8 months among those with unclassified cardiomyopathy, and 36.0 months among those with restrictive cardiomyopathy (P=0.003 for the overall comparison). In total, 63.4 percent of the patients presented before the age of 12 months.Sex
The association between the type of cardiomyopathy and sex was significant (P=0.001 for the overall comparison). Of the 184 children with dilated cardiomyopathy, 103 were girls (56.0 percent), as were 25 of the 80 children with hypertrophic cardiomyopathy (31.2 percent), 4 of the 8 with restrictive cardiomyopathy (50.0 percent), and 16 of the 42 with unclassified cardiomyopathy (38.1 percent). The last group included seven children with the Barth syndrome,17 an X-linked cardiomyopathy.
Ethnic Group
Table 2Table 2
Annual Incidence of Each Type of Cardiomyopathy According to Whether or Not the Children Were Indigenous. shows the incidence of each type of cardiomyopathy during the study period, according to ethnic background. Indigenous children had an annual incidence of dilated cardiomyopathy that was almost three times as high as that among nonindigenous children (1.52 vs. 0.57 per 100,000 children).Familial Cardiomyopathy
Familial cardiomyopathy was present in 19.7 percent of children. Table 3Table 3
Frequency of a Family History of Cardiomyopathy and Median Age at Presentation. shows the frequency of a family history of cardiomyopathy and the median age at presentation in each subgroup of children with cardiomyopathy. Children with dilated cardiomyopathy were less likely to have a family history of cardiomyopathy (27 of 184, 14.7 percent) than were those with either hypertrophic cardiomyopathy (19 of 80, 23.8 percent) or unclassified cardiomyopathy (15 of 42, 35.7 percent) (P=0.01). Children with familial dilated cardiomyopathy presented significantly earlier than those with nonfamilial dilated cardiomyopathy, and children with familial hypertrophic cardiomyopathy presented significantly later than those with nonfamilial hypertrophic cardiomyopathy.Parental Consanguinity
As a potential marker of recessively inherited conditions, parental consanguinity was documented in 21 of 314 children (6.7 percent), and the parental consanguinity status was unknown in 33 of 314 (10.5 percent). Of those whose status was known, parental consanguinity was present in 14 of 160 with dilated cardiomyopathy (8.8 percent), 2 of 73 with hypertrophic cardiomyopathy (2.7 percent), and 5 of 40 with unclassified cardiomyopathy (12.5 percent) (P=0.20).
Syndromal Malformations
The most common underlying syndrome was Noonan's syndrome, present in 23 of 80 children with hypertrophic cardiomyopathy (28.8 percent). Two siblings with dilated cardiomyopathy had Leber's disease, and there was one case each of Costello's, Beckwith–Wiedemann, and Fukuyama's syndromes. Six children with multiple congenital extracardiac abnormalities (1.9 percent) had no definable syndrome.
Metabolic and Mitochondrial Diseases
Of the 314 children, 28 (8.9 percent) had a metabolic disease etiologically linked to cardiomyopathy. These included a respiratory-chain enzyme deficiency in 10 children, the Barth syndrome in 8, a carnitine transporter defect in 4, and fatty-acid oxidation defects in 4. Seven of the eight children with the Barth syndrome had left ventricular noncompaction, and the eighth had dilated cardiomyopathy. The association between the type of cardiomyopathy and metabolic disease was significant, with 14 of 42 children with unclassified cardiomyopathy (33.3 percent) having a metabolic abnormality, as compared with 12 of 184 with dilated cardiomyopathy (6.5 percent) and 2 of 80 with hypertrophic cardiomyopathy (2.5 percent) (P<0.001). Among the children with unclassified cardiomyopathy, 7 of 9 children with combined myocardial hypertrophy and systolic dysfunction at presentation (77.8 percent) had a metabolic abnormality, as did 7 of 29 with left ventricular noncompaction (24.1 percent). The age at presentation was unrelated to the presence of a metabolic abnormality.
Lymphocytic Myocarditis
Lymphocytic myocarditis was present in 25 of 70 children with dilated cardiomyopathy who underwent cardiac histologic examination (35.7 percent), and in 25 of 62 children who underwent histologic examination within two months after presentation (40.3 percent).
Overall, one of the potential causes listed above was present in 66 of 184 children with dilated cardiomyopathy (35.9 percent), 44 of 80 with hypertrophic cardiomyopathy (55.0 percent), 1 of 8 with restrictive cardiomyopathy (12.5 percent), and 23 of 42 with unclassified cardiomyopathy (54.8 percent).
The proportion of children with dilated cardiomyopathy for which a potential cause was identified was significantly higher among those who underwent cardiac histologic examination within two months after presentation than among those who did not undergo histologic examination (36 of 62 children [58.1 percent] vs. 35 of 114 [30.7 percent], P<0.001).
Discussion
This study documents the incidence and presenting features of childhood cardiomyopathy in a national, population-based cohort. The acquisition of multicenter data was facilitated by the centralization of pediatric specialty services, with 9 pediatric cardiology centers and 21 pediatric cardiologists serving a population of approximately 18 million people. The inclusion of data obtained at autopsy and from children seen by rural physicians and those treating adults ensured as far as possible that the study cohort was representative of the spectrum of children with cardiomyopathy. The uniformity of diagnostic criteria was ensured by having a single cardiologist systematically categorize the cases, reviewing all imaging information and using a single set of normal echocardiographic values. This may well account for the relatively high incidence — 9.2 percent — of left ventricular noncompaction.
There are few published epidemiologic data on childhood cardiomyopathy. Among adults with hypertrophic cardiomyopathy, selection bias may skew outcomes and result in misconceptions about the severity of disease.18
In a population-based epidemiologic study of childhood cardiomyopathy in Finland,19 Arola et al. excluded patients with lymphocytic myocarditis and those who had spontaneous improvement within six months after presentation. Since post-viral cardiomyopathy may not be associated with lymphocytic myocarditis,20 we recruited patients according to the findings at presentation, rather than on the basis of any outcome measure. Grenier et al. have described the North American Pediatric Cardiomyopathy Registry,21 which includes children with progressive neuromuscular or multisystem metabolic diseases. In the North American21 and Finnish19 studies, the criteria for dilated cardiomyopathy included a left ventricular fractional shortening (or ejection fraction) that was less than 2 SD below the normal mean and a left ventricular dimension that was more than 2 SD above the normal mean. We used similar criteria for left ventricular systolic dysfunction in children with symptoms and those with familial dilated cardiomyopathy, but we used a fractional shortening of 20 percent or less as a cutoff point in children with other types of dilated cardiomyopathy so as to minimize the inclusion of asymptomatic patients with borderline or mild left ventricular dysfunction of uncertain clinical significance. Because congestive heart failure is present in 90 percent of children with dilated cardiomyopathy,19 the number of children with sporadic cases who were excluded from our study was probably small.
In our study the annual incidence of cardiomyopathy was 1.24 per 100,000 children younger than 10 years of age. This parallels the incidence of 1.13 per 100,000 in the North American study, reported elsewhere in this issue of the Journal, 22 but exceeds the incidence of 0.74 per 100,000 reported in the Finnish study.19 The exclusion of subjects with self-limiting cardiomyopathy from the Finnish study may explain these differences.
A closer comparison of the three studies can be made with respect to patients presenting before one year of age. For all types of cardiomyopathy, the annual incidence in our study was 7.84 per 100,000 children, as compared with 4.1 per 100,000 in Finland19 and 8.34 per 100,000 in North America.22 The annual incidence of dilated cardiomyopathy was 4.76 per 100,000 children, as compared with 3.8 per 100,000 in the Finnish study.19 Despite the use of similar inclusion criteria, the differences were more marked for infants with hypertrophic cardiomyopathy, with an annual incidence of 1.89 per 100,000 children in our study and 0.26 per 100,000 in the Finnish study.19
In our study, death was the presenting symptom in 4.9 percent of cases of dilated cardiomyopathy and 3.5 percent of all cases. In the Finnish study,19 12 percent of cases were diagnosed at autopsy. Hypertrophic cardiomyopathy is the most common cause of sudden death from cardiac causes in healthy young adults,23 but we found no cases of hypertrophic cardiomyopathy in which death was the presenting symptom. This probably reflects the young age of the study cohort.
Familial cardiomyopathy in our study was related to the age at presentation for both dilated and hypertrophic cardiomyopathy. Over 60 percent of the study population presented before one year of age, and the peak incidence of all types of cardiomyopathy except restrictive cardiomyopathy occurred before the age of three months. This finding is consistent throughout the regional studies6,7,24 and the larger epidemiologic studies.19,22 Dilated cardiomyopathy due to lymphocytic myocarditis25 and some cytoskeletal protein abnormalities26 may develop early in life. In contrast, familial hypertrophic cardiomyopathy due to contractile protein abnormalities usually develops after the first decade.27
Previous studies of cardiomyopathy19,24 have shown increasing rates of both dilated and hypertrophic cardiomyopathy in childhood, in contrast to our findings. Increasing rates of ascertainment might be explained by the increasing use of two-dimensional echocardiography since the early 1980s. Once indigenous or nonindigenous ethnic origin was taken into account, we found no significant regional differences in the Australian population.
We found a preponderance of boys among children with hypertrophic and unclassified cardiomyopathy (68.8 percent and 61.9 percent, respectively). The latter was largely accounted for by the presence of the Barth syndrome, an X-linked condition17 that was strongly associated with left ventricular noncompaction. Similar sex-based differences in hypertrophic cardiomyopathy were also reported in the Finnish19 and North American22 studies.
Despite the small numbers of indigenous children in our study, an increased risk of dilated cardiomyopathy was found in this group (relative risk, 2.67). Indigenous Australian children are also at increased risk for cardiovascular disease and death from rheumatic fever.28 Ethnic differences in the incidence of cardiomyopathy were also found in the North American study.22 Both genetic and environmental factors may contribute to these differences. Decreased availability of health care among indigenous subjects may explain the higher rate of death as a presenting symptom in this group, but it could also have diluted the observed difference in the incidence of cardiomyopathy, owing to the lower rates of diagnosis.
A known or presumed cause was identified in 114 of 314 children (42.7 percent) in our study. Lymphocytic myocarditis was present in 40.3 percent of children with dilated cardiomyopathy who underwent cardiac histologic examination within two months after presentation, increasing the number of cases of dilated cardiomyopathy with a known or probable cause from 30.7 percent to 58.1 percent. These data confirm the importance of lymphocytic myocarditis as a cause of dilated cardiomyopathy in childhood. By comparison, only 10 percent of adults with dilated cardiomyopathy have lymphocytic myocarditis,29 despite evidence of prior echovirus or adenovirus infection, each in approximately 10 to 15 percent of cases.30
Familial cardiomyopathy was ascertained in 19.8 percent of our study subjects and in 23 percent of those in the Finnish study.19 With prospective screening, the incidence of familial cardiomyopathy may have been even higher, owing to the inclusion of more subjects with latent cardiac dysfunction.31 Parental consanguinity, consistent with an autosomal recessive inheritance of cardiomyopathy, was documented in 6.7 percent of the children in our study. Advances in molecular genetics may identify the cause of autosomal recessively inherited cardiomyopathy.32
Retrospective enrollment of patients may have led to incomplete case ascertainment. We attempted to minimize this possibility by using multiple data bases at each center, with the inclusion of patients seen by physicians who treat adults and by rural physicians, and examination of autopsy records. Subjects who were phenotypically negative but genotypically positive for cardiomyopathy were not included, since routine genetic testing was not available at the time of the study.
During the study period, advances in the diagnosis of genetic, infectious, and metabolic abnormalities were gradually incorporated into clinical protocols. Failure to perform all relevant investigations would have limited the diagnostic yield. However, the proportion of cases with an identified cause was at least similar to that in the prospective North American study.22
This national population-based study documents the incidence and presenting features of childhood cardiomyopathy in Australia. The causes of childhood cardiomyopathy are diverse, and most cases are diagnosed in early infancy. As compared with nonindigenous children, indigenous Australian children have a higher incidence of dilated cardiomyopathy and a higher risk of death as the presenting symptom. In children with dilated cardiomyopathy, early cardiac histologic examination significantly increases the diagnostic yield. Left ventricular noncompaction is more common than previously recognized. The type of cardiomyopathy, as well as genetic and ethnic factors, determines the timing and severity of presentation of cardiomyopathy in childhood.
Supported by grants from the Murdoch Children's Research Institute (98001) and the National Heart Foundation of Australia (G98M0159).
We are indebted to Nicki Craze for assistance with data-base management.
Source Information
From the Departments of Cardiology (A.W.N., P.E.F.D., M.C., L.C.W., A.M.D., J.L.W., R.G.W.) and Anatomic Pathology (C.W.C.), Royal Children's Hospital, Melbourne; the Clinical Epidemiology and Biostatistics Unit, Murdoch Children's Research Institute, Melbourne (P.C., J.B.C.); the Departments of General Practice (P.C.) and Paediatrics (J.B.C., S.G.K.), University of Melbourne; and Genetic Health Services, Victoria (S.G.K.) — all in Australia.
Address reprint requests to Dr. Weintraub at the Department of Cardiology, Royal Children's Hospital, Flemington Rd., Parkville, VIC 3052, Australia, or at robert.weintraub@rch.org.au.
Appendix
The National Australian Childhood Cardiomyopathy Study comprises the following medical institutions and physicians: Princess Margaret Hospital for Children, Perth: Dr. J. Ramsay, Dr. L. D'Orsogna; Women's and Children's Hospital, Adelaide: Dr. B. Knight, Dr. M. Richardson; Prince Charles Hospital, Brisbane: Dr. D. Radford, Dr. C. Whight, Dr. A. Galbraith, Dr. R. Justo; Mater Children's Public Hospital, Brisbane: Dr. C. Ward; Children's Hospital at Westmead, Sydney: Dr. G. Sholler, Dr. R. Hawker, Dr. S. Cooper, Dr. K. Lau; Sydney Children's Hospital, Sydney: Dr. O. Jones; John Hunter Children's Hospital, Newcastle: Dr. G. Warner; Royal Children's Hospital, Melbourne: Dr. T. Goh, Dr. B. Edis, Dr. L. Fong; Monash Medical Centre, Melbourne: Professor S. Menahem; other participating physicians include Dr. G. Wheaton, Dr. P. Adams, Dr. R. Jeremy, Dr. R. Fryda, Dr. P. Robinson, and Dr. L. Lee.
- References
References
1
Boucek MM ,Faro A ,Novick RJ ,Bennett LE ,Keck BM ,Hosenpud JD . The Registry of the International Society for Heart and Lung Transplantation: Fourth Official Pediatric Report -- 2000. J Heart Lung Transplant 2001;20:39-52
CrossRef | Web of Science | Medline2
Matitiau A ,Perez-Atayde A ,Sanders SP , et al. Infantile dilated cardiomyopathy: relation of outcome to left ventricular mechanics, hemodynamics, and histology at the time of presentation. Circulation 1994;90:1310-1318
Web of Science | Medline3
Burch M ,Siddiqi SA ,Celermajer DS ,Scott C ,Bull C ,Deanfield JE . Dilated cardiomyopathy in children: determinants of outcome. Br Heart J 1994;72:246-250
CrossRef | Web of Science | Medline4
Yetman AT ,Hamilton RM ,Benson LN ,McCrindle BW . Long-term outcome and prognostic determinants in children with hypertrophic cardiomyopathy. J Am Coll Cardiol 1998;32:1943-1950
CrossRef | Web of Science | Medline5
Rivenes SM ,Kearney DL ,Smith EO ,Towbin JA ,Denfield SW . Sudden death and cardiovascular collapse in children with restrictive cardiomyopathy. Circulation 2000;102:876-882
Web of Science | Medline6
Wiles HB ,McArthur PD ,Taylor AB , et al. Prognostic features of children with idiopathic dilated cardiomyopathy. Am J Cardiol 1991;68:1372-1376
CrossRef | Web of Science | Medline7
Venugopalan P ,Houston AB ,Agarwal AK . The outcome of idiopathic dilated cardiomyopathy and myocarditis in children from the west of Scotland. Int J Cardiol 2001;78:135-141
CrossRef | Web of Science | Medline8
Richardson P ,McKenna W ,Bristow M , et al. Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of Cardiomyopathies. Circulation 1996;93:841-842
CrossRef | Web of Science | Medline9
Chin TK ,Perloff JK ,Williams RG ,Jue K ,Mohrmann R . Isolated noncompaction of left ventricular myocardium: a study of eight cases. Circulation 1990;82:507-513
CrossRef | Web of Science | Medline10
Colan SD ,Parness IA ,Spevak PJ ,Sanders P . Developmental modulation of myocardial mechanics: age- and growth-related alterations in afterload and contractility. J Am Coll Cardiol 1992;19:619-629
CrossRef | Web of Science | Medline11
Aretz HT ,Billingham ME ,Edwards WD , et al. Myocarditis: a histopathologic definition and classification. Am J Cardiovasc Pathol 1987;1:3-14
Medline12
Estimated resident population by sex and age, states and territories of Australia, June 1987 to June 1992. Canberra: Australian Bureau of Statistics, 1993 (catalog no. 3201.0).
13
Population by age and sex, Australian states and territories, June 1992 to June 1997. Canberra: Australian Bureau of Statistics, 1997 (catalog no. 3201.0).
14
Experimental estimates of the Aboriginal and Torres Strait Islander population, June 1986 to June 1991. Canberra: Australian Bureau of Statistics, 1994 (catalog no. 3230.0).
15
Experimental estimates of the Aboriginal and Torres Strait Islander population, 30 June 1991–30 June 1996. Canberra: Australian Bureau of Statistics, 1998 (catalog no. 3230.0).
16
Stata statistical software: release 6.0. College Station, Tex.: Stata Corporation, 1999.
17
Ades LC ,Gedeon AK ,Wilson MJ , et al. Barth syndrome: clinical features and confirmation of gene localisation to distal Xq28. Am J Med Genet 1993;45:327-334
CrossRef | Web of Science | Medline18
Spirito P ,Chiarella F ,Carratino L ,Berisso MZ ,Bellotti P ,Vecchio C . Clinical course and prognosis of hypertrophic cardiomyopathy in an outpatient population. N Engl J Med 1989;320:749-755
Full Text | Web of Science | Medline19
Arola A ,Jokinen E ,Ruuskanen O , et al. Epidemiology of idiopathic cardiomyopathies in children and adolescents: a nationwide study in Finland. Am J Epidemiol 1997;146:385-393
Web of Science | Medline20
Martin AB ,Webber S ,Fricker FJ , et al. Acute myocarditis: rapid diagnosis by PCR in children. Circulation 1994;90:330-339
Web of Science | Medline21
Grenier MA ,Osganian SK ,Cox GF , et al. Design and implementation of the North American Pediatric Cardiomyopathy Registry. Am Heart J 2000;139:S86-S95
CrossRef | Web of Science | Medline22
Lipshultz SE ,Sleeper LA ,Towbin JA , et al. The incidence of pediatric cardiomyopathy in two regions of the United States. N Engl J Med 2003;348:1647-1655
Full Text | Web of Science | Medline23
Maron BJ ,Thompson PD ,Puffer JC , et al. Cardiovascular preparticipation screening of competitive athletes: a statement for health professionals from the Sudden Death Committee (clinical cardiology) and Congenital Cardiac Defects Committee (cardiovascular disease in the young), American Heart Association. Circulation 1996;94:850-856
Web of Science | Medline24
Ferencz C ,Neill CA . Cardiomyopathy in infancy: observations in an epidemiologic study. Pediatr Cardiol 1992;13:65-71
CrossRef | Web of Science | Medline25
Nugent AW ,Davis AM ,Kleinert S ,Wilkinson JL ,Weintraub RG . Clinical, electrocardiographic, and histologic correlations in children with dilated cardiomyopathy. J Heart Lung Transplant 2001;20:1152-1157
CrossRef | Web of Science | Medline26
Bowles NE ,Bowles KR ,Towbin JA . The “final common pathway“ hypothesis and inherited cardiovascular disease: the role of cytoskeletal proteins in dilated cardiomyopathy. Herz 2000;25:168-175
CrossRef | Web of Science | Medline27
Maron BJ . Hypertrophic cardiomyopathy: a systematic review. JAMA 2002;287:1308-1320
CrossRef | Web of Science | Medline28
Carapetis JR ,Currie BJ . Mortality due to acute rheumatic fever and rheumatic heart disease in the Northern Territory: a preventable cause of death in aboriginal people. Aust N Z J Public Health 1999;23:159-163
CrossRef | Web of Science | Medline29
Mason JW ,O'Connell JB ,Herskowitz A , et al. A clinical trial of immunosuppressive therapy for myocarditis: The Myocarditis Treatment Trial Investigators. N Engl J Med 1995;333:269-275
Full Text | Web of Science | Medline30
Pauschinger M ,Bowles NE ,Fuentes-Garcia FJ , et al. Detection of adenoviral genome in the myocardium of adult patients with idiopathic left ventricular dysfunction. Circulation 1999;99:1348-1354
Web of Science | Medline31
Michels VV ,Moll PP ,Miller FA , et al. The frequency of familial dilated cardiomyopathy in a series of patients with idiopathic dilated cardiomyopathy. N Engl J Med 1992;326:77-82
Full Text | Web of Science | Medline32
Olson TM ,Karst ML ,Whitby FG ,Driscoll DJ . Myosin light chain mutation causes autosomal recessive cardiomyopathy with mid-cavitary hypertrophy and restrictive physiology. Circulation 2002;105:2337-2340
CrossRef | Web of Science | Medline
- Citing Articles (105)
Citing Articles
1
Jeffrey A. Towbin. 2012. Cardiomyopathies. , 826-854.
CrossRef2
R. J. Ing, W. A. Ames, N. A. Chambers. (2012) Paediatric cardiomyopathy and anaesthesia. British Journal of Anaesthesia 108:1, 4-12
CrossRef3
Anna Sabaté Rotés, Mireia del Toro Riera, Dimpna C. Albert Brotons, José Antonio Arranz Amo, Antonio Carrascosa Lezcano, Josep Girona Comas. (2011) Miocardiopatía en niños con errores innatos del metabolismo: descripción de 12 casos. Medicina Clínica 137:13, 596-599
CrossRef4
Jean-Charles Pierre-Yves, Li Yue-Jin, Nan Chang-Long, Huang Xu-Pei. (2011) Insights into restrictive cardiomyopathy from clinical and animal studies. Journal of Geriatric Cardiology 8:3, 168-183
CrossRef5
Joshua J. Blinder, Hugo R. Martinez, William J. Craigen, John Belmont, Ricardo H. Pignatelli, John L. Jefferies. (2011) Noncompaction of the left ventricular myocardium in a boy with a novel chromosome 8p23.1 deletion. American Journal of Medical Genetics Part A 155:9, 2215-2220
CrossRef6
Ola A. Elmasry, Terez B. Kamel, Naglaa F. El-Feki. (2011) Pediatric cardiomyopathies over the last decade. Journal of the Egyptian Public Health Association 86:3 and 4, 63-67
CrossRef7
James D. Wilkinson, Jonathan P. Zebrowski, Juanita A. Hunter, George A. Mensah, Majid Ezzati, Mohammad H. Forouzanfar, Steven D. Colan, Jeffrey A. Towbin, Daphne T. Hsu, Ana O. Mocumbi, Charles E. Canter, Robert G. Weintraub, Michael Burch, Steven E. Lipshultz. (2011) Assessing the global and regional impact of primary cardiomyopathies: The Global Burden of Diseases, Injuries and Risk Factors (GBD 2010) Study. Progress in Pediatric Cardiology 32:1, 55-63
CrossRef8
M. Juhani Junttila, Agustin Castellanos, Heikki V. Huikuri, Robert J. Myerburg. (2011) Risk markers of sudden cardiac death in standard 12-lead electrocardiograms. Annals of Medicine1-16
CrossRef9
E. Oechslin, R. Jenni. (2011) Left ventricular non-compaction revisited: a distinct phenotype with genetic heterogeneity?. European Heart Journal 32:12, 1446-1456
CrossRef10
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CrossRef11
S.R. Foerster, C.E. Canter. (2011) Contemporary etiology, outcomes, and therapy in pediatric myocarditis. Progress in Pediatric Cardiology 31:2, 123-128
CrossRef12
David N. Rosenthal, Gregory B. Hammer. (2011) Cardiomyopathy and heart failure in children: anesthetic implications. Pediatric Anesthesia 21:5, 577-584
CrossRef13
George A. Porter, Jennifer R. Hom, David L. Hoffman, Rodrigo A. Quintanilla, Karen L. de Mesy Bentley, Shey-Shing Sheu. (2011) Bioenergetics, mitochondria, and cardiac myocyte differentiation. Progress in Pediatric Cardiology 31:2, 75-81
CrossRef14
Robert G. Weintraub, Alan W. Nugent, Andrew Davis, Ingrid King, Tara Bharucha, Piers E.F. Daubeney. (2011) Presentation, echocardiographic findings and long-term outcomes in children with familial dilated cardiomyopathy. Progress in Pediatric Cardiology 31:2, 119-122
CrossRef15
Annette Y. Schure, Barry D. Kussman. (2011) Pediatric heart transplantation: demographics, outcomes, and anesthetic implications*. Pediatric Anesthesia 21:5, 594-603
CrossRef16
Hugo R. Martinez, John W. Belmont, William J. Craigen, Michael D. Taylor, John L. Jefferies. (2011) Left ventricular noncompaction in Sotos syndrome. American Journal of Medical Genetics Part A 155:5, 1115-1118
CrossRef17
Yakup Ergul, Kemal Nisli, Muhammet Ali Varkal, Naci Oner, Memduh Dursun, Aygun Dindar, Umrah Aydogan, Rukiye Eker Omeroglu. (2011) Electrocardiographic Findings at Initial Diagnosis in Children with Isolated Left Ventricular Noncompaction. Annals of Noninvasive Electrocardiology 16:2, 184-191
CrossRef18
HuiJuan Lv, Evis Havari, Sheena Pinto, Raju V.S.R.K. Gottumukkala, Lizbeth Cornivelli, Khadir Raddassi, Takashi Matsui, Anthony Rosenzweig, Roderick T. Bronson, Ross Smith, Anne L. Fletcher, Shannon J. Turley, Kai Wucherpfennig, Bruno Kyewski, Myra A. Lipes. (2011) Impaired thymic tolerance to α-myosin directs autoimmunity to the heart in mice and humans. Journal of Clinical Investigation 121:4, 1561-1573
CrossRef19
Alexandra Menchise. (2011) Myocarditis in the Setting of RSV Bronchiolitis. Fetal & Pediatric Pathology 30:1, 64-68
CrossRef20
Jin Hee Oh, Young Mi Hong, Jae Young Choi, Soo Jin Kim, Jo Won Jung, Sejung Sohn, Myung Chul Hyun, Chung Il Noh, Joo Won Lee, In Sook Park. (2011) Idiopathic Cardiomyopathies in Korean Children. Circulation Journal 75:9, 2228-2234
CrossRef21
Hugo R. Martinez, Mary C. Niu, V. Reid Sutton, Ricardo Pignatelli, Matteo Vatta, John L. Jefferies. (2011) Coffin-Lowry syndrome and left ventricular noncompaction cardiomyopathy with a restrictive pattern. American Journal of Medical Genetics Part An/a-n/a
CrossRef22
Josef Finsterer. (2010) Left ventricular non-compaction and its cardiac and neurologic implications. Heart Failure Reviews 15:6, 589-603
CrossRef23
Susan W. Denfield, Steven A. Webber. (2010) Restrictive Cardiomyopathy in Childhood. Heart Failure Clinics 6:4, 445-452
CrossRef24
Daphne T. Hsu, Charles E. Canter. (2010) Dilated Cardiomyopathy and Heart Failure in Children. Heart Failure Clinics 6:4, 415-432
CrossRef25
James D. Wilkinson, David C. Landy, Steven D. Colan, Jeffrey A. Towbin, Lynn A. Sleeper, E. John Orav, Gerald F. Cox, Charles E. Canter, Daphne T. Hsu, Steven A. Webber, Steven E. Lipshultz. (2010) The Pediatric Cardiomyopathy Registry and Heart Failure: Key Results from the First 15 Years. Heart Failure Clinics 6:4, 401-413
CrossRef26
Kalim U. Aziz, Najma Patel, Tareen Sadullah, Habiba Tasneem, Hasina Thawerani, Saeed Talpur. (2010) Acute viral myocarditis: role of immunosuppression: a prospective randomised study. Cardiology in the Young 20:05, 509-515
CrossRef27
Uwe Kühl, Heinz-Peter Schultheiss. (2010) Myocarditis in Children. Heart Failure Clinics 6:4, 483-496
CrossRef28
Shi Wei Yang, Marc-Phillip Hitz, Gregor Andelfinger. (2010) Ventricular septal defect and restrictive cardiomyopathy in a paediatric TNNI3 mutation carrier. Cardiology in the Young 20:05, 574-576
CrossRef29
Brian Feingold, Gaurav Arora, Steven A. Webber, Kenneth J. Smith. (2010) Cost-Effectiveness of Implantable Cardioverter-Defibrillators in Children With Dilated Cardiomyopathy. Journal of Cardiac Failure 16:9, 734-741
CrossRef30
Sravanthi Nagavalli, James L. Vacek. (2010) Approach to Incidentally Diagnosed Isolated Ventricular Noncompaction of Myocardium. Southern Medical Journal 103:7, 662-668
CrossRef31
Gerhard K. Wolf, Michael A. Frakes, Michael Gallagher, Catherine K. Allan, Suzanne K. Wedel. (2010) Management of Suspected Myocarditis During Critical-Care Transport. Pediatric Emergency Care 26:7, 512-517
CrossRef32
Kenneth T.E. Chang, Glenn P. Taylor, Wendy S. Meschino, Paul F Kantor, Ernest Cutz. (2010) Mitogenic cardiomyopathy. Human Pathology 41:7, 1002-1008
CrossRef33
Marla C Levine, Darren Klugman, Stephen J Teach. (2010) Update on myocarditis in children. Current Opinion in Pediatrics 22:3, 278-283
CrossRef34
Gabriella Captur, Petros Nihoyannopoulos. (2010) Left ventricular non-compaction: Genetic heterogeneity, diagnosis and clinical course. International Journal of Cardiology 140:2, 145-153
CrossRef35
Thomas E Callis, Brian C Jensen, Karen E Weck, Monte S Willis. (2010) Evolving molecular diagnostics for familial cardiomyopathies: at the heart of it all. Expert Review of Molecular Diagnostics 10:3, 329-351
CrossRef36
Giuseppe Limongelli, Giuseppe Pacileo, Roberta Ancona, Giuseppina Eusebio, Antonello D'Andrea, Massimo Romano, Giovanni Di Salvo, Alessandra Rea, Paolo Calabró, Giampaolo Romano, Ciro Maiello, Raffaele Calabró. (2010) Clinical Course and Risk Profile in Adolescents With Idiopathic Dilated Cardiomyopathy. The American Journal of Cardiology 105:5, 716-720
CrossRef37
I. Ostman-Smith, A. Wisten, E. Nylander, E.-L. Bratt, A. d.-W. Granelli, A. Oulhaj, E. Ljungstrom. (2010) Electrocardiographic amplitudes: a new risk factor for sudden death in hypertrophic cardiomyopathy. European Heart Journal 31:4, 439-449
CrossRef38
Akash R Patel, Robert E Shaddy. (2010) Role of β-blocker therapy in pediatric heart failure. Pediatric Health 4:1, 45-58
CrossRef39
Cesare M. Terracciano, Leslie W. Miller, Magdi H. Yacoub. (2010) Contemporary Use of Ventricular Assist Devices. Annual Review of Medicine 61:1, 255-270
CrossRef40
Darren Klugman, John T. Berger, Craig A. Sable, Jianping He, Sachin G. Khandelwal, Anthony D. Slonim. (2010) Pediatric Patients Hospitalized with Myocarditis: A Multi-Institutional Analysis. Pediatric Cardiology 31:2, 222-228
CrossRef41
Lori A. Blauwet, Leslie T. Cooper. (2010) Myocarditis. Progress in Cardiovascular Diseases 52:4, 274-288
CrossRef42
Aris Lacis, Inta Bergmane, Valts Ozolins, Inguna Lubaua, Valerija Groma, Elina Ligere, Eriks Jakobsons, Andrejs Erglis. (2010) First Results of using Stem Cell Transplantation for Pediatric Patients in Case of Dilated Cardiomyopathy. Acta Chirurgica Latviensis 10:2, 76-79
CrossRef43
Indrani S. Bhattacharya, Marc Dweck, Andrew Gardner, Mark Jones, Mark Francis. (2010) Isolated Ventricular Noncompaction Syndrome in a Nigerian Male: Case Report and Review of the Literature. Cardiology Research and Practice 2010, 1-5
CrossRef44
Mark Lewin. (2010) Left Ventricular Noncompaction: Travelling the Road from Diagnosis to Outcomes. Journal of the American Society of Echocardiography 23:1, 54-57
CrossRef45
Juan Pablo Kaski, Perry Elliott. 2010. Cardiomyopathies. , 1003-1034.
CrossRef46
Anne I. Dipchand, David C. Naftel, Brian Feingold, Robert Spicer, Delphine Yung, Beth Kaufman, James K. Kirklin, Tina Allain-Rooney, Daphne Hsu. (2009) Outcomes of Children With Cardiomyopathy Listed for Transplant: A Multi-institutional Study. The Journal of Heart and Lung Transplantation 28:12, 1312-1321
CrossRef47
Laurie E. Profitlich, Brian Kirmse, Melissa P. Wasserstein, George A. Diaz, Shubhika Srivastava. (2009) High prevalence of structural heart disease in children with cblC-type methylmalonic aciduria and homocystinuria. Molecular Genetics and Metabolism 98:4, 344-348
CrossRef48
Richard Kirk, David Naftel, Timothy M. Hoffman, Christopher Almond, Gerard Boyle, Randall L. Caldwell, James K. Kirklin, Kirstie White, Anne I. Dipchand. (2009) Outcome of Pediatric Patients With Dilated Cardiomyopathy Listed for Transplant: A Multi-institutional Study. The Journal of Heart and Lung Transplantation 28:12, 1322-1328
CrossRef49
Sudhir Vashist, Gautam K. Singh. (2009) Acute myocarditis in children: Current concepts and management. Current Treatment Options in Cardiovascular Medicine 11:5, 383-391
CrossRef50
Stefan Rupp, Jürgen Bauer, Torsten Tonn, Volker Schächinger, Stefanie Dimmeler, Andreas M. Zeiher, Dietmar Schranz. (2009) Intracoronary administration of autologous bone marrow-derived progenitor cells in a critically ill two-yr-old child with dilated cardiomyopathy. Pediatric Transplantation 13:5, 620-623
CrossRef51
Luca Ragni, Elena Biagini, Fernando M. Picchio, Daniela Prandstraller, Ornella Leone, Alessandra Berardini, Antonella Perolo, Francesco Grigioni, Lara di Diodoro, Gaetano Gargiulo, Eloisa Arbustini, Claudio Rapezzi. (2009) Heart transplantation in infants with idiopathic hypertrophic cardiomyopathy. Pediatric Transplantation 13:5, 650-653
CrossRef52
V Tsang, M Yacoub, S Sridharan, M Burch, R Radley-Smith, A Khaghani, B Savoldo, PJ Amrolia. (2009) Late donor cardiectomy after paediatric heterotopic cardiac transplantation. The Lancet 374:9687, 387-392
CrossRef53
M. Papadakis, S. Basavarajaiah, J. Rawlins, C. Edwards, J. Makan, S. Firoozi, L. Carby, S. Sharma. (2009) Prevalence and significance of T-wave inversions in predominantly Caucasian adolescent athletes. European Heart Journal 30:14, 1728-1735
CrossRef54
A. Garnier, G. Girod. (2009) Cardiac re-synchronization therapy in a patient with isolated ventricular non-compaction: a case report. European Journal of Echocardiography 10:5, 713-715
CrossRef55
STEVEN ZANGWILL, ROBERT HAMILTON. (2009) Restrictive Cardiomyopathy. Pacing and Clinical Electrophysiology 32, S41-S43
CrossRef56
Carline Koh, Pui-Wah Lee, Tak-Cheung Yung, Kin-Shing Lun, Yiu-Fai Cheung. (2009) Left Ventricular Noncompaction in Children. Congenital Heart Disease 4:4, 288-294
CrossRef57
Antonios A Pantazis, Perry M Elliott. (2009) Left ventricular noncompaction. Current Opinion in Cardiology 24:3, 209-213
CrossRef58
Cooper, Leslie T. Jr., . (2009) Myocarditis. New England Journal of Medicine 360:15, 1526-1538
Full Text59
Olufemi Jaiyesimi, Mohamed Kasem. (2009) Clinical profiles and outcomes for Omani children with dilated cardiomyopathy seen in a regional referral hospital. Cardiology in the Young 19:02, 145
CrossRef60
Iris Schrijver, Lynn M. Pique, Ilana Traynis, Curt Scharfe, Amy J. Sehnert. (2009) Mitochondrial DNA analysis by multiplex denaturing high-performance liquid chromatography and selective sequencing in pediatric patients with cardiomyopathy. Genetics in Medicine 11:2, 118-126
CrossRef61
Charles B. Huddleston. (2009) Indications for heart transplantation in children. Progress in Pediatric Cardiology 26:1, 3-9
CrossRef62
Mitsuhiro Kamisago, Takashi Ohkubo, Makoto Watanabe, Ei Ikegami, Ryuji Fukazawa, Shunichi Ogawa. (2009) Two Cases of Restrictive Cardiomyopathy in Children. Journal of Nippon Medical School 76:6, 313-318
CrossRef63
J. Mangat, C. Carter, G. Riley, Y. Foo, M. Burch. (2009) The clinical utility of brain natriuretic peptide in paediatric left ventricular failure. European Journal of Heart Failure 11:1, 48-52
CrossRef64
Andrea Badertscher, Urs Bauersfeld, Urs Arbenz, Matthias R. Baumgartner, Albert Schinzel, Christian Balmer. (2008) Cardiomyopathy in newborns and infants: a broad spectrum of aetiologies and poor prognosis. Acta Paediatrica 97:11, 1523-1528
CrossRef65
Paul R. Lurie. (2008) The perspective of ventricular noncompaction as seen by a nonagenarian. Cardiology in the Young 18:03,
CrossRef66
J.-D. Fine, M. Hall, M. Weiner, K.-P. Li, C. Suchindran. (2008) The risk of cardiomyopathy in inherited epidermolysis bullosa. British Journal of Dermatology???-???
CrossRef67
Mark A. Walsh, Lee N. Benson, Anne I. Dipchand, Andrew N. Redington, Christopher A. Caldarone, Glen S. Van Arsdell, Paul F. Kantor. (2008) Surgical Repair of the Mitral Valve in Children With Dilated Cardiomyopathy and Mitral Regurgitation. The Annals of Thoracic Surgery 85:6, 2085-2088
CrossRef68
Morita, Hiroyuki, Rehm, Heidi L., Menesses, Andres, McDonough, Barbara, Roberts, Amy E., Kucherlapati, Raju, Towbin, Jeffrey A., Seidman, J.G., Seidman, Christine E., . (2008) Shared Genetic Causes of Cardiac Hypertrophy in Children and Adults. New England Journal of Medicine 358:18, 1899-1908
Full Text69
James D. Wilkinson, Lynn A. Sleeper, Jorge A. Alvarez, Natalya Bublik, Steven E. Lipshultz. (2008) The Pediatric Cardiomyopathy Registry: 1995–2007. Progress in Pediatric Cardiology 25:1, 31-36
CrossRef70
Gabriel Somarriba, Jason Extein, Tracie L. Miller. (2008) Exercise rehabilitation in pediatric cardiomyopathy. Progress in Pediatric Cardiology 25:1, 91-102
CrossRef71
Shaji C. Menon, Timothy M. Olson, Virginia V. Michels. (2008) Genetics of familial dilated cardiomyopathy. Progress in Pediatric Cardiology 25:1, 57-67
CrossRef72
Steven A. Webber. (2008) Primary restrictive cardiomyopathy in childhood. Progress in Pediatric Cardiology 25:1, 85-90
CrossRef73
RICHARD ING, WARWICK AMES. (2008) Children with sick hearts: towards anesthesia safety. Pediatric Anesthesia 18:3, 195-197
CrossRef74
David S. Crossland, Katy Edmonds, Doris Rassl, Fiona Black, John H. Dark, Jon Smith, John J. O’Sullivan. (2008) Histology of the explanted hearts of children transplanted for dilated cardiomyopathy. Pediatric Transplantation 12:1, 85-90
CrossRef75
Renee Margossian. (2008) Contemporary management of pediatric heart failure. Expert Review of Cardiovascular Therapy 6:2, 187-197
CrossRef76
Gerald F. Cox. (2007) Diagnostic approaches to pediatric cardiomyopathy of metabolic genetic etiologies and their relation to therapy. Progress in Pediatric Cardiology 24:1, 15-25
CrossRef77
Tracie L. Miller, Daniela Neri, Jason Extein, Gabriel Somarriba, Nancy Strickman-Stein. (2007) Nutrition in pediatric cardiomyopathy. Progress in Pediatric Cardiology 24:1, 59-71
CrossRef78
A. J. Bograd, S. Mital, J. C. Schwarzenberger, R. S. Mosca, J. M. Quaegebeur, L. J. Addonizio, D. T. Hsu, J. M. Lamour, J. M. Chen. (2007) Twenty-Year Experience With Heart Transplantation for Infants and Children With Restrictive Cardiomyopathy: 1986–2006. American Journal of Transplantation 0:0, 071105081616015-???
CrossRef79
Jasveer Mangat, Tracy Lunnon-Wood, Philip Rees, Martin Elliott, Michael Burch. (2007) Successful cardiac transplantation in Barth syndrome - single-centre experience of four patients. Pediatric Transplantation 11:3, 327-331
CrossRef80
Edward K. Rhee, Charles E. Canter, Susan Basile, Steven A. Webber, David C. Naftel. (2007) Sudden Death Prior to Pediatric Heart Transplantation: Would Implantable Defibrillators Improve Outcome?. The Journal of Heart and Lung Transplantation 26:5, 447-452
CrossRef81
Vitor Manuel P. Azevedo, Marco Aurelio Santos, Francisco M. Albanesi Filho, M'árcia B. Castier, Bernardo R. Tura, Jose Geraldo C. Amino. (2007) Outcome factors of idiopathic dilated cardiomyopathy in children – a long-term follow-up review. Cardiology in the Young 17:02, 175
CrossRef82
Christian Kranz, Christoph Jungeblut, Jonas Denecke, Anne Erlekotte, Christina Sohlbach, Volker Debus, Hans Gerd Kehl, Erik Harms, Anna Reith, Sonja Reichel, Helfried Gröbe, Gerhard Hammersen, Ulrich Schwarzer, Thorsten Marquardt. (2007) A Defect in Dolichol Phosphate Biosynthesis Causes a New Inherited Disorder with Death in Early Infancy. The American Journal of Human Genetics 80:3, 433-440
CrossRef83
Marina L. Hughes, Bendix Carstensen, James L. Wilkinson, Robert G. Weintraub. (2007) Angiographic diagnosis, prevalence and outcomes for left ventricular noncompaction in children with congenital cardiac disease. Cardiology in the Young 17:01, 56
CrossRef84
Reiner Buchhorn, Andreas Eicken, Hans Peter Gildein, Joachim Kreuder, Thomas Paul, Achim A. Schmaltz, Ingram Schulze-Neick. 2007. Erkrankungen des Herzens. , 917-965.
CrossRef85
Hong Ryang Kil. (2007) The myocarditis and cardiomyopathy in children. Korean Journal of Pediatrics 50:11, 1049
CrossRef86
Lara Shekerdemian, Desmond Bohn. (2006) Acute viral myocarditis: Epidemiology and pathophysiology. Pediatric Critical Care Medicine 7:Supplement, S2-S7
CrossRef87
JEFFREY A. TOWBIN, NEIL E. BOWLES. (2006) Dilated Cardiomyopathy: A Tale of Cytoskeletal Proteins and Beyond. Journal of Cardiovascular Electrophysiology 17:8, 919-926
CrossRef88
Benito Morentin, M. Paz Suárez-Mier, Beatriz Aguilera, Andrés Bodegas. (2006) Mortalidad por enfermedades del miocardio en niños y jóvenes. Estudio observacional de base poblacional. Revista Española de Cardiología 59:3, 238-246
CrossRef89
L. T. Cooper, R. Virmani, N. M. Chapman, A. Frustaci, R. J. Rodeheffer, M. W. Cunningham, D. M. McNamara. (2006) National Institutes of Health-Sponsored Workshop on Inflammation and Immunity in Dilated Cardiomyopathy. Mayo Clinic Proceedings 81:2, 199-204
CrossRef90
Leslie T. Cooper. (2005) The natural history and role of immunoadsorption in dilated cardiomyopathy. Journal of Clinical Apheresis 20:4, 256-260
CrossRef91
Eric C. Hoppa, John C. Brancato. (2005) Dilated Cardiomyopathy in a 7-Year-Old Girl. Pediatric Emergency Care 21:11, 767-769
CrossRef92
L. Silva Melchor, J. Ortigosa Aso, L. Alonso Pulpón. (2005) Miocardiopatía hipertrófica. Medicine - Programa de Formación Médica Continuada Acreditado 9:42, 2790-2798
CrossRef93
Charles E. Canter. (2005) Therapy for pediatric myocarditis. Current Treatment Options in Cardiovascular Medicine 7:5, 411-417
CrossRef94
Sivasubramonian Sivasankaran, Gurleen K. Sharland, John M. Simpson. (2005) Dilated cardiomyopathy presenting during fetal life. Cardiology in the Young 15:4, 409-416
CrossRef95
Robert M. Freedom, Shi-Joon Yoo, Don Perrin, Glenn Taylor, Steffen Petersen, Robert H. Anderson. (2005) The morphological spectrum of ventricular noncompaction. Cardiology in the Young 15:4, 345-364
CrossRef96
Hemmi N. Bhagavan, Raj K. Chopra. (2005) Potential role of ubiquinone (coenzyme Q10) in pediatric cardiomyopathy. Clinical Nutrition 24:3, 331-338
CrossRef97
Karla R Bowles, Neil E Bowles. (2004) Genetics of inherited cardiomyopathies. Expert Review of Cardiovascular Therapy 2:5, 683-697
CrossRef98
Anna E. Tsirka, Kathryn Trinkaus, Su-Chiung Chen, Steven E. Lipshultz, Jeffrey A. Towbin, Steven D. Colan, Vernat Exil, Arnold W. Strauss, Charles E. Canter. (2004) Improved outcomes of pediatric dilated cardiomyopathy with utilization of heart transplantation. Journal of the American College of Cardiology 44:2, 391-397
CrossRef99
Josef Finsterer, Claudia Stöllberger. (2004) Left ventricular noncompaction requires the neurologist. Journal of the American Society of Echocardiography 17:7, 811-812
CrossRef100
Sulafa K.M Ali. (2004) Reply. Journal of the American Society of Echocardiography 17:7, 812
CrossRef101
Perry Elliott, William J McKenna. (2004) Hypertrophic cardiomyopathy. The Lancet 363:9424, 1881-1891
CrossRef102
J. Kreuder. (2004) Kardiomyopathien. Monatsschrift Kinderheilkunde 152:6, 620-631
CrossRef103
R. Santer. (2004) Metabolische Kardiomyopathien. Monatsschrift Kinderheilkunde 152:6, 639-648
CrossRef104
Lipshultz, Steven E., Sleeper, Lynn A., Towbin, Jeffrey A., Lowe, April M., Orav, E. John, Cox, Gerald F., Lurie, Paul R., McCoy, Kristina L., McDonald, Melissa A., Messere, Jane E., Colan, Steven D., . (2003) The Incidence of Pediatric Cardiomyopathy in Two Regions of the United States. New England Journal of Medicine 348:17, 1647-1655
Full Text105
Strauss, Arnold, Lock, James E., . (2003) Pediatric Cardiomyopathy — A Long Way to Go. New England Journal of Medicine 348:17, 1703-1705
Full Text
