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PubMed1999

Results of 102 cases of complete repair of congenital heart defects in patients weighing 700 to 2500 grams.

BACKGROUND: Published data suggest that low birth weight is a risk factor for poor outcome in corrective surgery for many cardiac defects. Congenital heart defects in low birth weight infants are typically managed with supportive therapy or palliative operations, with definitive repair delayed. The morbidity associated with such approaches is high. METHODS: Since 1990 complete repair of congenital heart defects (other than patent ductus arteriosus) has been performed in 102 infants no larger than 2500 g (median 2100 g, range 700-2500 g), including 16 no larger than 1500 g. Defects included ventricular septal defect (n = 22), tetralogy of Fallot complexes (n = 20), transposition complexes (n = 13), aortic coarctation (n = 12), interrupted arch (n = 10), truncus arteriosus (n = 8), atrioventricular septal defect (n = 6), total anomalous pulmonary venous return (n = 5), and other (n = 6). RESULTS: Preoperative morbidity was more common among patients referred late for surgical correction. There were 10 early deaths (10%) attributable to cardiac failure (n = 4), arrhythmia (n = 1), multiorgan failure (n = 1), sepsis (n = 1), idiopathic coronary artery intimal necrosis (n = 1), foot gangrene (n = 1), and pulmonary hemorrhage (n = 1). No patient had postbypass intracerebral hemorrhage. At follow-up (median 36 months) there were 8 late deaths, and 8 patients underwent 10 reinterventions. There was no evidence of neurologic sequelae attributable to the operation. CONCLUSIONS: In general, delaying repair of congenital heart defects in low birth weight infants does not confer a benefit and is associated with higher preoperative morbidity. Complete repair of both simple and complex lesions can be achieved in such cases with good results. Growth after repair approximates the normal curve for low birth weight infants without heart disease. It is recommended that such infants, especially when they have symptoms, undergo early surgical repair rather than prolonged medical management or other forms of palliation.

Actuarial Analysis↗
PubMed2006

Long-term neuromotor outcome at school entry of infants with congenital heart defects requiring open-heart surgery.

OBJECTIVES: Increased survival in infants with complex congenital heart defects (CHDs) has resulted in greater focus on morbidity. This prospective study was conducted to investigate whether or not neuromotor impairments evident acutely persist long-term. STUDY DESIGN: A total of 94 infants with CHD were reassessed at school entry (age 64.2 +/- 11.3 months) by blinded examiners using the Peabody Developmental Motor Scale and neurologic examination. RESULTS: Neurologic abnormalities were noted in 28.4% of the subjects, with hypotonia and developmental delay most commonly observed. Microcephaly was documented in 15.4% of subjects, with head circumference >50th percentile in only 14.1%. Mean gross and fine motor quotients were shifted downward (82.7 +/- 12.3 and 86.2 +/- 16.3, respectively), and gross and fine motor delays were prevalent (49.4% and 39.0%, respectively). Severe disability was rare (<5%). Predictors of neurologic impairment included type of surgery (palliative/corrective), abnormal postoperative neurologic examination, and presence of microcephaly at initial surgery. Gross motor delay was more likely if palliated. Deep hypothermic circulatory arrest time, palliative surgery, microcephaly, and number of hospitalizations were associated with fine motor delay. CONCLUSIONS: Neurologic impairments and motor delay are common in survivors of open-heart surgery, persisting to age of school entry. Early indicators of medical complications and acute neurologic compromise are associated with increased risk. Early identification and intervention may optimize performance in those at risk.

Cardiac Surgical Procedures↗
PubMed2004

The influence of pulmonary artery morphology on the results of operations for major aortopulmonary collateral arteries and complex congenital heart defects.

OBJECTIVE: Congenital heart defects with major aortopulmonary collateral arteries show marked variability in the size and distribution of native pulmonary arteries. We sought to classify the size and distribution of native pulmonary arteries and to determine their influence on surgical outcome. METHODS: Between 1989 and 2002, 164 patients underwent surgical intervention for congenital heart defects with major aortopulmonary collateral arteries (median age, 10 months). Three patterns of native pulmonary arteries were identified: intrapericardial native pulmonary arteries present (group I); confluent intrapulmonary native pulmonary arteries without intrapericardial native pulmonary arteries (group II); and nonconfluent intrapulmonary native pulmonary arteries (group III). Thirty-seven (23%) patients had single-stage and 76 (47%) patients had multistage complete repair. Thirty (18%) patients await septation, and 8 (5.0%) patients are not septatable. Follow-up is 98% complete (median follow-up, 5.8 years). RESULTS: In the 164 patients there were 15 (9.1%) early and 12 (7.3%) late deaths. Early mortality after complete repair was 4.4% (n = 5). Actuarial survival was 90% +/- 3% and 85% +/- 4% at 1 and 10 years, respectively. Actuarial freedom from surgical or catheter reintervention in septated patients was 77% +/- 4% and 45% +/- 8% at 1 and 10 years, respectively. On multivariate analysis, the morphology of the native pulmonary arteries was the only factor that influenced actuarial survival after complete repair (P =.04). Group III had the highest risk of death after septation (P =.008). Group II fared better than group III after the initial operation (P <.05). CONCLUSIONS: Current classifications of congenital heart defects with major aortopulmonary collateral arteries are based on the presence or absence of intrapericardial pulmonary arteries. We have identified a subgroup without intrapericardial native pulmonary arteries but with confluent intrapulmonary native pulmonary arteries. This group has a better outcome than those with nonconfluent intrapulmonary native pulmonary arteries.

Abnormalities, Multiple↗
PubMed1989

Occurrence of congenital heart defects in siblings of patients with univentricular heart and tricuspid atresia.

Because of the rarity of univentricular heart and tricuspid atresia, no study of a large number of patients has been made to determine the empiric occurrence risks of a congenital heart defect in their siblings. A retrospective chart review was performed of 223 patients with univentricular heart and 113 with classic tricuspid atresia evaluated from 1982 to 1987. Thirty-four patients with univentricular heart and 17 with tricuspid atresia had no siblings and were excluded. Eleven of the total 388 siblings (2.8%) of the 189 patients with univentricular heart had a congenital heart defect. Of the siblings born after the index case of univentricular heart, 7 of 169 (4.1%) had a congenital heart defect. Two of the 210 siblings (1.0%) of the 96 patients with tricuspid atresia had a congenital heart defect. The patients with univentricular heart were subdivided into 4 groups: (1) double-inlet left ventricle; (2) complex univentricular heart with single or common inlet, or with a ventricle of common or right ventricular morphology; (3) complex univentricular heart with asplenia; and (4) complex univentricular heart with polysplenia. One of the 202 siblings (0.5%) of the 102 patients with double-inlet left ventricle had a congenital heart defect, compared with 7 of the 140 siblings (5.0%) of the 69 patients with complex univentricular heart, 1 of the 29 siblings (3.4%) of the 14 patients with complex univentricular heart and asplenia, and 2 of the 7 siblings (28.6%) of the 4 patients with complex univentricular heart and polysplenia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

[Seasonal differences in the occurrence of congenital heart defects].

Incidence of congenital heart defects was studied prospectively in all 664,218 children born in 1977 to 1984. Those suspected of having a heart disease were examined at the center specialized in pediatric cardiology. All children who died were autopsied and those in whom a heart defect was proved were included in our series. In total, 4409 infants (6.64/1000 live births) were born with a heart defect in Bohemia. Differences from one year to another were not statistically significant. The incidence of infants with a heart defect was highest in October, lowest in December, June and July (p less than 0.05). Seasonal incidence of individual forms of heart defects differed as well. The seasonal variation was not influenced by the total number of live births. High incidence of congenital heart defects in infants born in October and November coincides with the epidemics of influenza in early pregnancy.

Czechoslovakia↗
PubMed1999

Atrioventricular canal defect and hypoplastic left heart syndrome as discordant congenital heart defects in twins.

We report on a twin pair presenting with atrioventricular canal defect (AVCD) with right ventricular dominance in one twin, and classic hypoplastic left heart syndrome (HLHS) in the other. According to the developmental-mechanistic approach, AVCDs belong to the group of extracellular matrix abnormalities, whereas classic HLHS is included among flow lesions. Twin pairs with congenital heart defect (CHD) generally have concordant defects by mechanistic group. The occurrence of AVCD and classic HLHS in twins or siblings has never been reported. Interestingly, hypoplasia of the left ventricle is the anatomic characteristic which unifies the discordant CHDs observed in our twins. The occurrence of CHD in both members of the twin pair implies a strong influence of genetic factors. At present, the genetic basis determining the different cardiac phenotypes observed in our twins is unknown. The report of these peculiar associations may be useful to stimulate further studies and shed light on the etiology of CHDs.

Child, Preschool↗
PubMed1989

[Pathologic anatomy of congenital heart defects].

The heart of neonates and infants with marked hypoplastic left- or right-heart-syndrome contains--despite the very low weight in the hypoplastic parts--myocytes of approximately the same size as in the non-hypoplastic ventricular wall. This means that the number of cells is not constant, because in contrast to the regularly developed right and left ventricular walls, the total number of myocytes in the hypoplastic parts is significantly lower. Hypertrophy of the myocardium in congenital heart disease shows histological and ultrastructural findings that are similar to those found in other forms of myocardial hypertrophy. Hypertrophy is reversible after successful surgical correction. However, regression is often incomplete, especially if surgery is delayed until adolescent or adult life. During this time scar formation in the hypertrophic ventricular wall may develop. In addition to these scars, also postoperative scar formation may contribute to the origin of arrhythmias. In hearts with cyanotic and non-cyanotic vitia distances between capillaries and capillary lengths are approximately the same as in normal hearts. Obviously, these parameters are genetically determined.

Arrhythmias, Cardiac↗
PubMed2000

[Heart rhythm variability of healthy newborns with congenital heart defects].

Short-term changes in heart rate (heart rate variability) are seen at every age and represent an important sign of normal homeostatic mechanisms of the cardiovascular system. The influence of premature birth on the maturation of the autonomic nervous system was established by studying heart rate variability in 12 pre-term newborns. The results were compared with a group of 88 full-term newborns and with a group of 14 newborns with congenital heart defects. Heart rate variability was measured by spectral- and time-domain analysis of interbeat intervals in 4-hour continuous ECG recordings. In comparison with full-term newborns, pre-term newborns had significantly lower (p < 0.05) time-domain indices (SDNN = 42.73 vs. 53.38; SDANN-i = 29.84 vs. 35.7) and spectral-domain indices (ULF = 7.91 vs. 10.29; VLF = 20.28 vs. 27.42; LF = 12.57 vs. 16.46). The present results point to a significant influence of gestational age on heart rate variability. Newborns with congenital heart defects present a different pattern of activity of the autonomic nervous system.

Arrhythmias, Cardiac↗
PubMed2000

[Disbiotic conditions in patients operated and reoperated for heart defects and ischemic heart disease].

Bacteriological examination of angiocardiac system, biocenosis of the intestine and upper respiratory tracts was made in 3473 patients who were to be operated or reoperated for congenital or acquired valvular defects in the presence of chroniosepsis and chronic septic endocarditis, complicated IHD. 375 patients with other diseases served control. 74 of them have undergone surgery for varicose veins of the legs. Preoperative contamination with opportunistic microflora was found in the heart, major vessels, veins of the majority of the patients. There was also dysbiosis of natural biotops. Patients with valvular defects to be reoperated 2-20 years after the initial operation on the heart had infection in the angiocardiac structures, severe dysbiosis of natural biotops, i.e. advanced dysbiosis--severe persistent condition with permanent source of endogenic infection complicated the underlying disease and bringing postoperative septic complications.

Adult↗
PubMed1978

Surgery for congenital heart disease in Ibadan. I: Non-cyanotic heart defects.

Congenital heart disease represents about 5% of all cardiovascular diseases in Nigeria today. Its incidence has increased in the last decade because of improved neonatal care, increased awareness and clinical acumen of physicians, better diagnostic tools and the introduction of newer techniques in cardiac catheterization. It is now possible to make the diagnosis with certainty and to define the extent of the pathology thus making it possible to select the appropriate surgical therapy for these children. This article reviews the commonest types of noncyanotic heart disease, the indications for surgery and the types of surgical procedures available in Nigeria today. The simple extracardiac defects, such as patent ductus arteriosus and coarctation of the aorta can be corrected with little or no mortality, but the more complex intracardiac defects can only be palliated pending the introduction of open heart surgery in Nigeria.

Aortic Coarctation↗
PubMed2005

Congenital heart defects and abnormal maternal biomarkers of methionine and homocysteine metabolism.

BACKGROUND: It is well established that folic acid prevents neural tube defects. Although the mechanisms remain unclear, multivitamins containing folic acid may also protect against other birth defects, including congenital heart defects. OBJECTIVE: Our goal was to establish a maternal metabolic risk profile for nonsyndromic congenital heart defects that would enhance current preventive strategies. DESIGN: Using a case-control design, we measured biomarkers of the folate-dependent methionine and homocysteine pathway among a population-based sample of women whose pregnancies were affected by congenital heart defects (224 case subjects) or unaffected by any birth defect (90 control subjects). Plasma concentrations of folic acid, homocysteine, methionine, S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), vitamin B-12, and adenosine were compared, with control for lifestyle and sociodemographic variables. RESULTS: After covariate adjustment, case subjects had higher mean concentrations of homocysteine (P < 0.001) and SAH (P < 0.001) and lower mean concentrations of methionine (P = 0.019) and SAM (P = 0.014) than did control subjects. Vitamin B-12, folic acid, and adenosine concentrations did not differ significantly between case and control subjects. Homocysteine, SAH, and methionine were identified as the most important biomarkers predictive of case or control status. CONCLUSIONS: The basis for the observed abnormal metabolic profile among women whose pregnancies were affected by congenital heart defects cannot be defined without further analysis of relevant genetic and environmental factors. Nevertheless, a metabolic profile that is predictive of congenital heart defect risk would help to refine current nutritional intervention strategies to reduce risk and may provide mechanistic clues for further experimental studies.

Adult↗