Asian Cardiovasc Thorac Ann 2006;14:501-504
© 2006 Asia Publishing EXchange Ltd
Valved Patch for Ventricular Septal Defect With Pulmonary Arterial Hypertension
Abbas Afrasiabi, MD,
Mahmoud Samadi, MD,
Hossein Montazergaem, MD
Cardiovascular Research Center, Madani Heart Hospital, University of Medical Sciences, Tabriz, Iran
For reprint information contact: Abbas Afrasiabi, MD Tel: 98 411 336 1175 Fax: 98 411 334 4021 Email: aafrasa{at}yahoo.com, Cardiovascular Research Center, Madani Heart Hospital, University of Medical Sciences, Tabriz, Iran.
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ABSTRACT
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From March 1998 to December 2004, 16 acyanotic patients aged 2 to 22 years (mean, 7 ± 5.7 years) with a large ventricular septal defect and elevated pulmonary vascular resistance (9.6 ± 3.8 Wood units) underwent surgery. A Gore-Tex patch with a 5–8 mm longitudinal slit in the center was used. A piece of pericardium was sewn around the slit on one side of the patch, except for the upper quarter. In all patients, the defect was closed with a trimmed patch and the pericardial aspect was placed on the left ventricular side to allow right-to-left shunting. Echocardiography on the day of operation revealed a right-to-left shunt in 6 cases. Two patients (12.5%) died in the early postoperative period due to frequent episodes of pulmonary hypertensive crisis and persistent severe pulmonary hypertension. In 3 years of follow-up, pulmonary vascular resistance gradually decreased in all but one patient in whom it increased with a right-to-left shunt and cyanosis. Insertion of a valved patch seems to be a promising technique to decrease morbidity and mortality in severe pulmonary arterial hypertension.
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INTRODUCTION
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A large ventricular septal defect (VSD) in infants may result in congestive heart failure. With increasing age and a continuing left-to-right shunt, pulmonary arterial pressure and pulmonary vascular resistance (PVR) may increase.1 Depending on the response to the increased flow and pressure, pulmonary vascular changes may develop. A non-operated large VSD is often complicated by irreversible changes in the pulmonary vascular bed. Closure of a large VSD with increased PVR is associated with significant morbidity and mortality.2 We report our experience of closure of a large VSD in patients with severe pulmonary hypertension, using a valved patch.
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PATIENTS AND METHODS
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Between March 1998 and December 2004, all 16 patients presenting at our institute with a large VSD and increased PVR were included in the study. The patients were evaluated preoperatively by history and physical examination, chest radiography, electrocardiography, echocardiography, and cardiac catheterization. Generally, patients with clinical cyanosis were excluded from surgery. Complete hemodynamic data and oximetry were determined by cardiac catheterization. Pulmonary and systemic flow and resistance were measured at rest and during high oxygen flow for 10 minutes. The decision for surgery was based on the judgment of the cardiologist and the cardiac surgeon and acceptance of the risk by the patient’s family. The mean age at surgery was 7 ± 5.7 years (range, 2 to 22 years) and 12 patients (76%) were male. One patient had Down syndrome and a secundum atrial septal defect and 2 others had a moderate-sized patent ductus arteriosus. Mean PVR was 9.6 ± 3.8 Wood units (range, 6.7 to 16.8 Wood units). Following administration of oxygen, an increase in the left-to-right shunt and reduction in PVR occurred in 3 patients. The mean PVR values before and after oxygen administration were 10.8 ± 3.6 and 7.4 ± 2 Wood units, respectively. A perimembranous VSD was diagnosed in 70% of patients. Preoperative hemodynamic data are given in Table 1
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All surgical procedures were performed by the same surgeon. Cardiopulmonary bypass with moderate hypothermia and cold blood cardioplegia were used in all patients. Preoperatively, VSD size and location were determined by echocardiography. A patch was constructed from a Gore-Tex patch (WL Gore, Newark, DE, USA) and a piece of the patient’s pericardium. Depending on the VSD size and PVR, a central perpendicular slit of 5 to 8 mm in length was created in the Gore-Tex patch and covered by a piece of pericardium which was continuously sutured around the lower three quarters of the slit to direct flow from the right ventricle to the aorta and eliminate the left-to-right shunt (Figure 1). The operative approach varied according to the location of the VSD, but it was preferred through the right atrium. Subpulmonic and subarterial VSDs were repaired through the main pulmonary artery and right ventricular infundibulum. The VSDs were closed with a trimmed Gore-Tex patch so that the pericardial aspect was located on the left ventricular side to open for a potential right-to-left shunt (Figure 2).
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Figure 2. Illustration of the constructed valved patch from (A) the right atrial and (B) the left ventricular aspect.
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After weaning from cardiopulmonary bypass, modified ultrafiltration was used in some cases and vasodilators were started. All patients were sedated with Fentanyl for 18–24 hr postoperatively, and mild to moderate hypocarbia was maintained. On the day of operation, cardiac chamber function and the valved patch were assessed by transthoracic echocardiography. All patients were followed up by echocardiography on discharge from the hospital, at the 1st, 3rd, and 6th month, and yearly thereafter for evaluation of pulmonary artery pressures and possible shunts. Results are expressed as mean ± standard deviation.
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RESULTS
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All patients were weaned off cardiopulmonary bypass, but 2 (12.5%) died in the early postoperative period. One patient with a PVR of 9.3 Wood units died on the 3rd postoperative day due to multi-organ failure; despite deep sedation on a ventilator, frequent episodes of pulmonary hypertensive crisis with right-to-left shunting and convulsions occurred. The other patient died on the 5th postoperative day from persistent severe pulmonary arterial hypertension, a right-to-left shunt, and low systemic oxygen saturation. In this patient, the PVR was 14.6 Wood units. On the day of operation, pulmonary hypertensive crises were detected in 6 patients. In these cases, a right-to-left shunt through the valved patch was determined by echocardiography. The other patients had an uneventful postoperative course.
At a mean follow-up of 3.2 years (range, 5 months to 6 years) one patient still suffered palpitations and cyanosis. He had undergone surgery at the age of 10 years with a basal PVR of 9 Wood units, and after 4 years, he was in New York Heart Association functional class III with echocardiographic and catheterization evidence of severe pulmonary hypertension and a right-to-left shunt through the valved patch. Two other patients were in functional class II with echocardiographic evidence of moderate pulmonary hypertension at 2.5 years postoperatively. They were operated on at the age of 18 and 22 years with a mean basal PVR of 7.1 Wood units. The others were asymptomatic with normal or near normal pulmonary artery pressure.
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DISCUSSION
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There are several surgical approaches to treat a large VSD with severe pulmonary hypertension.3 Pulmonary artery banding was described as a means of reducing a large left-to-right shunt and improving survival.4 Operative mortality for this procedure is considerable in small infants, and many of these patients have a significant residual pulmonary artery deformity after reconstruction.5 Primary closure of the VSD with a fenestrated patch has been suggested as an alternative to two-stage management.2 In this repair, a large VSD is modified to a smaller VSD with a bidirectional shunt in the early postoperative period. In sustained or progressive PVR, a right-to-left shunt through the fenestration would occur, as in our valved patch repair technique. By reducing pulmonary artery pressure, in contrast to a unidirectional valved patch, fenestration allows a left-to-right shunt with the risk of endocarditis. Novick and colleagues7 used a flap-valved double-patch for closure of VSDs in children with increased PVR. They attached a secondary patch to the superior rim of the fenestration, directing the flow to open the valve toward the left ventricular apex. Contrary to our technique, flap-valve flow is not in the direction of left ventricular flow, and it seems to interfere with flow when the pressure in the left ventricle starts to rise.
A unidirectional valved patch for closure of a large VSD with pulmonary hypertension was reported to have acceptable morbidity and mortality.6,7 A one-way shunt through the valved patch is important in the early postoperative period. After the operation, pulmonary hypertensive crisis may occur and it can be associated with acute right heart failure and death. It is vital to ease refractory pulmonary arterial hypertension to reduce the risk of death. During hypertensive episodes, unloading of the right ventricle through the valved patch can occur. In our study,6 patients experienced pulmonary hypertensive crisis with right-to-left shunting. Creation of a one-way shunt may sometimes have deleterious effects in the early and even late postoperative period in patients with sustained elevated PVR. Compared to the bidirectional shunt with a fenestrated patch, these patients have only a right-to-left shunt which may lead to low systemic oxygen saturation and prolonged intubation in the early postoperative period. In the later phase, persistent pulmonary hypertension may lead to early cyanosis compared to non-operated cases with a large VSD; one patient in our series was found to be cyanotic 4 years after surgery.
The prognosis for patients undergoing closure of a large VSD with increased PVR is dependent on the age and degree of PVR on presentation.1,8 Although the patients in our study were older with high PVR, surprisingly, the mortality occurred in younger children. One patient (aged 2.5 years) died on the 3rd postoperative day with frequent episodes of pulmonary hypertensive crisis and the other, a 4 years old, died because of sustained elevated PVR with a right-to-left shunt via the valved patch. This patient could not achieve more than 90% arterial O2 saturation. If nitric oxide was available in our center, presumably it might improve oxygenation and hemodynamic indices in the short-term in these patients, but as Kannan and colleagues9 have reported, the rapid progression of PVR in younger children is a risk factor for significant morbidity and mortality compared to older patients with a similar elevation of PVR. Surgery on older patients was found to have a more favorable outcome in our study. In the early postoperative period, pulmonary hypertensive episodes did not occur, but arrhythmia was a common finding, which responded well to medication. In comparison to younger children, PVR gradually decreased in these patients but did not return to normal levels with good exercise capability. This may be due to permanent histopathologic changes in the pulmonary vascular bed.
The duration of intubation after the operation is a problem in these patients. The pulmonary vasoconstrictive effects of cardiopulmonary bypass and exacerbation of pulmonary vasoconstriction in the early postoperative period are well known.10,11 Sometimes, the development of pulmonary hypertensive episodes mandates delayed extubation.12 Novick and colleagues7 recommended rapid extubation of children to prevent adverse events. In our experience of early extubation, pulmonary hypertensive episodes occurred in 3 cases, which led to a right-to-left shunt and re-intubation. Due to the hazards of re-intubation and pulmonary hypertensive crisis, we abandoned rapid extubation. When PVR regresses and pulmonary artery pressure decreases, the pericardium in the valved patch adheres to the Gore-Tex to prevent left-to-right shunting. As there is only a slit in the Gore-Tex patch and pericardium is a flexible tissue, evidence of left ventricular outflow tract obstruction or pericardial aneurysm through the slit was not found during the follow-up.
It was concluded that a valved patch in cases of severe pulmonary artery hypertension seems to be a promising technique to decrease morbidity and mortality, but in sustained elevated PVR, it may have deleterious effects in the early and late postoperative periods.
Presented at the 7th Congress of the Pediatric Cardiac Society of India, Hyderabad, India, July 15–17, 2005.
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ABSTRACT
INTRODUCTION
