You are in: eMedicine Specialties > Radiology > CARDIAC Ventricular Septal DefectArticle Last Updated: Aug 19, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Vibhuti N Singh, MD, MPH, FACC, FSCAI, Director, Suncoast Cardiovascular Center; Chair, Cardiology Division and Cath Labs, Department of Medicine, Bayfront Medical Center; Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine Vibhuti N Singh is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Florida Medical Association Coauthor(s): Rakesh K Sharma, MBBS, FACC, FACP, Interventional Cardiologist, The Heart and Vascular Institute of Florida; Hanumanth K Reddy, MD, FACC, Clinical Professor of Medicine, St Louis University Medical School; Associate Chief, Department of Cardiovascular Services, Three Rivers Healthcare; Navin C Nanda, MD, FACC, Director, Heart Station and Echocardiography Laboratories, Professor, Department of Internal Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham Editors: Justin D Pearlman, MD, PhD, ME, MA, Director of Dartmouth Advanced Imaging Center, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; John D Newell, Jr, MD, FACR, FCCP, FASER, Co-Director of Thoracic Imaging, UCDHSC; Director of Lung Imaging Center, Professor of Radiology and Professor of Medicine, Department of Radiology, University of Colorado Health Sciences Center, National Jewish Medical and Research Center; Univ. Colorado Hospital; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Eugene C Lin, MD, Clinical Assistant Professor of Radiology, University of Washington Medical School Author and Editor Disclosure Synonyms and related 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 INTRODUCTIONSection 2 of 12
  BackgroundVentricular septal defect (VSD) is the second most common cardiac malformation, accounting for approximately one fifth of all congenital cardiac anomalies. It is usually diagnosed during childhood. In adults, it is diagnosed less often, owing to the fact that, during the patient's early years, large VSDs are corrected surgically, and smaller VSDs close spontaneously. A VSD is a defect in the interventricular septum, which is composed of muscular and membranous segments. VSDs are classified into 3 main categories according to their location and the appearance of the margins of defects. The clinical significance of the VSD depends on its size and location, the level of pulmonary pressure, and the left ventricular (LV) outflow resistance associated with the VSD. A restrictive VSD produces a small shunt and does not cause significant hemodynamic derangement. In contrast, a large VSD may progressively lead to higher pulmonary resistance and, finally, to irreversible pulmonary vascular changes, producing the so-called Eisenmenger syndrome (reversal of shunt to right-to-left shunt). Clinically, VSDs produce a characteristic systolic murmur and are associated with recurrent upper respiratory infections. The anatomic localization of all VSDs is facilitated by using 2-dimensional (2D) echocardiographic images with a Doppler system and by superimposing a color-coded direction and velocity of blood flow on the real-time images. Clinically significant VSDs require surgical correction; clinical outcomes are usually excellent. For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education article Ventricular Septal Defect. PathophysiologyThe functional disturbance caused by a ventricular septal defect depends primarily on its size and the status of the pulmonary vascular bed rather than on the location of the defect. The physical size of the VSD is a major, but not the only, determinant of the size of the left-to-right shunt. The magnitude of the shunt is also determined by the level of pulmonary vascular resistance relative to the systemic vascular resistance. The magnitude of intracardiac shunts is usually described by the Qp:Qs ratio, where Qp is the pulmonary resistance and Qs is the systemic resistance. If the left-to-right shunt is small (Qp:Qs < 1.75:1), the cardiac chambers are not appreciably enlarged, and the pulmonary vascular bed is likely normal. If the shunt is large (Qp:Qs > 2:1), left atrial and LV volume overload occurs, as does right ventricular and pulmonary arterial hypertension. The main pulmonary artery, left atrium, and LV are enlarged. When a small communication is present (usually <0.5 cm2), the VSD is called restrictive, and the right ventricular pressure is normal. Such a VSD produces a significant pressure gradient between the LV and the right ventricle. It is accompanied by a small (<1.5/1.0) shunt, and it does not cause significant hemodynamic derangement. A small VSD with high resistance to flow permits only a small left-to-right shunt. A moderately restrictive VSD is accompanied by a moderate shunt (Qp:Qs = 1.5-2.5:1.0) and poses a hemodynamic burden on the LV. This leads to left atrial and LV dilation and dysfunction, as well as a variable increase in pulmonary vascular resistance. Important atrial arrhythmias and, less often, ventricular arrhythmias may occur. In large nonrestrictive VSDs (usually >1.0 cm2), right and LV pressures are equalized. In these defects, the direction of shunting and the shunt magnitude are determined by the ratio of pulmonary resistance to systemic vascular resistance. Such a VSD results initially in LV volume overload early in life, with a progressive increase in pulmonary artery pressure. The natural history of VSDs has a wide spectrum of findings, ranging from spontaneous closure to congestive cardiac failure and death in early infancy. Within this spectrum are the possible development of pulmonary vascular obstruction, right ventricular outflow tract obstruction, aortic regurgitation, and infective endocarditis. After patients with a large VSD are born, pulmonary vascular resistance may remain higher than normal, and thus, the size of the left-to-right shunt may initially be limited. As pulmonary vascular resistance continues to decrease in the first few weeks after birth, owing to the normal involution of the media of small pulmonary arterioles, the size of the left-to-right shunt increases. Eventually, a large left-to-right shunt ensues, and clinical symptoms become apparent. In most cases during early infancy, pulmonary vascular resistance is only slightly elevated, and the major contribution to pulmonary hypertension is the extremely large pulmonary blood flow. However, in some infants with a large VSD, pulmonary arteriolar medial thickness never decreases. With continued exposure of the pulmonary vascular bed to high systolic pressure and high flow, pulmonary vascular obstructive disease develops. When the ratio of pulmonary to systemic resistance approaches 1:1, the shunt becomes bidirectional, signs of heart failure abate, and the patient becomes cyanotic (Eisenmenger physiology). FrequencyUnited StatesVentricular septal defects are the second most common congenital anomalies of the heart, accounting for approximately 20% of all congenital cardiac malformations.1, 2 Mortality/Morbidity
RaceNo particular racial predilection has been reported for ventricular septal defect. SexNo difference in the incidence of ventricular septal defect in male and female patients has been reported. AgeVentricular septal defect is usually diagnosed in children.
AnatomyThe ventricular septum comprises 4 compartments: the membranous septum; the inlet septum; the trabecular septum; and the outlet, or infundibular, septum. Defects result from a deficiency of growth or a failure of alignment or fusion of component parts. Defects are most commonly classified as occurring in or adjacent to 1 or more of the septal components. The most common defects occur in the region of the membranous septum and are referred to as paramembranous or perimembranous defects because they are larger than the membranous septum itself and are associated with a muscular defect at a portion of their perimeter. They also are known as infracristal, subaortic, or conoventricular defects. These perimembranous defects also may be defined by their adjacent areas as an inlet, trabecular, or outlet defect. A second type of defect is one with an entirely muscular rim. Such muscular defects also may be defined as inlet, trabecular, central, apical, marginal or Swiss cheese, or outlet types. They vary greatly in size, shape, and number. A third type of defect occurs when the outlet septum is deficient. This is commonly referred to as supracristal, subpulmonary, outlet, infundibular, or conoseptal. Because the aortic and pulmonary valves are in fibrous continuity, this type of defect also may be referred to as a doubly committed subarterial defect. A septal deficiency of the site of the atrioventricular (AV) septum characterizes defects called AV septal, AV canal, or inlet septal defects. The other feature of any defect may be a malalignment of the septal components. Either the inlet septum or the outlet septum may be malaligned. Malalignment of the inlet septum produces either mitral or tricuspid valve override and/or straddle. Malalignment of the outlet septum may be to the right or the left of the trabecular septum. When it is to the left of the trabecular septum, the VSD is characteristic of tetralogy of Fallot; double-outlet ventricle; truncus arteriosus; and, in some cases, transposition of the great arteries. Clinical DetailsThe clinical presentation of patients with a ventricular septal defect varies according to the size of the defect and the pulmonary blood flow and pressure.3, 4, 5, 6, 7 Symptoms Small VSDs with trivial left-to-right shunts and normal pulmonary arterial pressures are the most common. Patients with these VSDs are asymptomatic; the cardiac lesion is usually found during routine physical examination. Patients with a moderately restrictive VSD often present with dyspnea in adult life. In patients with large nonrestrictive VSDs, the condition frequently progresses to Eisenmenger syndrome. Signs Physical examination typically reveals a displaced cardiac apex with a similar holosystolic murmur, as well as an apical diastolic rumble and third heart sound (S3) at the apex, caused by the increased flow through the mitral valve. Characteristically, a loud, harsh, or blowing holosystolic murmur is best heard over the lower left sternal border in the third or fourth intercostal space. This is frequently accompanied by a thrill. Sometimes, the murmur ends before the second heart sound, presumably because of closure of the defect during late systole. A short, harsh systolic murmur localized at the apex in a neonate is often a sign of a tiny muscular VSD. In the immediate neonatal period, the left-to-right shunt may be minimal because of higher right-sided pressures; thus, the systolic murmur may not be audible during the first few days of life. In premature infants, the murmur may be heard early because pulmonary vascular resistance decreases more rapidly. Large VSDs with excessive pulmonary blood flow and pulmonary hypertension are responsible for dyspnea, feeding difficulties, poor growth, profuse perspiration, recurrent pulmonary infections, and cardiac failure in early infancy. Cyanosis is usually absent, but duskiness is sometimes noted during periods of infection or when crying. Prominence of the left precordium is common, as are a palpable parasternal lift, a laterally displaced apical impulse and apical thrust, and a systolic thrill. The holosystolic murmur of a large VSD is usually less harsh than that of a small VSD and is more blowing in nature because of the absence of a significant pressure gradient across the defect. It is even less likely to be audible in newborns. The pulmonic component of the second heart sound may be increased, indicating pulmonary hypertension. The presence of a mid-diastolic, low-pitched rumble at the apex is caused by increased blood flow across the mitral valve and indicates a Qp:Qs of 2:1 or greater. Natural history The natural course of a VSD depends to a large degree on the size of the defect. A significant number (30-50%) of small defects close spontaneously, most frequently during the first 2 years of life. Small muscular VSDs are more likely to close (as many as 80%) than membranous VSDs (as many as 35%). The vast majority of defects that close do so before the patient is 4 years of age, although spontaneous closure has been reported in adults. Most children with small defects remain asymptomatic, without evidence of an increase in heart size, pulmonary arterial pressure, or resistance. One of the long-term risks for these patients is infective endocarditis. Some long-term studies of adults with small VSDs that are not treated with surgery indicate an increase in the incidence of arrhythmia, subaortic stenosis, and exercise intolerance. The Council on Cardiovascular Disease in the Young of the American Heart Association states that an isolated, small, hemodynamically insignificant VSD is not an indication for surgery. More commonly, infants with large defects have repeated episodes of respiratory infection and heart failure despite optimal medical management. Many of these infants experience heart failure, manifested as a failure to thrive. Pulmonary hypertension occurs as a result of high pulmonary blood flow. These patients are at risk for the eventual development of pulmonary vascular disease if the defect is not repaired. Patients with VSD are also at risk for the development of aortic valve regurgitation; the risk is greatest for patients with supracristal VSD. A VSD that either decreases in size or closes completely during the first year of life presents no problem to the practicing physician. Spontaneous closure occurs by 3 years of age in about 45% of patients born with VSD. In some patients, spontaneous closure does not occur until 8-10 years or age, or even later. Spontaneous closure is more common in patients born with a small VSD; nonetheless, about 7% of infants with a large defect who experience congestive heart failure early in life also experience spontaneous closure. Partial, rather than complete, closure is common in patients with both large and small VSDs. Spontaneous closure of a perimembranous VSD (from tricuspid leaflet tissue apposition) or of a small muscular VSD during adulthood is uncommon (<10%). Preferred ExaminationEchocardiography Two-dimensional and Doppler color-flow mapping may be used to identify the type of defect in the ventricular septum. Perimembranous VSDs are characterized by septal dropout in the area adjacent to the septal leaflet of the tricuspid valve and below the right border of the aortic annulus. The subaortic or anterior malalignment type of VSD appears just below the posterior semilunar valve cusps, entirely superior to the tricuspid valve. Subpulmonary VSD appears as echo dropout within the outflow septum and extending to the pulmonary annulus. One or two of the aortic cusps may be seen to be protruding through the defect into the right ventricular outflow tract. The inlet AV septal-type of VSD extends from the fibrous annulus of the tricuspid valve into the muscular septum; it is often entirely beneath the septal tricuspid leaflet. Muscular defects may appear anywhere throughout the ventricular septum. They may be either large and single or small and multiple. The anatomic localization of all VSDs is facilitated by coupling 2D sonograms with a Doppler system and by superimposing a color-coded direction and velocity of blood flow on the real-time images. Chest radiography In patients with small VSDs, the results of chest radiographs are usually normal. With medium-size VSDs, minimal cardiomegaly and a borderline increase in pulmonary vasculature may be observed. In large VSDs, the chest radiograph shows gross cardiomegaly with prominence of both ventricles, the left atrium, and the pulmonary artery. The pulmonary vascular markings are increased, and frank pulmonary edema, including pleural effusions, may be present. Electrocardiography The ECG mirrors the size of the shunt and the degree of pulmonary hypertension. Small restrictive VSDs usually produce a normal tracing. Medium-size VSDs produce a broad, notched P wave characteristic of left atrial overload. Signs of LV volume overload — namely, deep Q and tall R waves with tall T waves in leads V5 and V6 — are present. In addition, signs of atrial fibrillation are often present. Large VSDs produce right ventricular hypertrophy with right-axis deviation. With further progression, the ECG shows biventricular hypertrophy; P waves may be notched or peaked. Limitations of TechniquesThe 2D echocardiogram shows the position and size of the ventricular septal defect. Small defects, especially those of the muscular septum, may be difficult to image; they might be visualized only by means of color Doppler examination. In defects of the membranous septum, a thin membrane may partially cover the defect and limit the volume of the left-to-right shunt. Although the membrane is called a ventricular septal aneurysm, it consists of tricuspid valve tissue. DIFFERENTIALSSection 3 of 12
Other Problems To Be ConsideredMembranous VSD RADIOGRAPHSection 4 of 12
FindingsThe chest radiograph reflects the magnitude of the shunt as well as the degree of pulmonary hypertension. A shunt of moderate size causes signs of left atrial, right ventricular, and LV dilation, with some pulmonary overcirculation. Over time, a large shunt produces pulmonary hypertension in association with enlarged central pulmonary arteries, peripheral pruning, and Eisenmenger physiology. With these developments, the enlarged cardiac chamber may normalize. Degree of ConfidenceThe findings are nonspecific for ventricular septal defect. CT SCANSection 5 of 12
FindingsCT scans may show cardiomegaly, left atrial enlargement, and vascular engorgement.8 MRISection 6 of 12
FindingsMRI has multiple capabilities in the evaluation of congenital heart disease. Morphologic information is provided by ECG-gated spin-echo and cine MRI. Ventricular volumes, mass, and function may be assessed by using cine MRI. The volumes of shunts, valvular function, and pressure gradients across valves and conduits may be estimated by use of velocity-encoded cine MRI (velocity-flow mapping). Echocardiography and Doppler techniques are now used for many of these purposes; the current clinical role of MRI is to supplement the information acquired by means of echocardiography. Reports from several centers indicate the effectiveness of MRI for the evaluation of both children and adults with congenital heart disease. In several studies in which the results of MRI were corroborated with those of angiography and/or 2D echocardiography, an accurate anatomic diagnosis of anomalies was achieved with MRI in more than 90% of patients. MRI has also shown substantial utility in the anatomic and functional evaluation of congenital heart disease after palliative and total correction. The visceroatrial situs, the type of ventricular loop, and the relationship of the great vessels may be identified in all patients in whom studies encompassing the entire heart are performed. The diagnostic accuracy of MRI exceeds 90% for abnormalities of arterioventricular connections; for great vessel anomalies, such as coarctation and vascular rings; for ventricular and atrial septal defects; and for abnormalities of venous connections.9, 10, 11, 12, 13 Degree of ConfidenceIn several studies in which the results of MRI were corroborated with those of angiography and/or 2D echocardiography, accurate anatomic diagnosis of anomalies was achieved by use of MRI in more than 90% of patients. Information provided by MRI may also be obtained by means of echocardiography, the equipment for which is more portable. Consequently, the current clinical role of MRI is to supplement the information acquired with echocardiography. False Positives/NegativesFalse-positive and false-negative results are uncommon regarding ventricular septal defect. ULTRASOUNDSection 7 of 12
FindingsDoppler color-flow and 2D mapping may be used to identify the type of defect in the ventricular septum. Perimembranous VSDs are observed as septal dropout in the area adjacent to the septal leaflet of the tricuspid valve and below the right border of the aortic annulus (see Image 1). The subaortic or anterior malalignment type of VSD appears just below the posterior semilunar valve cusps, entirely superior to the tricuspid valve. Subpulmonary VSD appears as echo dropout within the outflow septum and extending to the pulmonary annulus. One or two of the aortic cusps may be seen to be protruding through the defect into the right ventricular outflow tract. The inlet AV septal-type of VSD extends from the fibrous annulus of the tricuspid valve into the muscular septum; it is often entirely beneath the septal tricuspid leaflet. Muscular defects may appear anywhere throughout the ventricular septum. They may be either large and single or small and multiple. The anatomic localization of all VSDs is facilitated by coupling 2D images with a Doppler system and by superimposing a color-coded direction and velocity of blood flow on the real-time images.14, 15, 16, 17, 18, 19, 20, 21, 22 Degree of ConfidenceThe degree of confidence is high. False Positives/NegativesFalse-positive and false-negative results are rare. ANGIOGRAPHYSection 8 of 12
FindingsCardiac catheterization and angiography The hemodynamics of a ventricular septal defect may be demonstrated by means of cardiac catheterization. Indications Catheterization is usually performed only under the following conditions: uncertainty remains regarding the size of the shunt following a comprehensive clinical evaluation; laboratory data do not fit well with the clinical findings; or pulmonary vascular disease is suspected. Oximetry demonstrates an increase in oxygen content in the right ventricle, because with some defects, blood is ejected almost directly into the pulmonary artery (a phenomenon known as streaming). This increase is occasionally apparent only when pulmonary arterial blood is sampled. Small, restrictive VSDs are associated with normal right-sided heart pressures and pulmonary vascular resistance. Large, nonrestrictive VSDs are associated with equal or near-equal pulmonary and systemic systolic pressures. Pulmonary blood flow may be 2-4 times greater than systemic blood flow. In patients with large, nonrestrictive VSDs who have hyperdynamic pulmonary hypertension, the pulmonary vascular resistance is only minimally elevated (pulmonary vascular resistance is equal to the pressure divided by the flow). If Eisenmenger syndrome is present, pulmonary artery systolic and diastolic pressures are elevated, the degree of left-to-right shunting is minimal, and desaturation of blood in the LV is encountered. The size, location, and number of ventricular defects are demonstrated by left ventriculography. Contrast medium passes across the defect or defects to opacify the right ventricle and the pulmonary artery. Degree of ConfidenceThe degree of confidence is high for ventricular septal defect. False Positives/NegativesFalse-positive and false-negative results are rare regarding ventricular septal defect. INTERVENTIONSection 9 of 12
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. Medical/Legal Pitfalls
Special Concerns
FURTHER READINGSection 10 of 12
Suspected congenital heart disease in the adult. MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
Ventricular Septal Defect excerpt Article Last Updated: Aug 19, 2008 | |||||||
