Objective We sought to determine if maternal bupropion treatment in early pregnancy is associated with congenital heart defects in the infant. Study Design We conducted a retrospective case-control ...study of birth defects risk factors. Data on 6853 infants with major heart defects were compared with 5869 control infants born in 1997–2004. Bupropion exposure was defined as any reported use between 1 month before and 3 months after conception. Results Mothers of infants with left outflow tract heart defects were more likely to have reported taking bupropion than mothers of control infants (adjusted odds ratio, 2.6; 95% confidence interval, 1.2–5.7; P = .01). Conclusion We identified a positive association between early pregnancy bupropion use and left outflow tract heart defects; however, the magnitude of the observed increased risk was small. Nevertheless, further studies are needed to confirm these results.
Objective The purpose of this study was to examine the risk of birth defects in relation to diabetes mellitus and the lack of use of periconceptional vitamins or supplements that contain folic acid. ...Study Design The National Birth Defects Prevention Study (1997-2004) is a multicenter, population-based case-control study of birth defects (14,721 cases and 5437 control infants). Cases were categorized into 18 types of heart defects and 26 noncardiac birth defects. We estimated odds ratios for independent and joint effects of preexisting diabetes mellitus and a lack of periconceptional use of vitamins or supplements that contain folic acid. Results The pattern of odds ratios suggested an increased risk of defects that are associated with diabetes mellitus in the absence vs the presence of the periconceptional use of vitamins or supplements that contain folic acid. Conclusion The lack of periconceptional use of vitamins or supplements that contain folic acid may be associated with an excess risk for birth defects due to diabetes mellitus.
Although several studies describe the 22q11.2 deletion, population-based data are scant. Such data are needed to evaluate properly the impact, distribution, and clinical presentation of the deletion ...in the population. Our goals were to assess the population-based birth prevalence of the 22q11.2 deletion and its associated phenotype and its impact on the occurrence of heart defects.
We evaluated data on infants who were born from 1994 through 1999 to women who resided in metropolitan Atlanta. We matched records from the Metropolitan Atlanta Congenital Defects Program (a population-based registry with active case ascertainment), the Sibley Heart Center at Children's Healthcare of Atlanta, and the Division of Medical Genetics at Emory University. We used birth certificate data for the denominators of the rates.
We identified 43 children with laboratory-confirmed 22q11.2 deletion among 255 849 births. The overall prevalence was 1 in 5950 births (95% confidence interval: 1 in 4417 to 1 in 8224 births). The prevalence was between 1 in 6000 and 1 in 6500 among whites, blacks, and Asians and 1 in 3800 among Hispanics. Most affected children (81%) had a heart defect, and many (1 in 3) had major extracardiac defects (other than velopalatal anomalies), including anomalies of the central nervous system. Overall, the deletion contributed to at least 1 of every 68 cases of major heart defects identified in the total birth cohort and, in particular, to 1 of every 2 cases diagnosed with interrupted aortic arch type B, 1 of every 5 with truncus arteriosus, and 1 of every 8 with tetralogy of Fallot.
The 22q11.2 deletion was common in this birth population. The clinical phenotype included a wide and variable spectrum of major cardiac and extracardiac anomalies. From these population-based data, one can estimate that at least 700 affected infants are born annually in the United States. Population-based estimates such as these should be useful to medical professionals and policy makers in planning for the optimal care of people with the 22q11.2 deletion.
Objective To examine associations between maternal reports of prenatal fever or influenza and congenital heart defects (CHDs), and to evaluate whether those associations varied with antipyretic use. ...Study design We analyzed case infants with CHD (n = 2361) and control infants without CHD (n = 3435) from the Baltimore-Washington Infant Study (1981-1989). Participating mothers were asked whether they experienced a “fever of 101°F or higher,” had “influenza (flu),” or used an antipyretic agent (ie, acetaminophen, salicylate, or nonsteroidal anti-inflammatory drug) during the period extending from 3 months before pregnancy through the end of the third month of pregnancy. We used logistic regression to compute ORs and 95% CIs while controlling for potential confounders. Results There were significant associations between fever and influenza and specific CHDs, namely right-sided obstructive defects (fever: OR, 2.04; 95% CI, 1.27 to 3.27; influenza: OR, 1.75; 95% CI, 1.16 to 2.62) and atrioventricular septal defects in infants with Down syndrome (fever: OR, 1.92; 95% CI, 1.10 to 3.38; influenza: OR, 1.66; 95% CI, 1.04 to 2.63). Maternal antipyretic use in the setting of fever or influenza tended to decrease these associations. Conclusions Prenatal maternal fever or influenza may be associated with right-sided obstructive lesions in all infants and with atrioventricular septal defects in infants with Down syndrome. The use of antipyretics might attenuate such associations.
Background Visceral adipose tissue (VAT) is associated with incident heart failure (HF) and HF with preserved ejection fraction, yet it is unknown how pericardial and abdominal adiposity affect HF ...and mortality risks in Black individuals. We examined the associations of pericardial adipose tissue (PAT), VAT, and subcutaneous adipose tissue (SAT) with incident HF hospitalization and all‐cause mortality in a large community cohort of Black participants. Methods and Results Among the 2882 Jackson Heart Study Exam 2 participants without prevalent HF who underwent body computed tomography, we used Cox proportional hazards models to examine associations between computed tomography–derived regional adiposity and incident HF hospitalization and all‐cause mortality. Fully adjusted models included demographics and cardiovascular disease risk factors. Median follow‐up was 10.6 years among participants with available VAT (n=2844), SAT (n=2843), and PAT (n=1386). Fully adjusted hazard ratios (95% CIs) of distinct computed tomography–derived adiposity measures (PAT per 10 cm 3 , VAT or SAT per 100 cm 3 ) were as follows: for incident HF, PAT 1.08 (95% CI, 1.02–1.14) and VAT 1.04 (95% CI, 1.01–1.08); for HF with preserved ejection fraction, PAT 1.13 (95% CI, 1.04–1.21) and VAT 1.07 (95% CI, 1.01–1.13); for mortality, PAT 1.07 (95% CI, 1.03–1.12) and VAT 1.01 (95% CI, 0.98–1.04). SAT was not associated with either outcome. Conclusions High PAT and VAT, but not SAT, were associated with incident HF and HF with preserved ejection fraction, and only PAT was associated with mortality in the fully adjusted models in a longitudinal community cohort of Black participants. Future studies may help understand whether changes in regional adiposity improves HF, particularly HF with preserved ejection fraction, risk predictions. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT00005485.
To determine whether insulin resistance (IR) measured by homeostasis model of insulin resistance (HOMA-IR) can further stratify diabetes risk in African Americans (AAs) beyond obesity and identify ...obese, low risk and non-obese, high risk individuals.
Using the Jackson Heart Study cohort, we categorized participants without diabetes into four phenotypes: non-obese/insulin-sensitive, non-obese/IR, obese/insulin-sensitive and obese/IR. Obesity was defined as BMI ≥ 30 or BMI 25–30 plus an increased waist circumference. IR was defined as HOMA-IR ≥ 2. We used modified Poisson regression models to estimate the incident risk-ratios (IRR) of diabetes across these phenotypes adjusting for potential confounders and HbA1c.
Among 3219 AAs without diabetes, 14.0% were non-obese/insulin-sensitive, 24.6% non-obese/IR, 6.2% obese/insulin-sensitive, and 55.3% obese/IR. The overall crude incidence rate of diabetes was 29.91 cases/1000 person-years. In fully-adjusted models, compared to the non-obese/insulin-sensitive group, the relative risk of diabetes was highest in obese/IR (IRR = 2.35; 95% CI: 1.53, 3.60), followed by non-obese/IR (IRR = 1.59; 95% CI: 1.02, 2.46), and non-significant for the obese/insulin-sensitive (IRR = 1.70; 95% CI: 0.97, 2.99) group.
HOMA-IR can further stratify diabetes risk in AA adults beyond obesity, identifying non-obese high-risk and lower-risk obese individuals. However, diabetes risk should still be carefully monitored in obese populations despite insulin sensitivity.
Objective The purpose of this study was to examine associations between prepregnancy body mass index (BMI) and congenital heart defects (CHDs). Study Design These analyses included case infants with ...CHDs (n = 6440) and liveborn control infants without birth defects (n = 5673) enrolled in the National Birth Defects Prevention Study (1997-2004). Results Adjusted odds ratios for all CHDs combined were 1.16 (95% confidence interval CI, 1.05–1.29), 1.15 (95% CI, 1.00–1.32), and 1.31 (95% CI, 1.11–1.56) for overweight status, moderate obesity, and severe obesity, respectively. Phenotypes associated with elevated BMI (≥25.0 kg/m2 ) were conotruncal defects (tetralogy of Fallot), total anomalous pulmonary venous return, hypoplastic left heart syndrome, right ventricular outflow tract (RVOT) defects (pulmonary valve stenosis), and septal defects (secundum atrial septal defect). Conclusion These results corroborated those of previous studies and suggested new associations between obesity and conotruncal defects and RVOT defects.
In the Atherosclerosis Risk in Communities (ARIC) Study and Jackson Heart Study (JHS) cohorts, serum potassium (K) is an independent predictor of diabetes risk, particularly among African-American ...participants. Experimental studies show that serum K levels affects insulin secretion. The KCNJ11 gene encodes for a K channel that regulates insulin secretion and whose function is affected by serum K levels. Variants in KCNJ11 are associated with increased diabetes risk. We hypothesized that there could be a gene-by-environment interaction between KCNJ11 variation and serum K on diabetes risk.
Evaluating a combined cohort of ARIC and JHS participants, we sought to determine if KCNJ11 variants are risk factors for diabetes; and if KCNJ11 variants modify the association between serum K and diabetes risk. Among participants without diabetes at baseline, we performed multivariable logistic regression to determine the effect of serum K, KCNJ11 variants, and their interactions on the odds of incident diabetes mellitus over 8-9 years in the entire cohort and by race.
Of 11,812 participants, 3220 (27%) participants developed diabetes. 48% and 47% had 1 or 2 diabetes risk alleles of rs5215 and rs5219, respectively. Caucasians had higher proportions of these risk alleles compared to African Americans (60% vs 17% for rs5215 and 60% vs 13% for rs5219, p<0.01). Serum K was a significant independent predictor of incident diabetes. Neither rs5215 nor rs5219 was associated with incident diabetes. In multivariable models, we found no statistically significant interactions between race and either rs5215 or rs5219 (P-values 0.493 and 0.496, respectively); nor between serum K and either rs5215 or rs5219 on odds of incident diabetes (P-values 0.534 and 0.687, respectively).
In this cohort, rs5215 and rs5219 of KCNJ11 were not significant predictors of incident diabetes nor effect modifiers of the association between serum K and incident diabetes.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Documenting the prevalence and trends of congenital heart defects provides useful data for pediatric practice, health-care planning, and causal research. Yet, most population-based studies use data ...from the 1970s and 1980s. We sought to extend into more recent years the study of temporal and racial variations of heart defects occurrence in a well-defined population.
We used data from the Metropolitan Atlanta Congenital Defects Program, a population-based registry with active case ascertainment from multiple sources. Heart defects were identified among liveborn infants up to 1 year old, among stillborn infants, and among pregnancy terminations to mothers residing in metropolitan Atlanta.
From 1968 through 1997, the registry ascertained 5813 major congenital heart defects among 937 195 infants, for a prevalence of 6.2 per 1000. The prevalence increased to 9.0 per 1000 births in 1995 through 1997. The prevalence of ventricular septal defects, tetralogy of Fallot, atrioventricular septal defects, and pulmonary stenosis increased, whereas that of transposition of the great arteries decreased. For some defects, prevalence and trends varied by race.
The prevalence of congenital heart defects is increasing. Whereas most findings likely result from improved case ascertainment and reporting, others might be because of changes in the distribution of risk factors in the population. The basis of the racial variations is incompletely understood.