Atrioventricular Valve

A method of measuring the displacement of the atrioventricular (AV) of the left ventricle plane during the cardiac cycle in 71 healthy persons is described. An echocardiographic equipment with two cursors was used. Measurements were performed from four sites in the AV plane situated about 90 degrees apart and corresponding to the septal, anterior, lateral and posterior myocardial walls. The mean displacement during systole was 16 mm towards the apex. There was no significant difference in the recordings from the four sites. The study population was divided into three groups with mean ages 28, 42 and 60 years (group I, II and III). The displacement was significantly smaller in group III compared with groups I and II. Fractional shortening, however, could not demonstrate such a difference. The determination of displacement of the AV plane may imply the introduction of a new and simple method in assessment of left ventricular function.

atrioventricular valve

Results: A total of 1,468 patients who underwent Fontan palliation were identified; complete follow-up data were available for 1,199 patients. Six hundred eighty-six patients had 2 atrioventricular valves, 286 had a single mitral valve, 130 had a common atrioventricular valve, and 97 had a single tricuspid valve. A total of 132 repairs were performed in 110 patients, and 15 replacements were performed in 13 patients. The cumulative incidence of atrioventricular valve failure at 25 years of age for patients with a common atrioventricular, single tricuspid, single mitral, and 2 atrioventricular valves was 56% (95% confidence interval [CI]: 46% to 67%), 46% (95% CI: 31% to 61%), 8% (95% CI: 4% to 12%), and 26% (95% CI: 21% to 30%), respectively. In patients without valve failure, freedom from Fontan failure at 10 and 20 years post-Fontan palliation was 91% (95% CI: 89% to 93%) and 77% (95% CI: 73% to 81%), respectively, compared with 77% (95% CI: 69% to 85%) and 54% (95% CI: 42% to 68%), respectively, in patients with valve failure (hazard ratio: 2.43; 95% CI: 1.74 to 3.39; p

Conclusions: Atrioventricular valve failure occurs frequently in patients undergoing Fontan palliation. Patients with valve failure are twice as likely to have their Fontan circulation fail than those without valve failure.

An atrioventricular septal defect (AVSD) is a heart defect in which there are holes between the chambers of the right and left sides of the heart, and the valves that control the flow of blood between these chambers may not be formed correctly. This condition is also called atrioventricular canal (AV canal) defect or endocardial cushion defect. In AVSD, blood flows where it normally should not go. The blood may also have a lower than normal amount of oxygen, and extra blood can flow to the lungs. This extra blood being pumped into the lungs forces the heart and lungs to work hard and may lead to congestive heart failure.

Infants who have surgical repairs for AVSD are not cured; they might have lifelong complications. The most common of these complications is a leaky mitral valve. This is when the mitral valve does not close all the way so that it allows blood to flow backwards through the valve. A leaky mitral valve can cause the heart to work harder to get enough blood to the rest of the body; a leaky mitral valve might have to be surgically repaired. A child or adult with an AVSD will need regular follow-up visits with a cardiologist (a heart doctor) to monitor his or her progress, avoid complications, and check for other health conditions that might develop as the child gets older. With proper treatment, most babies with AVSD grow up to lead healthy, productive lives.

The atrioventricular septal defect is a congenital cardiac malformation that is characterized by a variable degree of the atrial and ventricular septal defect along with a common or partially separate atrioventricular orifice. Diagnosis of AVSD in fetal life or early neonatal period is essential in order to initiate appropriate medical treatment and to plan early surgical repair. In order to avoid the high morbidity and mortality associated with this condition, it must be promptly diagnosed and treated. This activity reviews the evaluation and treatment of AVSD and highlights the role of the interprofessional team in evaluating and treating patients with this condition.

Objectives:Identify the etiology of atrioventricular septal defects.Outline the evaluation of atrioventricular septal defects.Review the management options available for atrioventricular septal defects.Access free multiple choice questions on this topic.

The atrioventricular septal defect is a congenital cardiac malformation that is characterized by a variable degree of the atrial and ventricular septal defect along with a common or partially separate atrioventricular orifice.[1] A partial atrioventricular septal defect is characterized by an ostium primum atrial septal defect, separate atrioventricular valves with a common junction, an inlet ventricular septal defect, and a cleft mitral valve. Whereas the complete form of the atrioventricular septal defect (AVSD) is characterized by a common atrioventricular valve with ostium primum atrial septal defect and an unrestricted ventricular septal defect of inlet type.[2]

In almost all patients, the atrioventricular septal defect is caused by genetic mutations, and most of the time, it is associated with syndromes. Every six patients with Down syndrome have associated atrioventricular septal defect, and Down syndrome cell adhesion molecule (DSCAM) gene has been described to be associated with an atrioventricular septal defect and other congenital heart diseases in these patients.[4][5]

The other syndromes associated with the atrioventricular septal defect may include CHARGE, Ellis-van-Creveld, Smith-Lemli-Opitz, and 3p. Other than its association with syndromes, gene mutations associated with the atrioventricular septal defect can also be inherited as an autosomal dominant trait. Gestational diabetes and maternal obesity have also been reported to increase the risk of non-syndromic atrioventricular septal defects.[6]

The incidence of an atrioventricular septal defect in the general population has been reported to be 0.24 to 0.31 per 1000 live births.[3] It accounts for 3% of all congenital cardiac malformations.[2] Although both male and female genders are affected equally, one of the studies suggests a female to male ratio of 1.3 to 1.0, especially in patients with Down syndrome.[7]

Endocardial cushions are paired (superior and inferior) mesenchymal structures located in the common atrioventricular canal in the early embryonic period, and there growth is of prime importance in the development of atrioventricular septum and atrioventricular valves.[8] These endocardial cushions fuse at the end of 4 weeks of development and form two atria and two ventricles. Failure of fusion results in a variable degree of the atrioventricular septal defect.

A complete atrioventricular septal defect is characterized by a common atrioventricular valve, ostium primum atrial septal defect and ventricular septal defect of inlet type. It is caused by the complete failure of the endocardial cushions to fuse.[9]

A partial atrioventricular septal defect is characterized by separate atrioventricular valves, an ostium primum atrial septal defect, a ventricular septal defect of inlet type, and cleft mitral valve. It is caused by incomplete fusion of endocardial cushions.[10]

In the complete form of the atrioventricular septal defect, a common atrioventricular valve has five leaflets, including superior bridging, interior bridging, left mural, right mural, and anterosuperior. Rastelli divided complete atrioventricular septal defect into three anatomical subgroups.[11]

Rastelli type A is associated with left-sided obstruction, type C is associated with tetralogy of Fallot and other complex congenital heart diseases, and type B is the least common form of the complete atrioventricular septal defect.

Clinical presentation of atrioventricular septal defects is influenced by the type of atrioventricular septal defect, the magnitude of the intracardiac shunt, and other associated cardiac malformations.[3] In patients with complete atrioventricular septal defect, signs of pulmonary congestion, and right heart failure develop in early infancy due to significant left to right shunt as pulmonary vascular resistance drops after birth. Heart failure and Eisenminger may develop even earlier if these patients have associated atrioventricular valve regurgitation, ventricular imbalance, or coarctation of the aorta.[12]

Patients with the partial atrioventricular septal defect without other complex congenital cardiac malformations and minimal atrioventricular valve regurgitation, usually remain asymptomatic in infancy and early childhood. They are diagnosed on the bases of incidental findings, including pulmonary or tricuspid flow murmur and a fixed splitting due to atrial septal defect.

Antenatal ultrasonography with a four-chamber view is the commonly used diagnostic test for the atrioventricular septal defect. The most common findings include a common atrioventricular valve and a defect in the atrial or ventricular septum. However, the sensitivity of antenatal ultrasound for the atrioventricular septal defect is very low.[13]

Electrocardiogram: The characteristic electrocardiographic findings include a superior axis in the frontal plan, right ventricular hypertrophy, and atrioventricular block. Other findings may include superior p wave axis and partial right bundle branch block.

Cardiac Magnetic Resonance Imaging: Magnetic resonance imaging reveals findings similar to an echocardiogram. It is more accurate in measuring the size of defects and regurgitation fraction through the atrioventricular valve.

It includes diuretics and vasodilators to reduce the preload and afterload to relieve the symptoms associated with pulmonary congestion and heart failure. Associated feeding problems and failure to thrive are managed by tube feeding and providing extra calories. In atrioventricular septal defects, medical treatment is usually directed at optimizing the condition of the patient for surgery.[3] 041b061a72