Incidence Of Ventricular Septal Defect Research Articles

Clinical Profile and Natural History of Children with Ventricular Septal Defects in Tripoli, Libya from 1996 through 2009

Introduction and Objectives: Ventricular septal defect (VSD) is the most common congenital heart diseases, it accounts 40%. This study carried out to describe the epidemiological characters and clinical presentation of patients with VSD in Western and Southern Libya, and to evaluate spontaneous versus surgical closure in different types.  Patients and Methods It is hospital case series study conducted by reviewing the medical records of 1092 patients followed at cardiology outpatient department (OPD) of Tripoli Children Hospital from 1996 through 2009, the data abstracted from medical records and filed in a worked sheet, Excel and SPSS software used to analyze the data.  Results We identified 1092 patients. The results revealed that 30.9% diagnosed during the first month, and 49.7% from1 to 12 months. From 1092 patients; 50.8% have peri- membranous VSD, 18.8% muscular, and 13% having an apical type. 97.2% of males have peri-membranous VSD where muscular and apical seen more in female, p value = 0.001. Cardiac murmur is the common presenting sign 61.3%, 9.3% have feature of Down syndrome. Positive Family history of CHD in 9.9% with significant relationship between family history and type of VSD (peri- membranous type), P value = 0.001. Small VSDs accounts 66.9%, large VSDs 16.1%, followed by medium size VSD 11.8% of cases. Patients with large VSDs more prone for hospital admission as 101 (57.4%) from 176 patients were admitted to hospital, followed by moderate size (45%), P value = 0.001. 70.3% of patients with large VSD need either medical or surgical treatment, P value = 0.001. Spontaneous closure seen in 17%, 0.6% died, while 41.9% still on follow up. Muscular VSD shows the highest tendency for spontaneous closer as 72% closed by the age of 2 years.  Conclusion We conclude that peri- membranous VSD is the most common type. Two thirds of patients had been diagnosed in the first year of life. Big defects and some of moderate VSDs need either medical or surgical treatment. Spontaneous closer is usually seen in the first 2 years of life.  Recommendations We highly recommend for further multi-center study all over the country to get reliable data on the prevalence of congenital heart diseases and the incidence of ventricular septal defect in our population.

Maternal MTR gene polymorphisms and their interactions with periconceptional folic acid supplementation in relation to offspring ventricular septal defects

To investigate how maternal MTR gene polymorphisms and their interactions with periconceptional folic acid supplementation are associated with the incidence of ventricular septal defects (VSD) in offspring. A case-control study was conducted, recruiting 426 mothers of infants with VSD under one year old and 740 mothers of age-matched healthy infants. A questionnaire survey collected data on maternal exposures, and blood samples were analyzed for genetic polymorphisms. Multivariable logistic regression analysis and inverse probability of treatment weighting were used to analyze the associations between genetic loci and VSD. Crossover analysis and logistic regression were utilized to examine the additive and multiplicative interactions between the loci and folic acid intake. The CT and TT genotypes of the maternal MTR gene at rs6668344 increased the susceptibility of offspring to VSD (P<0.05). The GC and CC genotypes at rs3768139, AG and GG at rs1050993, AT and TT at rs4659743, GG at rs3768142, and GT and TT at rs3820571 were associated with a decreased risk of VSD (P<0.05). The variations at rs6668344 demonstrated an antagonistic multiplicative interaction with folic acid supplementation in relation to VSD (P<0.05). Maternal MTR gene polymorphisms significantly correlate with the incidence of VSD in offspring. Mothers with variations at rs6668344 can decrease the susceptibility to VSD in their offspring by supplementing with folic acid during the periconceptional period, suggesting the importance of periconceptional folic acid supplementation in genetically at-risk populations to prevent VSD in offspring.

Incidence and risk factors of congenital ventricular septal defect in Qingdao

Objective: To analyze the incidence and risk factors of ventricular septal defect (VSD) in Qingdao. Methods: A prospective cohort study design was used to include pregnant women who underwent prenatal screening in Qingdao between August 2018 and June 2020 (the whole population coverage). VSD was diagnosed according to the pulse oxygen saturation and heart auscultation, and the final diagnosis was made according to the echocardiography of VSD positive newborns within postnatal day 7. Results: The study included 115 238 live births, among which 388 were diagnosed as VSD, with an incidence of 3.37‰. The results of multivariate logistic regression analysis showed that mother with postgraduate level (OR=1.61, 95%CI: 1.00-2.58, P=0.049) (compared with junior high school and below), preterm birth history (OR=2.90, 95%CI: 1.47-5.70, P=0.002), and pregnancy history of congenital heart disease (OR=5.98, 95%CI: 2.63-14.73, P<0.001) were risk factors for VSD. Compared with female infants, the overall risk of VSD in male infants was relatively low (OR=0.74, 95%CI: 0.60-0.91, P=0.005). Conclusions: The incidence of VSD in Qingdao is 3.37‰. The risk factors of VSD include higher maternal education level, pregnancy history of congenital heart disease and preterm birth history. Moreover, the overall risk of VSD in male infants is low.

The Incidence of Isolated Ventricular Septal Defect in Libyan Newborns

This study aimed to evaluate the incidence and spontaneous closure of ventricular septal defects in a randomly selected newborn population, using color Doppler echocardiographic screening. Color flow Doppler echocardiographic screening was performed in 635 neonates within the first week of life. Patients with a ventricular septal defect were also followed up for 6 months to detect spontaneous closure rate and its timing. The incidences of a ventricular septal defect in all neonates, preterm neonates, and term neonates were found as 48.8/1,000, 64/1,000, and 48.1/1,000 live births, respectively. Only three patients were symptomatic. 21 cases had a muscular ventricular septal defect and 10 cases had a perimembranous ventricular septal defect. Most of them had a small ventricular septal defect (≤3 mm). Spontaneous closure was observed in 64.5% of ventricular septal defects within 6 months Closure rate was found as 80% for preterm infants and 66.8% for term infants (p&gt;0.05). The incidence of a ventricular septal defect was considerably high in neonates when routine color flow Doppler echocardiographic examination was performed. Despite the increased incidence of ventricular septal defect, spontaneous closure rate was remarkably high within the first 6 months of life. These defects may result from delayed physiologic development and have a good prognosis.

Modern aspects of surgical treatment of post-infarction ventricular septal defect

Determination of the anatomical location of the ventricular septal defect (VSD), one of the complications that may develop after acute myocardial infarction (MI), affects the surgical intervention and surgical success. Improved surgical techniques and heart protection methods, increased anesthesia and reanimation experience with new prosthetic patches have increased the success of surgical intervention in post-MI VSD. Long-term survivals of patients treated surgically have been reported to be better than those who did not undergo surgery. In autopsy studies, the incidence of VSD after acute myocardial infarction is 1-2%. According to epidemiological studies, post-MI VSD occurs more frequently in male patients 65 years of age and older who have a single-vessel disease and who have had an infarction for the first time. Post-MI VSD, which develops because of anterior MI, which constitutes 60% of myocardial infarctions, is the most common anteroapical septum, and VSDs, which are formed because of inferior MI (20-40%), are usually located in the posterior septum. In this study, we investigated the risk factors affecting hospital mortality retrospectively in patients who developed post-MI VSD and operated.

RF31 IS ISOLATED TYPE I VENTRICULAR SEPTAL DEFECT STILL RARE IN ITALIAN POPULATION COMPARED TO ASIAN?

Background: Type I Ventricular Septal Defect (VSD) is less common in Western Countries (5-6% of all VSDs) than in Asia (30% of all VSDs) despite the incidence of VSD is similar (25-30% of all Congenital Heart Defects). In the last 2 years we operated on several isolated Type I VSDs. Methods: A retrospective study reviewing VSDs surgical repair from March 2016 to April 2018 was conducted. In total 14 patients received surgical correction of a isolated VSD. The diagnosis was made primarily on transthoracic 2-dimensional echocardiography,standard cardiac catherization. Patients with associated major cardiovascular anomalies were excluded. The classification of VSD type is according to the nomenclature for VSD reviewed by The Society of Thoracic Surgeons in 2000. Results: In 4 out of 14 patients Type I VSD was identified (28,5%),in 9 Type II (64,3%) and in 1 Type III (7,2%). Focusing on patients with Type I they were all female and surprisingly all Italian with no Asian relatives at all. Age at operation ranged from 2 to 13 months (mean 7,7 mo) and weight ranged from 3,8 to 10 kg (mean 6,8 kg). Surgical repair was done via transpulmonary arterial access. All patients are alive and well with no aortic nor pulmonary valve problems at 24 months of follow up. Conclusions: We are surprised to find out such a incidence of Type I VSD in Italian population. We are fully aware of the weak statistical power of our series so we look forward to propose an Italian multicenter study to verify the hypothesis of a changing incidence of Type I VSD in Italy.

Investigation of the teratogenic potential of VLA-4 antagonist derivatives in rats.

Very late antigen-4 (VLA-4), which is concerned with cell-cell adhesion, plays important roles in development of the heart, and some VLA-4 antagonists cause cardiac anomalies. In this study, we evaluated the teratogenic potential of VLA-4 antagonist derivatives as screening, and investigated the conditions that induce cardiac anomalies. Seventeen compounds were orally administered to pregnant rats throughout the organogenesis period, and fetal examinations were performed. In addition, drug concentrations in the embryos were assayed. As a result, the incidence of ventricular septal defect (VSD) ranged from 0 to 100% depending on the compound. Plasma drug concentrations in the dams were related to increased incidence of VSD; however, these incidences were not increased when the concentration of the compound in the embryos at 24h after dosing was low. It is considered that continuous pharmacological activity in the embryo for more than 24h might disrupt closure of the ventricular septum.

Reproductive and developmental toxicity studies of T-3761 in rats

We carried out reproductive and developmental toxicity studies (i.e. fertility study, teratological study, and perinatal and postnatal study) of T-3761, a new quinolone derivative, in S.D. rats. T-3761 was administered orally at the dose of 60, 300 and 1,500 mg/kg/day as suspension in 5% acacia solution. 1. Fertility study T-3761 was administered to male rats for 9 weeks prior to mating and to female rats for 2 weeks prior to mating and until day 7 of gestation. In parent rats, soft stools, slight depression of body weight gain and increase in water intake were observed at the dose of 1,500 mg/kg. Cecum weight was increased at the dose of 300 mg/kg and more in male and at the dose of 1,500 mg/kg in female. No effects on reproductive performance were discernible in the T-3761 treated groups. In fetuses, external, skeletal and visceral examinations revealed no teratological abnormalities. Slightly retarded ossification, however, was observed at the dose of 1,500 mg/kg. From these findings, the no-effect dose of T-3761 in fertility study was considered to be 300 mg/kg/day for parent rats and fetuses. 2. Teratological study T-3761 was administered from day 7 to day 17 of gestation. In dams, soft stools, transient decrease in food intake, increase in water intake, depression of body weight gain and increase in cecum weight were observed at the dose of 1,500 mg/kg. In fetuses, slight increase in incidence of ventricular septal defect and slightly retarded ossification were observed at the dose of 1,500 mg/kg. In the postnatal examination, there were no effects in the T-3761 treated groups. From these findings, the no-effect dose of T-3761 in teratological study was considered to be 300 mg/kg/day for dams and next generations. 3. Perinatal and postnatal study T-3761 was administered from day 17 of gestation to day 21 of lactation. In dams, cecum weight was increased at the dose of 300 mg/kg and more. And soft stools, transient decrease in food intake, increase in water intake, transient depression of body weight gain and slight extension of gestation period were observed at the dose of 1,500 mg/kg. In the postnatal examination, there were no effects in the T-3761 treated groups. From these findings, the no-effect dose of T-3761 in perinatal and postnatal study was considered to be 300 mg/kg/day for dams and more than 1,500 mg/kg/day for next generations.

Transcatheter closure of a traumatic ventricular septal defect using an amplatzer™ atrial septal occluder device

A relatively rare occurrence, the incidence of ventricular septal defect (VSD) complicating penetrating cardiac trauma has been reported at 4.5%. Closing such defects may be challenging especially in an unstable patient where cardiopulmonary bypass may exponentially increase the surgical risk. In such patients, catheter-based device closure is a reliable and effective alternative. We describe case of a 30 year old man who presented with a stab wound to his anterior mediastinum. His injuries involved laceration to right and left ventricles and a VSD. His lacerations were repaired on a beating heart and the VSD was not addressed due to patient hemodynamic instability. The VSD was semi-electively closed using a 24 mm Amplatzer™ device as the patient demonstrated significant left to right shunt. Post-device closure, the patient developed hemolysis attributed to an intra- device residual leak. The hemolysis resolved without any complications by conservative medical management. At latest follow-up the patient is in NYHA functional class I-II.

Moderately high intake of folic acid has a negative impact on mouse embryonic development

The incidence of neural tube defects has diminished considerably since the implementation of food fortification with folic acid (FA). However, the impact of excess FA intake, particularly during pregnancy, requires investigation. In a recent study, we reported that a diet supplemented with 20-fold higher FA than the recommended intake for rodents had adverse effects on embryonic mouse development at embryonic days (E)10.5 and 14.5. In this report, we examined developmental outcomes in E14.5 embryos after administering a diet supplemented with 10-fold higher FA than recommended to pregnant mice with and without a mild deficiency of methylenetetrahydrofolate reductase (MTHFR). Pregnant mice with or without a deficiency in MTHFR were fed a control diet (recommended FA intake of 2 mg/kg diet for rodents) or an FA-supplemented diet (FASD; 10-fold higher than the recommended intake [20 mg/kg diet]). At E14.5, mice were examined for embryonic loss and growth retardation, and hearts were assessed for defects and for ventricular wall thickness. Maternal FA supplementation was associated with embryonic loss, embryonic delays, a higher incidence of ventricular septal defects, and thinner left and right ventricular walls, compared to mothers fed control diet. Our work suggests that even moderately high levels of FA supplementation may adversely affect fetal mouse development. Additional studies are warranted to evaluate the impact of high folate intake in pregnant women. Birth Defects Research (Part A), 2013. © 2012 Wiley Periodicals, Inc.

Complex Trait Analysis of Ventricular Septal Defects Caused by Nkx2-5 Mutation

The occurrence of a congenital heart defect has long been thought to have a multifactorial basis, but the evidence is indirect. Complex trait analysis could provide a more nuanced understanding of congenital heart disease. We assessed the role of genetic and environmental factors on the incidence of ventricular septal defects (VSDs) caused by a heterozygous Nkx2-5 knockout mutation. We phenotyped >3100 hearts from a second-generation intercross of the inbred mouse strains C57BL/6 and FVB/N. Genetic linkage analysis mapped loci with lod scores of 5 to 7 on chromosomes 6, 8, and 10 that influence the susceptibility to membranous VSDs in Nkx2-5(+/-) animals. The chromosome 6 locus overlaps one for muscular VSD susceptibility. Multiple logistic regression analysis for environmental variables revealed that maternal age is correlated with the risk of membranous and muscular VSD in Nkx2-5(+/-) but not wild-type animals. The maternal age effect is unrelated to aneuploidy or a genetic polymorphism in the affected individuals. The risk of a VSD is not only complex but dynamic. Whereas the effect of genetic modifiers on risk remains constant, the effect of maternal aging increases over time. Enumerable factors contribute to the presentation of a congenital heart defect. The factors that modify rather than cause congenital heart disease substantially affect risk in predisposed individuals. Their characterization in a mouse model offers the potential to narrow the search space in human studies and to develop alternative strategies for prevention.

Spontaneous Closure of a Ventricular Septal Defect in a Horse

Spontaneous Closure of a Ventricular Septal Defect in a Horse

Ventricular septal defect complicating acute myocardial infarction—still an unsolved problem in the invasive treatment era

Post-acute myocardial infarction (AMI) ventricular septal defect (VSD) is a rare but catastrophic complication. The aim of study was to delineate the incidence and risk factors of VSD in patients after AMI treated with successful primary percutaneous coronary intervention (pPCI). In the years 2004-2006, a total of 1835 patients with AMI underwent successful pPCI in our hospital. Thirteen patients (0.71%) developed VSD after pPCI. Mean time of occurrence of VSD was 24.46 ± 9.32 h. Patients with VSD had longer time from the AMI onset to pPCI vs. patients without VSD (7.77 ± 2.83 vs. 4.49 ± 4.45, P<.001). In the VSD group, most of the patients were nonsmokers, had arterial hypertension, and had no previous history of coronary artery disease (CAD). Neither group differed in administered antiplatelet therapy. According to univariate log-regression analysis, the presence of VSD was strongly associated with age >70 years (OR=4.66; P=.007), female gender (OR=5.73; P=.004), anterior infarction (OR=3.86; P=.04), single-vessel CAD (OR=3.74; P=.03), body mass index (BMI) <25 (OR=2.98; P=.04), and left ventricular wall hypertrophy (OR=3.39; P=.03). Our study demonstrated that the incidence of VSD after AMI appears to have declined in patients treated with pPCI. The pathomechanism of VSD in the invasive treatment era is the consequence of several processes and needs further investigation. Advanced age, female gender, anterior infarction, single-vessel CAD, left ventricular wall hypertrophy, and low BMI are strong risk factors of this complication after AMI, which remain invariable over the years.

Methionine synthase reductase deficiency results in adverse reproductive outcomes and congenital heart defects in mice

Low dietary folate and polymorphisms in genes of folate metabolism can influence risk for pregnancy complications and birth defects. Methionine synthase reductase (MTRR) is required for activation of methionine synthase, a folate- and vitamin B12-dependent enzyme. A polymorphism in MTRR (p.I22M), present in the homozygous state in 25% of many populations, may increase risk for neural tube defects. To examine the impact of MTRR deficiency on early development and congenital heart defects, we used mice harboring a gene-trapped (gt) allele in Mtrr. Female mice (Mtrr+/+, Mtrr+/gt, and Mtrrgt/gt) were mated with male Mtrr+/g mice. Reproductive outcomes and cardiac phenotype (presence of defects and myocardial thickness) were assessed at E14.5. Mtrr-deficient mothers had more resorptions and more delayed embryos per litter (resorptions per litter: 0.29±0.13; 1.21±0.41; 1.87±0.38 and delayed embryos per litter: 0.07±0.07; 0.14±0.14; 0.60±0.24 in Mtrr+/+, Mtrr+/gt, and Mtrrgt/gt mothers respectively). Placentae of Mtrrgt/gt mothers were smaller and their embryos were smaller, with myocardial hypoplasia and a higher incidence of ventricular septal defects (VSD) per litter (0; 0.57±0.30; 1.57±0.67 in Mtrr+/+, Mtrr+/gt, and Mtrrgt/gt groups respectively). Embryonic Mtrrgt/gt genotype was associated with reduced embryonic length, reduced embryonic and placental weight, and higher incidence of VSD, but did not affect myocardial thickness or embryonic delay. We conclude that Mtrr deficiency adversely impacts reproductive outcomes and cardiac development in mice. These findings may have implications for nutritional prevention of heart defects, particularly in women with the common MTRR polymorphism.

Non-steroidal anti-inflammatory drugs are not fully safe for fetus: comments on the article Treating common ear problems in pregnancy: what is safe? by Vlastarakos et al.

Sir, I read with great interest an article by Vlastarakos et al. [1] entitled Treating common ear problems in pregnancy: what is safe? The paper was written by clinicians based on information collected from various databases. However, certain interpretations and conclusions regarding non-steroidal anti-inXammatory drugs (NSAIDs) should be clariWed from the teratological point of view. It is true that speciWc NSAIDs, presently known as nonselective cyclooxygenase (COX) inhibitors, have not proven to be human teratogens with the exception of high doses of aspirin [2–5]. However, in a recently published paper by Ofori et al. [5]––conducted on a large (n = 36,387) representative population––a greater risk for all the structural congenital anomalies (OR = 2.21; CI = 1.72–2.85), especially cardiac septal defects (OR = 3.34; CI = 1.87–5.98), was revealed due to the use of NSAIDs. This article is the only fully available document that presents human prenatal toxicity of selective COX-2 inhibitors (COXIBs). It should also be noted that according to Kozer et al. [4] (OR = 2.37; CI = 1.44–3.88) and Martinez-Frias et al. [6] (OR = 3.47), a signiWcantly higher risk of gastroschisis was highly dependent on the use of aspirin along with maternal age and smoking. The above mentioned results were conWrmed by animal data presented in various meta-analyses that showed a higher incidence of ventricular septal defects (VSD), celosomy (gastroschisis, umbilical hernia), and diaphragmatic hernia [7–9]. Additionally, in the case of congenital VSD in rats, an insigniWcantly higher ratio was calculated for ibuprofen (106.5/ 10,000 exposed fetuses) and aspirin (46.26/10,000) when compared with various control groups (4.56–19.72/10,000) [9]. For celosomy, it was found that only aspirin (56.41/ 10,000), as a single drug, signiWcantly increased the risk of abdominal wall defects that in untreated rat populations ranged 0.3–1.54/10,000 [7, 8]. It is worth mentioning that a signiWcant decrease of fetal body weight was noted in COX-inhibitor-exposed groups when compared with corresponding controls [8]. The above Wnding carries importance, because intrauterine growth retardation is one of the most common signs of prenatal toxicity [10], even though it was not revealed in human epidemiological studies for NSAIDs [11]. It is also unclear why there is no information about risk of miscarriage in the article. Epidemiological, retrospective studies showed that NSAIDs increased incidence of fetal death and the results depended on the time of treatment [11]. The risk increased from 1.26 (CI = 0.85–1.87) to 6.99 (CI = 2.75–17.74) when the drugs were used for 10– 12 weeks or just a week before miscarriage, respectively. Even with all the limitation to the study by Nielsen et al. [11], the results are important since they were proved later by Li et al. [12]. The risk was much higher when drugs were used around conception (OR = 5.6; CI = 2.3–13.7) or longer than 1 week (OR = 8.1; CI = 2.8–23.4). Other complications, like the ductus arteriosus constriction with secondary persistent pulmonary hypertension and reduced renal perfusion that led to oligohydramions, were pointed by Vlastarakos et al. [1]. F. Burdan (&) Experimental Teratology Unit of the Human Anatomy Department, Medical University of Lublin, 4 Jaczewskiego Str, 20090 Lublin, Poland e-mail: fb3@wp.pl 1 odds ratio 2 95% conWdence interval

Increasing incidence of ventricular septal defects caused by improved detection rate.

In a population-based study in children born alive during the 10-year period from 1982 to 1991 (n = 22,810), ventricular septal defects (VSDs) were diagnosed in 127 cases, an incidence of 5.6 per 1000. The incidence was significantly higher in the cohort of children born during the 6-year period from 1986 to 1991 than among those born in the preceding 4-year period, 1982-1985 (6.5 and 4.0 per 1000 respectively; p < 0.05). The increase was caused entirely by an increased detection rate of small defects in the muscular part of the interventricular septum after introducing echocardiography as a standard method for investigating suspect congenital heart defects in the neonatal period. This also explained entirely an increase in the total incidence of congenital heart defects to 10.6 per 1000 in the last period from 8.4 per 1000 in the first, although this increase was not significant (p > 0.05). More children born in 1986-1991 had spontaneous closure of their VSDs (75.5%) than those born in 1982-1985 (51.5%) (p < 0.05). In 69.3% of patients the VSDs closed during the first year of life. For the cohort born in 1986-1991, 84.6% of the defects located in the muscular part of the septum closed spontaneously. Small defects in the muscular part of the interventricular septum with spontaneous closure in early life may represent the tail of a normal developmental process, and not defects in the sense of malformations.

Role of second trimester sonography in detecting trisomy 18: A review of 70 cases

To investigate the role of second-trimester sonographic examination in the prenatal diagnosis of trisomy 18. Out of 22,150 fetal chromosomal analyses performed between 1990 and 2004, 70 trisomy 18 fetuses were found. The sonographic findings of this aneuploidy were analyzed. The average maternal age was 32.4 years; the average gestational age was 19.5 weeks. Major anomalies were seen in 61 (87.1%) of the 70 fetuses with trisomy 18; among these, cardiac anomalies were the most common (47.1%), with a 27.1% incidence of ventricular septal defects. Anomalies of the central nervous system were seen in 35.7% of cases; abnormal head shape was the most frequently detected anomaly in this group (12.9%). Fifty-six (80%) of the fetuses had at least 1 minor anomaly; of these, choroid plexus cyst was the most common (38.6%). Increased nuchal fold thickness was detected in 17.1% of cases. The vast majority of trisomy 18 fetuses have sonographically detectable abnormalities in the second trimester. Both the 87.1% frequency of major anomalies and the 80% frequency of minor anomalies are substantially higher than multiple biochemical marker tests could achieve. It was also demonstrated that fetal echocardiography plays a pivotal role in the diagnosis of trisomy 18.

Invited commentary

Invited commentary

The double switch operation with accent on the Senning component

In congenitally corrected transposition (ccTGA) the most common configuration is atrial situs solitus with left ventricular loop and left transposition of the great arteries (SLL). Less common is ccTGA with atrial siti inversus (IDD). In both configurations there is a high incidence of ventricular septal defect, pulmonary stenosis, or atresia and some anatomic abnormality of the morphologic tricuspid valve (mTV). The morphologic right ventricle (mRV) is the systemic ventricle and prone to premature failure, particularly in the presence of early TV regurgitation, atrial arrhythmias conduction defects, and prior surgical ventricular septal defect closure. With a long experience with the Senning operation and then the arterial switch, it seemed feasible that these could be combined in ccTGA to restore the mLV to the systemic circuit. This was first attempted in 1989 by the author and was successful. Many of the more recently graduated congenital heart surgeons have little or no experience with the inflow switch. For this reason, the author was asked to write this article, accenting the technical details of the inflow switch. The author uses the Senning operation, with those modifications needed to accommodate the differences between the morphologic right atrium, conduction system, and quite frequent discordance between the atrial situs and the position of the apex of the heart, in ccTGA as compared with TGA.

Transcatheter Closure of Traumatic Ventricular Septal Defect : An Alternative to Surgery

The incidence of ventricular septal defect (VSD) occurs in up to 4.5% of penetrating cardiac trauma. We report a patient with persistent VSD who underwent surgical repair with significant left-to-right shunt and signs of heart failure. We performed a successful transcatheter closure of the VSD with an Amplatzer septal occluder (AGA Medical Corporation; Golden Valley, MN).