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Ann Thorac Surg 1995;60:1245-1248
© 1995 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Unidirectional Valve Patch for Repair of Cardiac Septal Defects With Pulmonary Hypertension

Department of Cardiac Surgery, Beijing Heart, Lung and Blood Vessel Medical Center, and Anzhen Hospital, Beijing, People's Republic of China

Accepted for publication June 3, 1995.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Background. Congenital septal defects with a large left-to-right shunt often cause pulmonary hypertension, which complicates surgical repair of the defects.

Methods. Twenty-four patients with congenital cardiac septal defects and severe pulmonary hypertension had operation to close the septal defect using a unidirectional valve patch during a 3-year period. The ratio of systolic pulmonary artery pressure to systolic arterial blood pressure was near to or more than 1.0 in all patients.

Results. Two patients died in the hospital after operation, and there have been no deaths during intermediate term follow-up. Mean pulmonary artery pressure decreased from 80 ± 12 mm Hg to 56 ± 18 mm Hg. The ratio of pulmonary artery pressure to systemic arterial pressure dropped from 1.1 ± 0.1 mm Hg to 0.7 ± 0.1 mm Hg. The unidirectional valve patch functioned allowing right to left shunting in 4 patients with a systolic pulmonary artery pressure more than systolic arterial blood pressure immediately after closure of a septal defect. The patch sealed or was effectively closed by the third postoperative day. There was impressive improvement in symptoms and exercise tolerance after operation during the 3-month to 3-year (mean, 1.1 year) follow-up period.

Conclusions. The unidirectional valve patch is useful for management of patients having operation to close cardiac septal defects in the presence of severe pulmonary hypertension.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
See also page 1249.

Congenital heart disease with septal defects and a large left-to-right shunt often causes pulmonary artery hypertension. The course of disease is variable and depends on the size of the defect, the magnitude of the left-to-right shunt, and the pulmonary vascular response to increased pulmonary flow and pressure [1]. Pulmonary artery pressure is hyperkinetic in the early phase but may eventually become a fixed elevation associated with a fixed increase of pulmonary vascular resistance [2]. The clinical symptomatic manifestations are decreased exercise tolerance, cyanosis, congestive heart failure, often hemoptysis, and finally death (Eisenmenger's syndrome). Eisenmenger's syndrome has been defined hemodynamically by Wood [3] as: Pulmonary hypertension at the systemic level due to a high pulmonary vascular resistance (more than 800 dynes • s^-1 • cm⁵) with reversed or bidirectional shunt through a septal defect. Patients having Eisenmenger's syndrome are often seriously handicapped and may be functionally improved by closure of the septal defect, although ``long-term'' survival may be unaltered. Unfortunately, ``short-term'' risk of death accompanying the operation is high. This report documents the experience of closure of septal defects in a group of patients with severe pulmonary hypertension using a univentricular valve patch (UVP) in an effort to reduce the risk of operation.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Patients
Twenty-four patients with congenital cardiac defects and severe hypertension underwent operation in our institute during the period from January 1, 1990, to December 31, 1993. There were 15 cases of isolated ventricular septal defect, 3 cases of ventricular septal defect in combination with atrial septal defect, 2 cases of ventricular septal defect in association with patent ductus arteriosus, 2 cases of patent ductus arteriosus and coarctation of aorta coexisted with a large ventricular septal defect, and 2 cases of isolated atrial septal defect. The age ranged from 5 to 28 years (average, 15.8 years). All patients had dyspnea on exertion. Cyanosis was present in 2 patients at rest and occurred with exercise in 19. Five patients reported hemoptysis. A systolic murmur was audible in 11 patients. The murmur was only grade I (soft) in 8 patients and it was absent in 5 patients. The second heart sound was increased at the left base in all patients. Eight patients were classified in New York Heart Association functional class II, 15 in class III, and 1 in class IV. The electrocardiogram showed right axis deviation in all patients. There was right ventricular hypertrophy in 16 patients and 8 showed biventricular hypertrophy. Chest roentgenogram showed dilation of the main pulmonary artery in all patients, with a tumor-like enlargement in 6 of them. Cardiothoracic ratio ranged from 0.45 to 0.67 (mean, 0.55 ± 0.1). Bidirectional shunt through the intracardiac or extracardiac defect was present in all patients by echocardiography and catheter flow studies. Cardiac catheterization showed the ratio of pulmonary to system flow ranged from 0.5 to 2.0 (mean, 1.2 ± 0.5), and was less than 1.0 in 10 patients. Calculated total pulmonary resistance ranged from 8 to 32 Wood units (mean, 16 ± 7 Wood units). Pulmonary resistance was more than 10 Wood units in 20 patients and in 7 of them it was more than 20 Wood units. Ratio of systolic pulmonary artery pressure to systolic systemic arterial blood pressure (SPAP/SABP) ranged from 1.0 to 1.3 mm Hg (mean, 1.1 ± 0.1 mm Hg) and in 22 patients it was equal to or more than 1.0 mm Hg. Mean pulmonary artery pressure ranged from 50 to 98 mm Hg (mean, 80 ± 12 mm Hg), and it was more than 80 mm Hg in 14 patients. Arterial oxygen saturation ranged from 82% to 93% (mean, 87% ± 4%), and was less than 90% in 17 patients. Biopsy of the lung was performed in the last 12 consecutive patients. Pulmonary vascular disease was graded by Heath-Edwards classification [4]. There was 1 patient in grade I, 9 in grade III, and 2 had grade IV pulmonary vascular disease.

Methods
Anesthesia was induced by thiopental infusion and intermittent positive-pressure ventilation with nitrous oxide, facilitated by muscle relaxants. Fentanyl was used for maintenance. Pressure in the pulmonary artery was measured by needle puncture before repair of the septal defect and at the completion of operation before closure of the wound. A flow-directed balloon catheter was inserted into the main pulmonary artery to monitor the hemodynamic changes continuously in 12 patients who underwent operation in 1993. Systemic blood pressure and central venous pressure were monitored in the radial artery and femoral vein. The unidirectional valve patch was used to close the ventricular septal defect (22 patients) or atrial septal defect (2 patients). Associated anomalies were corrected simultaneously. The UVP was constructed from a Dacron patch approximately as large as the defect to be closed. A hole about 0.5 to 1.0 cm in diameter was made in the patch somewhat off the center. A piece of quadrangular pericardium was attached by suture to the surface of the Dacron patch. The three edges of pericardium were continuously sutured and one edge was left unattached. This unattached edge of pericardium should provide a small opening, not to exceed 0.5 cm, and appropriate tension should be maintained on the pericardial edge so that the valve mechanism will not be loose and incompetent. Nevertheless, the tension should not be too great and completely attach the pericardium to the Dacron patch and lose its valve effectiveness (Fig 1). The pericardial flap valve is placed on the left side (systemic) of the defect.

View larger version (36K): [in this window] [in a new window]   Fig 1. . Construction of a unidirectional valve patch for closure of atrial septal defect from Dacron with a 0.5- to 1.0-cm hole somewhat off center. Three sides of the pericardial patch are attached and one side is open to function as a valve. The pericardial flap valve is placed on the left side (systemic) of the defect. This allows blood to flow from the right atrium (RA) to the left atrium (LA) or across the ventricular septum when used to close a ventricular septal defect.

Sedation and oxygen supplement were considered to be important to these patients in the postoperative care. Prostaglandin E₁ was the pulmonary vasodilator of choice. The support time of respiration using endotracheal tube and respirator-assisted ventilation ranged from 44 to 93 hours (average, 58 hours).

Results were presented as mean ± standard error of the mean. Paired t tests were used to assess the difference between data at each time point. Spearman's correlation tests were performed to evaluate the relationships. Values were considered to be statistically significant when p was less than 0.05.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Two patients died after the operation. These patients were among those treated in the initial application of UVP. One died of acute right heart failure at the fourth postoperative day and the other died at the second postoperative day because of respirator failure, although the hemodynamics had improved after operation. The perioperative mortality was 8.3%. One patient with patch dehiscence and left-to-right shunt required reoperation. Cerebral air emboli occurred in 1 patient who gradually recovered with supporting therapy.

The follow-up period was 3 months to 3 years (average, 1.1 ± 0.9 years). The symptoms of dyspnea on exertion were relieved, cyanosis disappeared, and hemoptysis did not reoccur. Functional class improved with 14 patients in class I and 10 patients in class II.

Hemodynamic changes after operation included a significant decrease in pulmonary artery pressure (mean pulmonary artery pressure, 56 ± 19 mm Hg versus 80 ± 12 mm Hg before repair) and in the SPAP/SABP, 0.7 ± 0.1 versus 1.1 ± 0.1 before repair (Table 1). Arterial oxygen saturation increased significantly after operation (mean, 96% ± 1% versus 88% ± 4% before operation; p < 0.001). Hemodynamics continuously monitored during and after operation in 12 patients treated in 1993 showed most change occurring intraoperatively and only a slight further decrease of pulmonary artery pressure and SPAP/SABP during the first 12 hours after operation.

Echocardiography at 2 weeks and 4 weeks after operation showed SPAP continued to decrease, but the diameter of the pulmonary artery did not change.

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
The surgical treatment of congenital heart disease with severe pulmonary hypertension is controversial [2, 5–8]. Perioperative mortality to close septal defects is high (22.7% to 50%) [9–12]. Acute congestive heart failure, pulmonary hypertensive crisis, and acute respiratory failure are the principal causes of perioperative death. It has been generally accepted that operation to close the septal defect should not be performed when the pulmonary vascular resistance is more than 10 Wood units, the ratio of pulmonary to system flow is less than 1.5, and the arterial oxygen saturation is less than 90% [2, 5, 13].

Pulmonary artery pressure and pulmonary vascular resistance are always significantly elevated in the patients with Eisenmenger's syndrome. Operation to correct the congenital cardiac defect requires use of cardiopulmonary bypass, infusion of protamine, and other factors that could cause the release of vasoactive substances such as thromboxane A₂ and catecholamines resulting in pulmonary vasoconstriction and acute pulmonary hypertension [14–18]. Pulmonary hypertensive crisis can be associated with acute congestive heart failure and death after operation in some of these patients. The univentricular valve patch was designed to function like the fossa ovalis of the atrial septum. It provides the advantage of opening to allow some blood to flow from right to left during pulmonary hypertensive episodes. This is akin to reducing risk by the technique of fenestration of the atrial septum after Fontan-type operations, which has been extensively documented in the literature. This could prevent pulmonary artery hypertension from becoming refractory while maintaining systemic blood pressure with the aim of reducing risk of death after operation. When pulmonary artery pressure diminishes after operation and pressure gradients between the right and left sides of the circulation normalize, the unidirectional valve closes and blocks the left-to-right shunt. The pericardium eventually adheres to the Dacron patch producing secure closure of the septal defect.

The data presented in this study indicated that the UVP has been a useful adjunct to management of patients having operations to close cardiac septal defects in the presence of severe pulmonary hypertension. Low operative mortality (8.3%) in these difficult operations is compelling evidence. Subjectively, systemic arterial blood pressure appears to remain quite stable during operation and during the critical early postoperative period and general management of the patient was easier. Postoperative epicardial echocardiography demonstrated that the valve actually opened and blood flowed from right to left circulation especially in those critical cases where pulmonary artery pressure was higher than systemic artery pressure. Blood was also shown to flow from the right to the left ventricle through the unidirectional valve during the 12-hour period after operation. As cardiac function improved and hemodynamics became more stable 1 to 3 days after operation, echocardiography showed that the UVP gradually closed and became less important.

Other aspects of perioperative management were certainly as important as the UVP for these patients. An endotracheal tube was in place and the patients' ventilation was supported by a respirator until cardiopulmonary function was stable and adequate. The period of respirative support was long for all patients, ranging from 44 to 93 hours (average, 58 hours). Prostaglandin E₁ was used liberally as the principal pulmonary vasodilator, because it is a relatively selective pulmonary vasodilator and had less effects to systemic circulation [19, 20]. Nitric oxide was not available for management of this group of patients and could be even more effective than the combination of the UVP and prostaglandin E₁. Inotropic agents were infused as required through the left atrial catheter to reduce pulmonary vasoconstriction.

Echocardiography was used to monitor structure and cardiac function in the operating room, during the postoperative period, and later after invasive catheters were removed. Pulmonary hypertension is considered to be the most common cause of functional tricuspid regurgitation [21]. Quantitation of tricuspid insufficiency by Doppler ultrasound provided an accurate noninvasive estimate of pulmonary artery pressure [22, 23] in the postoperative follow-up of these patients. Echocardiography was also useful in monitoring flow direction patterns across the septal defect closed by the UVP. Echocardiography showed the UVP had ceased functioning by 3 days after operation and the cardiac defect was completely closed. Structural abnormality, such as size of the pulmonary artery, did not change during follow-up although hemodynamics improved dramatically.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
We express thanks to Donald B. Doty, MD, for assistance in preparation of the manuscript.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Address reprint requests to Dr Zhou, Beijing Heart, Lung and Blood Vessel Medical Center, Anding Menwai, Beijing 100029, People's Republic of China.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 

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