Ventricular Septal Defect: A Vanishing Disease

     The heart is an amazing organ because it has the ability to supply the entire body system with oxygen-rich blood. The approximate weight of a healthy adult heart is about 7-12 ounces. It beats over 100,000 times per day pumping approximately 1,800 gallons of blood to all the cells so homeostasis can be present. Each time the heart beats, a portion of the blood is siphoned through the coronary arteries which nourish the heart itself; and sometimes the blood is shunted incorrectly between the chambers. This is because of a defect found in the septal wall or in the outer lining known as the 'pericardium'.

     The defects are attributed to a congenital failure or from drug and alcohol abuse while in-utero. Primary cardiomyopathies have no relationship with cardiovascular or systemic diseases accounting for the myocardial abnormality. These generally happen in the embryonic, fetal, and newborn stages with a hereditary and congenital origin. The incidence of total congestive heart defects is 8% and VSD, Ventricular Septal Defect, is the most predominant of the anomalies noted.

     In the case of VSD, a massive shunting of blood flowing from left to right occurs causing pulmonary hypertension. {McNulty, 1995} There are three different locations a VSD can be detected. The first which is most common, involves the membranes inferior to crista in 80% of all cases. The second location is much less common and involves the muscular septum in about 10% of the cases. The third, most rare, is discovered in 5% of the cases and involves the supracristal type which involves the right ventricular and aortic outflow regions. This is seen in conotruncal anomalies particularly 'Tetralogy of Fallot' which refers to the combination of 4 (tetrad) anatomic defects. The severity of this disease is related to the amount of pulmonary artery stenosis the body is capable of maintaining.

     In a newborn with a VSD, a noticeable 'hole' is seen between the left and right ventricles. If the 'hole' is small the babies are usually asymptomatic and natural closure can occur within the first six weeks to eighteen years. If it is monitored and no problems arise during childhood, surgical intervention is not an option. A moderate size VSD produces symptoms of hyperventilation, distress, slow at feeding and resulting in poor weight gain leaving the infant or child prone to a myriad chest infections. These symptoms are more exagerated when the 'hole' is significantly larger, like more than 8mm making it more dangerous to the infants overall normal development.

     While in most cases nothing can be done before the baby is born, but with technology advanced as it is we can now see the defect early enough in childhood, to correct it and add a few more years to the life expectancy. Academic medical centers have the capability well-established in prenatal diagnosis and perinatal treatment which encourage the eradification and hopeful extinction of this defect.

     The corrective surgical procedure commonly available to patients affected by a VSD, is a patch. This patch is inserted between the membranes and fused from both sides to grow within the 'hole', surround it and function as it normally would. This patch is generally designed from a dacron material or other synthetic fiber that functions homeostatically within the connective tissues support system. In time, the patch becomes natural to the pericardium and hearts tissue and is subject to all and any other foreign material as if it were 'born with the infant'.

     After surgery, the patient is monitored for up to six weeks. An array of post-surgical follow-up diagnostics are performed since the heart has taken an unusual toll early in its development. Tests include the chest x-ray, cardiac catheterization and a cardiac angiography. Each procedure provides a detailed list of diagnostic information on how the heart and invasive repair are adjusting. This information can provide for essential therapeutic measures to strengthen the prognosis (final outcome) for the patient.

     An issue of concern regarding the necessity of intervention surgically allows for two other non-surgical options to exist for patients born with a VSD. The use of diuretics such as Frusemide and Spironolactone, used to control fluid retention back about 10-15 years ago, still work today only the medication names are probably different. These diuretics are used to to promote excessive output while reducing blood volume in the circulatory process thus producing less overflow and overload to the renal system. In conjunction with diuretics, the use of Digoxin is added so as to increase heart muscle contraction to produce adequate blood flow to necessary regions. This kind of drug therapy is usually reserved for those with a small VSD that within time can close itself and available post-surgically to those that may experience any complications.

     Some complications are due to pre-existing conditions such as Congestive Heart failure, infective endocharditis, aortic insufficiency and 'delayed growth and failure to thrive' syndrome in infancy. This is why monitoring for at least six weeks is common, recommended and welcomed by parents whose children are affected with this defect. It may be common in occurence but it is being reduced in severity because technology has been given insight to things we could not see even twenty years ago !

     Children are not asked to be born . . . let alone born with a tremendous barrier at the beginning of life that could keep them from ever living a 'normal' life and I thank our determination as medical diagnosticians to seek answers and better treatments at the very sign of trouble, so as to correct it as soon as humanly possible. 11-20-1999 Copyright ©eih

References

http://www.healthcentral.com/mhc/top/001099.cfm

http://en.wikipedia.org/wiki/Ventricular_septal_defect

http://www.americanheart.org/presenter.jhtml?identifier=11066

Piscatella, Joseph. C. Choices for A Healthy Heart, Workman Publishing Company, Inc., New York, NY 1987

Snider, Rebecca. A. Echocardiography in Pediatric Heart Disease. Mosby-Year Book, Inc., St. Louis, MO 1990