eMedicine Specialties > Radiology > Cardiac
Ventricular Septal Defect: Follow-up
Updated: Aug 19, 2008
Intervention
General principles, techniques, and goals
Parents of patients with small ventricular septal defects should be reassured of the relatively benign nature of the lesion, and the child should be encouraged to live a normal life, with no restrictions on physical activity. Surgical repair is currently not recommended.
As a protection against infective endocarditis, the integrity of primary and permanent teeth should be carefully maintained; antibiotic prophylaxis should be provided for dental visits (including cleanings), tonsillectomy, adenoidectomy, and other oropharyngeal surgical procedures, as well as for instrumentation of the genitourinary and lower intestinal tracts. These patients may be followed by means of a combination of clinical examinations and noninvasive laboratory tests until the VSD has closed spontaneously.
In these patients, electrocardiography is an excellent means of screening for possible pulmonary hypertension or pulmonary stenosis, which is indicated by right ventricular hypertrophy. Echocardiography is used to screen for the development of LV outflow tract pathology (subaortic membrane or aortic regurgitation) and to confirm spontaneous closure.
In infants with a large VSD, medical management has 2 aims: to control heart failure and to prevent the development of pulmonary vascular disease.
Clamshell-type catheter occlusion devices are being tested as a means of closing apical muscular VSDs. Successful transcatheter device closure of trabecular (muscular) and perimembranous VSDs has been reported. Trabecular VSDs have proved more amenable to this technique because of their relatively straightforward anatomy and the presence of a muscular rim, to which the device attaches well. The closure of perimembranous VSDs is technically more challenging and should be considered experimental.
Therapeutic measures are aimed at the control of symptoms of heart failure and the maintenance of normal growth. If early treatment is successful, the shunt may diminish in size and improve spontaneously, especially during the first year of life. The clinician must be alert not to confuse clinical improvement caused by a decrease in defect size with clinical changes caused by the development of Eisenmenger physiology. Because surgical closure may be performed with low risk in most infants, medical treatment should not be pursued in symptomatic infants after an initial trial is unsuccessful. Pulmonary vascular disease may be prevented when surgery is performed within the first year of life.23,24,25,26
Indications and contraindications
Surgical closure of VSD is indicated (1) for patients of any age with large VSDs in whom clinical symptoms and failure to thrive cannot be controlled medically; (2) for infants 6-12 months of age who have large defects associated with pulmonary hypertension, even if symptoms are controlled by medication; and (3) for patients older than 24 months with a Qp:Qs ratio greater than 2:1.
Patients with supracristal VSD of any size are usually referred for surgery because of the high risk of aortic valve regurgitation.
Severe pulmonary vascular disease is a contraindication to surgical closure of a VSD.
Pulmonary arterial palliative banding with repair in later childhood is reserved for complicated cases or very premature infants. Surgical risks are higher for defects in the muscular septum, particularly apical defects and multiple (Swiss cheese–type) VSDs. Patients with these conditions may require pulmonary arterial banding if they are symptomatic; these patients undergo subsequent debanding and repair of multiple VSDs at an older age.
The presence of a significant VSD in the absence of irreversible pulmonary hypertension warrants surgical closure. Signs of significant VSD include the following: the presence of symptoms; a Qp:Qs ratio greater than 1.5:1.0; pulmonary artery systolic pressure greater than 50 mm Hg; enlarged LV and left atrium; and deteriorating LV function.
Severe pulmonary hypertension is defined as pulmonary arteriolar resistance greater than two thirds the systemic arteriolar resistance. For patients with severe pulmonary hypertension, surgical closure may be safely undertaken under the following conditions: the net left-to-right shunt is at least 1.5:1.0; there is strong evidence of pulmonary reactivity when a pulmonary vasodilator challenge (with oxygen or nitric oxide) is undertaken; or the results of lung biopsy suggest that pulmonary arterial changes are reversible.
Other relative indications for surgical closure include the presence of a perimembranous or outlet VSD with more than mild aortic regurgitation and a history of endocarditis, especially if recurrent.
Outcomes
Results of primary surgical repair are excellent, and complications resulting in long-term problems (eg, residual ventricular shunts requiring repeat operation or heart block requiring a pacemaker) are rare.
After the obliteration of the left-to-right shunt, the hyperdynamic heart becomes quiet, the size of the heart decreases toward the normal range, thrills and murmurs are abolished, and pulmonary artery hypertension regresses. The patient's clinical status improves markedly. Most infants begin to thrive, and cardiac medications are no longer required. Catch-up growth occurs in the majority of patients over the next 1-2 years.
In some instances, after successful operation, systolic ejection murmurs of low intensity may persist for months.
The long-term prognosis after surgery is excellent. Patients with a small VSD and those who have undergone surgical closure without residua are considered to be at standard risk for the purposes of insurability.
For patients with good to excellent functional class and whose LV function was good before surgical closure, life expectancy after surgical correction is close to normal. The risk of progressive aortic regurgitation is markedly reduced after surgery, as is the risk of endocarditis, unless a residual VSD persists. Intraventricular conduction disturbances are slightly increased after surgical closure and may be responsible for the slight increase in risk of sudden death encountered in this patient population.
Follow-up
Yearly cardiac evaluation is suggested for patients not undergoing surgical repair; in patients with Eisenmenger syndrome; in adults with significant atrial or ventricular arrhythmias; and in patients with associated cardiac lesions, such as right ventricular outflow tract obstruction (RVOTO), LV outflow tract obstruction (LVOTO), or aortic regurgitation.
Cardiac surveillance is also recommended for patients who undergo late repair of moderate or large defects, which are often associated with LV impairment and elevated pulmonary artery pressure at the time of surgery. Residual patch or device leaks are seldom of hemodynamic importance, but they may predispose patients to endocarditis. Good dental hygiene and antibiotic prophylaxis are important in these patients.
Medicolegal Pitfalls
- Ventricular septal defects are usually diagnosed in infants and children.
- Small VSDs cause louder murmurs due to higher pressure gradients, whereas large VSDs cause murmurs that may be missed unless listened to carefully.
- Therefore, careful clinical cardiac evaluation of all infants is warranted not to miss this common cardiac defect, which is treatable with surgery.
Special Concerns
- Physicians must remember to recommend subacute bacterial endocarditis prophylaxis for all patients with ventricular septal defect, large or small.
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 Follow-up: Ventricular Septal Defect |
| Multimedia: Ventricular Septal Defect |
| References |
| Further Reading |
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Further Reading
Suspected congenital heart disease in the adult.
American College of Radiology - Medical Specialty Society. 1998 (revised 2007). 8 pages. NGC:005988
Keywords
ventricular septal defect, VSD, interventricular septal defect, heart septal defect, membranous VSD, cardiac malformation, congenital cardiac anomaly, interventricular septum, restrictive ventricular septal defect, restrictive VSD, Eisenmenger syndrome, interventricular foramen, congenital heart defect, congenital heart disease, septal defect
