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Ventricular Septal Disease


A ventricular septal defect (VSD) is a type of heart malformation present at birth or congenital heart disease (CHD). The heart with a VSD has a hole in the wall (the septum) between its two lower chambers (the ventricles).
VSD is a hole in the wall (septum) separating the ventricles of the heart. VSD is the most common type of heart malformation present at birth (congenital

heart disease).
VSD lets blood shunt from the left ventricle to the right ventricle. VSD can overwork the heart. VSD can cause excess pressure in the blood vessels to the lungs (pulmonary

VSD, if small, usually needs no treatment. VSD, if large, needs medical management and then surgery to repair the VSD. VSD generally has an excellent long-term outlook.

How common is a VSD? CHD is the most frequent class of major congenital malformations (birth defects). CHD affects conservatively 8 per 1,000 newborns. VSD, in turn, is the most common type of CHD, accounting for 25-30% of all CHD. Thus, at least 2 per 1,000 babies is born with a VSD, one baby in every 500. What is the normal design of the heart? Normally the two ventricles are completely separated from each other. Blood from the right ventricle flows under relatively low pressure to the lungs where it receives oxygen. The blood then comes back to the heart where it is pumped by the left ventricle under relatively high pressure through the aorta into the body. Predisposing & Risk Factors - Birth defects - Congenital heart defects - Coronary angiogram - Genetics Tube partitioning process does not occur completely (leaving an opening in the ventricular septum) - defect in a gene - a chromosome abnormality The heart is forming during the first 8 weeks of fetal development. It begins as a hollow tube, then partitions within the tube develop that eventually become the septa (or walls) dividing the right side of the heart from the left. Ventricular septal defects occur when the partitioning process does not occur completely, leaving an opening in the ventricular septum. Some congenital heart defects may have a genetic link, either occurring due to a defect in a gene, a chromosome abnormality, or environmental exposure, causing heart problems to occur more often in certain families. Most ventricular septal defects occur sporadically (by chance), with no clear reason for their development. Signs & Symptoms:

fatigue sweating rapid breathing heavy breathing congested breathing disinterest in feeding, or tiring while feeding (infants) poor weight gain

Diagnostic Procedures: chest x-ray, ECG, Echocardiogram, Cardiac Catherization Medical Management
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digoxin - a medication that helps strengthen the heart muscle, enabling it to pump more efficiently. diuretics - the body's water balance can be affected when the heart is not working as well as it could. These medications help the kidneys remove excess fluid from the body.

How do VSDs cause problems? When there is a VSD, the two ventricles are not separate. Blood from the left ventricle shunts through the septal defect into the right ventricle because of the difference in pressures between the ventricles. The right ventricle has to do extra work to handle the additional blood. It may have trouble keeping up with the load and enlarge. The lungs receive too much blood under too much pressure. The arterioles (small arteries) in the lungs thicken up in response to the excess blood under excess pressure. Permanent vascular damage can be done to the lungs. It makes a considerable difference whether the VSD is small or large. How is a small VSD treated? A third to a half of all small VSDs close spontaneously (on their own). This seemingly miraculous event occurs most often before the baby is a year of age, almost always before age 4. It is due to the small VSD being located between heart fibers which increase in size and tourniquet the VSD closed. Even if a small VSD does not close spontaneously, surgical repair is usually not recommended. However, long-term follow-up is required. What if the VSD is large? With a large VSD (usually one greater than 1.0 square cm in area), there is a significant shunt into the right ventricle, excessive blood flow into the lungs, and pulmonary hypertension. The child may have labored breathing, difficulty feeding, and grow poorly. How is a large VSD treated? Medically, the heart should be kept strong. And vascular disease in the lungs must not be allowed to develop. Surgery should be done to close a large VSD.

What is the outlook (prognosis) after a VSD is repaired? After a successful surgical repair of the VSD, the two ventricles are entirely separate from each other and the circulation of the blood within the heart is normal. If the heart was enlarged, it should return toward normal size. And the high pressure in the pulmonary artery should begin dropping. If the child's growth had slowed, catch up occurs usually within a year or two. Long- term follow-up is required. The long-term prognosis is usually excellent.

Complications of VSD surgery Complications with VSD surgery are not common. They include residual openings in the septum that require a second surgery and heart block (impairment of conduction of electrical excitation of the heart) which may require a pacemaker. Unusual cases of VSD There are rare cases of VSD that may be harder to treat. For example, cases with the VSD well down in the septum (in what is called the muscular septum), especially defects near the tip (apex) of the heart (apical VSDs), can be more difficult to treat. Cases with multiple VSDs ("Swiss cheese" defects) are also harder to treat. Long-term precautions with VSDs No matter what size a VSD is, small or large, a VSD creates an increased risk for infections of the heart walls and valves (endocarditis). To help prevent endocarditis, everyone with a VSD needs to take antibiotics before dental hygiene and other dental care, before surgical procedures on the mouth or throat, and before any instrumentation of the urinary tract or lower intestinal tract.

TREND: MI Development and Evaluation of a New Canine Myocardial Infarction Model Using a ClosedChest Injection of Thrombogenic Material.
A new canine myocardial infarction model using thrombi induced by closed-chest injection of thrombin and autogenous blood with fibrinogen into coronary arteries was developed. Occlusive thrombi were formed in all treated animals. Occluded vessels did not spontaneously reperfuse 1 day after occlusion, but did so within 3 days. Infarction was confirmed by increased levels of creatine kinase-MB, glutamate-oxaloacetate transaminase and .ALPHA.-hydroxybutyrate dehydrogenase. Additionally, the left ventricular ejection fraction (LVEF) decreased within 0.5h after occlusion and had not improved 4 weeks later. After 1 week, extensive transmural anteroinferior myocardial infarction was observed and heart mass had increased. By 4 weeks after occlusion, pulmonary capillary wedge pressure and central venous pressure were increased, and oxygen pressure was decreased. Dropout of nuclei in cardiomyocytes and increased amount of collagen fiber were observed in myocardial infarct regions of hearts excised 4 weeks after occlusion. This canine model may be useful and convenient in evaluating treatment efficacy and the long-term outcome of acute myocardial infarction. Ref. http://sciencelinks.jp/j-east/article/200006/000020000699A0955818.php