Editorial, see p XXXBACKGROUND: More children with congenital heart disease (CHD) are surviving to adulthood, and CHD is associated with risk factors for dementia. We compared the risk of dementia in CHD adults to that of the general population. METHODS:In this cohort study, we used medical registries and a medical record review covering all Danish hospitals to identify adults with CHD diagnosed between 1963 and 2012. These individuals with CHD were followed from January 1, 1981, 30 years of age, or date of first CHD registration (index date for matched members of the general population cohort) until hospital diagnosis of dementia, death, emigration, or end of study (December 31, 2012). For each individual with CHD, we identified 10 members of the general population utilizing the Danish Civil Registration System matched on sex and birth year. We computed cumulative incidences and hazard ratios (HRs) of dementia, adjusting for sex and birth year. RESULTS:The cumulative incidence of dementia was 4% by 80 years of age in 10 632 adults with CHD (46% male). The overall HR comparing adults with CHD with the general population cohort was 1.6 (95% confidence interval [CI], 1.3−2.0). The HR among individuals with CHD without extracardiac defects was 1.4 (95% CI, 1.1−1.8). Adults with mild-to-moderate CHD had an HR of 1.5 (95% CI, 1.1−2.0), whereas the HR was 2.0 (95% CI, 1.2−3.3) for severe CHD, including univentricular hearts. The HR for early onset dementia (<65 years of age) was 2.6 (95% CI, 1.8−3.8), whereas the late-onset HR was 1.3 (95% CI, 1.0−1.8).CONCLUSIONS: CHD was associated with an increased risk of dementia compared with the general population, in particular for early onset dementia. Further understanding of dementia risk in the population with CHD is a potential target for future investigation.
BackgroundLong‐term survival for persons born with congenital heart disease (CHD) is improved, but limited knowledge exists of this growing population's acquired cardiovascular risk profile. This study's purpose was to assess CHD survivors’ risk for type 2 diabetes mellitus (T2DM) with attention to the impact of cyanotic CHD.Methods and ResultsThis population‐based cohort study included Danish subjects with CHD who were born between 1963 and 1980 and were alive at age 30 years. For each CHD case, we identified 10 individuals from the general population matched by sex and birth year, by using the Danish Civil Registration System. Complete follow‐up was obtained through Danish public registries for death, emigration, and T2DM (diagnosis and prescriptions record). We computed cumulative incidences and hazard ratios of developing T2DM after age 30 for 5149 CHD subjects compared with the general population. After adjusting for CHD severity, as well as age, sex, preterm birth, and extracardiac defects, we analyzed the impact of cyanotic compared with acyanotic CHD. By age 45 years, the cumulative incidence of T2DM after age 30 was 4% among subjects with CHD. Subjects with CHD were more likely to develop T2DM than the general population (hazard raio 1.4, 95% CI 1.1–1.6). Subjects CHD who had cyanotic defects were more likely to develop T2DM than were subjects with acyanotic CHD (hazard ratio 1.9, 95% CI 1.1–3.3).Conclusions CHD survivors had an increased risk of developing T2DM after age 30. Patients with cyanotic CHD are at particular risk. Given the cardiovascular health burden of T2DM, attention to its development in CHD survivors seems warranted.
The rate of introduction of neutral mutations is lower in man than in other primates, including the chimpanzee. This species is generally regarded as our closest relative among the great apes. We present here an analysis of sequences of X chromosomal alphoid repetitive DNA from man and the great apes, which supports the closer relationship between man and chimpanzee and indicates a considerably increased rate of recombination in the human repeat DNA. These results indicate that the ‘molecular clock’ is running more quickly in man.
Centromeric alphoid DNA in primates represents a class of evolving repeat DNA. In humans, chromosomes 13 and 21 share one subfamily of alphoid DNA while chromosomes 14 and 22 share another subfamily. We show that similar pairwise homogenizations occur in the chimpanzee (Pan troglodytes), where chromosomes 14 and 22, homologous to human chromosomes 13 and 21, share one partially homogenized alphoid DNA subfamily and chromosomes 15 and 23, homologous to human chromosomes 14 and 22, share another extensively homogenized subfamily. Such a pattern of homogenization presumably predates speciation 3-10 million years ago. However, the alphoid DNA on these human and chimpanzee chromosomes is not orthologous but originates from two evolutionarily different repeat families. It follows that dramatic sequence evolution has occurred in a concerted fashion among the chromosomes in one or both species during or after separation.Molecular data support a view concerning human origins that groups chimpanzees (Pan) and gorillas (Gorilla) with humans rather than with orangutans (Pongo) (1). Orthologous nonrepetitive DNAs share a high overall identity (98%) between humans and the great African apes, whereas analyses of pseudogene DNA sequences and protein structure suggest that humans and chimpanzees are more closely related and diverged from a common ancestor 3-10 million years ago (1-5). High-resolution banding patterns of prophase chromosomes also link humans with chimpanzees (6), but these conclusions have been challenged by recent studies on gene structure (7). Compared to chimpanzee, the human lineage has experienced rapid phenotypic evolution (8) and at the same time has had the lowest mutation rate yet found, 0.1% per million years (3)(4)(5)9). The dramatic morphological changes may therefore be more easily explained by increased frequency of rearrangement of preexisting DNA sequences rather than by fixation of mutations (10).
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