Within the last several decades, there has been an explosion of interest in interventional cardiac catheterization techniques. This interest was sparked in 1966 by Drs. Rashkind and Miller, who described a catheter technique for the nonsurgical creation of atrial septal defects in newborns with complete transposition of the great arteries. ' This procedure has since gained worldwide acceptance as a palliative approach to the treatment of several congenital cardiac lesions, not only complete transposition of the great arteries, but also total anomalous pulmonary venous return and tricuspid atresia. Recently, other interventional cardiac catheterization techniques for palliation of congenital heart disease have been described and have achieved limited acceptance, including transcatheter patch atrial septal defect repair, transcatheter patent ductus arteriosus occlusion, and balloon dilatation of stenosed arteries or veins, shunts, and coarctation of the aorta.2 None of these new procedures has gained the widespread acceptance, use, and reproducibility of percutaneous balloon dilatation technique for pulmonary valve stenosis. 3
Our method of angioplasty is similar to that described by Kan3 and others.4 Standard premedication and local anesthesia are administered and the patient is draped under sterile conditions. A right and left heart catheterization for hemodynamic evaluation is performed. Placement of an arterial catheter is avoided in those patients in whom the approach to the left heart can be made by traversing a patent foramen ovale. Angiographie studies are obtained in both ventricles and, where appropriate, in the main pulmonary artery. From the postero-anterior and lateral right ventricular angiogram, the severity, type, and position of the pulmonic stenosis are determined. Using correction factors calculated from size markers on "scout" xrays to eliminate distortion and magnification, the pulmonary valve anulus is measured directly from the angiograms.
Figure 1. Balloon dilatation catheter showing guide wire through one port and syringe connected to second port for balloon inflation.
Balloon dilatation catheters are double-lumen catheters which allow through one port inflation of an elongated 3 cm balloon, and through the other port passage of a guide wire, injection of contrast material or measurement of intracardiac pressures (Figure 1). The balloons are constructed of plastic polymers which permit rapid inflation and deflation and retain their predetermined diameter without excessive distortion in the areas proximal and distal to the area of stenosis. Balloon diameters range from 4 mm to 25 mm and are applied to 7 or 10 French catheters. The recommended maximum inflation for the largest catheter is 4 atmospheres while that for the smallest catheter is considerably higher at up to 7.5 atmospheres.
Angioplasty catheters are advanced over an exchange wire positioned in a lower lobe pulmonary artery. The deflated balloon catheter is "washed" with carbon dioxide and advanced across the pulmonary valve, where it is rapidly inflated by hand using contrast and normal saline in a 1 to 1 dilution. This procedure is performed under constant fluoroscopic control until indentation ("waisting") caused by the stenotic valve disappears (Figure 2). A second or third inflation may be necessary to achieve maximum effect and to document the absence of waisting. Inflation/ deflation cycles last 10 to 15 seconds. After angioplasty, the balloon catheter is replaced by an angiographie catheter and hemodynamic data are obtained.
Figure 2. Upper panel: Inflated balloon catheter across stenotic pulmonary valve showing "waisting. " An angiographie catheter is placed in the right ventricle to measure right ventricular pressure. The guide wire for the angioplastic catheter is in a left lower lobe pulmonary artery to allow for anchoring the catheter. Lower panel: Waisting disappears after successful dilatation of a stenotic valve.
Selection of the appropriate dilatation catheter size is crucial. In early studies, the balloon used was either smaller than or about the same size as the valve anulus. Reported average grathent reduction was somewhat less than that provided by standard surgical technique.5 Recent reports suggest that percutaneous balloon valvuloplasty with catheters 20% to 40% larger than the valve anulus is the treatment of choice.6 In large patients, a dual balloon technique may be necessary to achieve "oversize" balloon dilatation. This may involve insertion of a second catheter in the opposite groin or the use of special catheters incorporating two or three balloons. These techniques may reduce hemodynamic compromise during maximum inflation because the residual spaces between the inflated balloons allow for some transvalvar flow. In some cases of severe pulmonic stenosis, we have tried sequential incremental dilatation, using a smaller balloon to create improved pulmonary flow and a larger balloon to more completely reduce valvar grathent.
Figure 3. Changes in aortic and right ventricular pressure with inflation and deflation are illustrated.
SELECTION OF PATIENTS
Our experience with balloon angioplasty for treatment of pulmonic stenosis has been limited to patients with primary valvar disease (as demonstrated by angiogram and hemodynamic data), right ventricular pressure greater than 50 mmHg, and no evidence of other congenital heart defects. We have excluded neonates and those with dysplastic pulmonary valves, as are seen with the Noonan syndrome. The experience of others with neonatal severe pulmonic stenosis has generally been unsuccessful,4 although more experience may change this. Perhaps smaller catheters will be developed. We believe that patients with dysplastic pulmonary valves require a relatively aggressive surgical approach, sometimes including excision of valve tissue and possible transanular patch. Some have, however, reported angioplastic success with this clinical entity and suggest that the size of the anulus rather than the morphology of the valve is the critical factor determining relief of grathent.7
Our results and those of others indicate that balloon angioplasty can be as successful as surgical intervention for the relief of valvular pulmonic stenosis. Radtke and colleagues reported mean grathent reduction of 74 ± 15% with the mean prevalvotomy grathent reduced from 65.0 ± 19 mmHg to 15.9 ± 7.5 mmHg.4 This compares favorably to long-term surgical reports which showed that 81% of patients had residual grathents of less than 25 mmHg several years postoperatively.8 The group from Ann Arbor, Michigan reported right ventricular outflow tract grathent reduced from a mean of 88 ± 26 mmHg to 38 ± 16 mmHg.7 European pediatrie cardiologists have demonstrated similar results.9
Pressure measurements recorded during a representative pulmonary valve balloon angioplastic procedure in our laboratory are illustrated in Figures 3 and 4. At the commencement of inflation, aortic pressure falls with a concomitant fall in cardiac output while right ventricular pressure rises acutely (Figure 3). With deflation, aortic pressure returns to baseline and right ventricular pressure to below baseline values. Following a successful valvuloplasty, right ventricular pressure is noted to diminish from systemic levels (approximately 105 mmHg) to upper limits of normal (approximately 32 mmHg) (Figure 4). Comparison of pulmonary artery and right ventricular pressures shows a significant reduction in transvalvular grathent. We have noted that right ventricular pressure continues to fall in the 15 to 30 minutes following valve dilatation. Transient but significant systemic pressure drop appears to be extremely well tolerated and many laboratories, including our own, no longer universally monitor arterial pressure.
Development of an infundibular grathent after balloon valvuloplasty has been well documented. 10 We have seen this in one patient with severe pulmonic stenosis and suprasystemic right ventricular pressure (165 mmHg). Natural history studies have shown that this may be expected to regress.11 Infundibular obstruction with right ventricular pressure greater after valvuloplasty than before has been reported as well.12
Figure 4. Pulmonary artery and fight ventricular pressures and pulmonary valve grathent before (left panel) and after (right panel) balloon angioplasty. Note difference in pressure scales for right and left panels.
Little data are available on the long-term results of balloon valvuloplasty. We and others have documented persistent long-term regression of right ventricular hypertrophy which is usually a sensitive indicator of diminution of right ventricular pressure. In some series» 30% to 40% of study patients were reevatuated by cardiac catheterization about one year after valvuloplasty and all showed residual pressure grathents similar to those measured at the termination of the valvuloplasty.4
Surgical observations have demonstrated that the mechanism of percutaneous balloon valvuloplasty is para-, extra- or commisurai tearing of the valve. 12
COMPLICATIONS AND SAFETY
Based on a large number of procedures performed at many institutions, percutaneous balloon valvuloplasty can be considered a procedure associated with low morbidity and low mortality. Neither we nor others have observed serious short- or long-term complications. Premature ventricular contractions (rarely in runs) and short-lived bradycardia are often encountered during the procedure. We have already commented on well tolerated transient systemic hypotension. A sensation of tightness of the chest invariably disappears with balloon deflation.
There may be a somewhat higher incidence of postprocedure bleeding, due to the large size of the catheters. Direct pressure to the femoral vein must often be applied for relatively lengthy periods (>20 minutes).
The incidence of femoral vein occlusion is not yet known. Some infants have experienced edema of that extremity. This seems to be transient; it is of low incidence and is similar to the edema that sometimes follows noninterventional cardiac catheterization in infants. Similarly, insertion and removal of the catheter often causes some local discomfort despite sedation and use of subcutaneous analgesics.
Rupture of the balloon may occur during the procedure but with appropriate preparation of the catheter (ie, CO2 "washing"), this is not associated with adverse effects. Perforation of the right ventricular infundibulum is a serious potential risk that is minimized by shorter balloons and distal placement of the catheter to avoid anterior protrusion of the catheter in the right ventricular outflow tract. Right ventricular hypertrophy protects the chamber from perforation.
Pulmonary insufficiency of mild degree was reported by Radtke and colleagues in 19% of patients after balloon vaivuloplasty.6 This figure compares favorably with the incidence of postsurgical valvotomy pulmonary régurgitation.8 It is of no physiologic consequence when there is no distal stenosis and no proximal shunt. Both of those possible situations are excluded prior to selection of patients with pure pulmonic stenosis for valvuloplasty.
At the present time, it appears that percutaneous balloon valvuloplasty using catheters larger than the pulmonary valve anulus is the procedure of choice for the treatment of moderate to severe valvular pulmonic stenosis in most children. We have reservations about the procedure in the palliation of neonates with severe valvular pulmonic stenosis and in the clinical setting of dysplastic pulmonary valves. The current wide acceptance and application of this angioplastic technique is heralding a new age of interventional cardiac catheterization for congenital heart disease. We will continue to employ this technique judiciously in other clinical settings where safety and significant hemodynamic improvement can be demonstrated.
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