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Is direct closure dangerous for treatment of doubly committed subarterial ventricular septal defect?
Is Direct Closure Dangerous for Treatment of Doubly Committed Subarterial Ventricular Septal Defect? Kouichi Hisatomi, MD, Akira Taira, MD, and Yukinori Moriyama, MD Second Department of Surgery, Faculty of Medicine, Kagoshima University, Kagoshima City, Japan
Background. We performed direct closure of doubly committed subarterial ventricular septal defects with aortic cusp prolapse. Postoperative echocardiographic studies showed that this method improved coaptation of the prolapsing aortic cusp, especially in patients with mild aortic regurgitation (AR). Methods. Twenty-one patients (mean age, 7.8 6 4.3 years; range, 2 to 18 years) with doubly committed subarterial ventricular septal defect underwent direct closure alone. Aortic valve prolapse was observed in all 21 patients, with mild AR found in 13 patients but not in the remaining 8. The site of the prolapsed aortic valve was in the right coronary cusp in all patients. We inserted an interrupted 4-0 or 5-0 polypropylene suture with a pledget from the lower margin of the ventricular septal defect to the pulmonary ring to increase protrusion of the prolapsed cusp by pushing it back and to improve coaptation of the aortic cusp. Results. The interval between surgical treatment and the last postoperative evaluation ranged from 3 to 24 months (median, 11 months). No residual ventricular
septal defect was detected in any patient. In the 8 patients who had aortic valve prolapse without AR preoperatively, no AR was found at follow-up. Of the 13 patients who had mild AR associated with aortic valve prolapse preoperatively, AR diminished in 7 and did not progress in the remaining 6. Furthermore, no anatomic changes in either the aortic or pulmonary annulus were found on follow-up echocardiography. In the group of 13 patients with mild preoperative AR, AR significantly persisted in patients who were more than 10 years old at operation (p < 0.05). Conclusions. Our findings suggest that direct closure for this type of ventricular septal defect is safe and reliable in improving mild AR and that direct closure is more effective for younger patients in whom the prolapsing aortic cusp is mobile enough to be protruded. However, further long-term follow-up studies will be needed to ascertain the adequacy and usefulness of the method.
R
Patients and Methods
ecently, the number of patients requiring aortic valve repair for aortic regurgitation (AR) associated with doubly committed subarterial ventricular septal defect (VSD) has markedly decreased because the mechanism of its occurrence is well understood, and patients are immediately referred for closure of the VSD when progression of prolapse of the aortic cusp or AR is detected [1–3]. Patch closure alone for this type of VSD, if the grade of the associated AR is mild or less, has been found to prevent further progression of AR in several recent postoperative follow-up studies [3–5]. In the present study, we used direct closure for this type of VSD to protrude the prolapsing cusp (to return the cusp to its normal position) and to diminish the AR rather than to prevent progression. We examined the results obtained by postoperative echocardiographic studies.
Accepted for publication Aug 6, 1998. Address reprint requests to Dr Hisatomi, Second Department of Surgery, Faculty of Medicine, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima City, 890-8520 Japan.
© 1999 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
(Ann Thorac Surg 1999;67:756 –9) © 1999 by The Society of Thoracic Surgeons
From November 1995, to October 1997, 21 patients with doubly committed subarterial VSD underwent operation. Patients ranged in age from 2 to 18 years (mean, 7.8 6 4.3 years). All but 3 patients, who were being treated with diuretic drugs and digitalis derivates, had no limitation of exercise preoperatively. Preoperative echocardiography and angiography were performed in all patients. Aortic valve prolapse was observed in all 21 patients; mild AR was found in 13 patients but not in the remaining 8. Pulmonary-to-systemic flow ratios ranged from 1.1 to 2.2 (mean, 1.4 6 0.3), and no other cardiac anomalies were observed in any of the patients. The operation was performed under moderate hypothermia with ascending aortic and bicaval cannulation, and hearts were arrested with antegrade infusion of blood cardioplegic solution after aortic cross-clamping. The pulmonary trunk was transversely incised approximately 1 cm above the pulmonary ring, and we were able to confirm that the principal location of the VSD was just beneath the pulmonary valve. The size of the defect, which was measured by the distance between the pulmonary ring and the lower margin of the defect, ranged 0003-4975/99/$20.00 PII S0003-4975(99)00004-1
Ann Thorac Surg 1999;67:756 –9
757
HISATOMI ET AL DIRECT CLOSURE OF SUBARTERIAL VSD
Table 1. Relation Between Presence of Residual Aortic Regurgitation and Age at Operation in 13 Patients With Mild Preoperative Aortic Regurgitation Age at Operation Postoperative AR
$ 10 y (n 5 6)
, 10 y (n 5 7)
Present (n 5 6) Absent (n 5 7)
83% (5) 14% (1)
17% (1) 86% (6)
AR 5 aortic regurgitation.
of AR by two-dimensional color Doppler flow imaging were based on the maximal distance reached by regurgitant blood flow images in the left ventricular outflow tract in the long-axis view [6]. Mild regurgitation was indicated by a regurgitant flow image localized in the subaortic region and corresponded to grade 11 AR according to the Sellers’ classification. Results are presented as mean 6 standard deviation. Correlations between the presence of residual AR and age at operation were analyzed by the Fisher’s exact test. A p value less than 0.05 indicated statistical significance.
Results
Fig 1. Direct closure performed through a transpulmonary approach. Top panel shows an interrupted polypropylene suture with a pledget inserted from the lower margin of the ventricular septal defect to the pulmonary ring. Bottom panel shows direct closure pushing the prolapsed sinus and cusp back, resulting in improved coaptation of the aortic cusp. (Ao 5 aorta; PA 5 pulmonary artery; IVS 5 interventricular septum.)
from 7 to 15 mm (median, 10 mm). The site of the prolapsed aortic valve was in the right coronary cusp in all patients. We inserted an interrupted 4-0 or 5-0 polypropylene suture with a pledget from the lower margin of the VSD to the pulmonary ring (Fig 1). The number of stitches varied from three to six. In some patients for whom orientation of the boundary between the prolapsed aortic cusp itself and the rim of the VSD was difficult, cardioplegic solution was infused to reveal the extent of the aortic cusp and to prevent its injury during repair. All patients were followed up carefully, and postoperative examination included color Doppler echocardiography (HDI 3000; Advanced Technology Laboratories Co, WA) in all patients. The criteria for assessing the severity
There were no early and late deaths in this series, and no patient has undergone reoperation. Postoperative complications occurred in only 1 patient who experienced pericardial effusion and was given aspirin for 2 weeks postoperatively. The interval between surgical treatment and the last postoperative evaluation ranged from 3 to 24 months (median, 11 months). All patients are now New York Heart Association functional class I. No residual VSD was detected in any patient. In the 8 patients who had aortic valve prolapse without AR preoperatively, no AR was found during follow-up study. In 7 of the 13 patients who had mild AR associated with aortic valve prolapse preoperatively, the AR diminished. In the remaining 6 patients, no AR occurred in 4, and AR lessened, becoming only slight in the subaortic area, in 2 patients, as determined by color Doppler flow imaging. Furthermore, no anatomic changes (distortion) in either the aortic or pulmonary annulus were found on follow-up echocardiography. In the group of 13 patients with mild preoperative AR (Table 1), AR significantly persisted in those who were older than 10 years at operation ( p 5 0.029).
Comment Since Spencer and associates [7] and Kawashima and colleagues [8] described the surgical procedure for patients with doubly committed subarterial VSD associated with AR, patch closure for this type of VSD has been considered the most reliable and definitive procedure for preventing residual VSD and disruption of the aortic annulus postoperatively. In 1991, Backer and colleagues [4] also suggested that direct closure appeared to have the risk of pulling the valve down to the septum and
758
HISATOMI ET AL DIRECT CLOSURE OF SUBARTERIAL VSD
making aortic valve insufficiency worse by producing a downward deflection of the aortic annulus and disruption of its commissural support, especially in doubly committed subarterial VSD. However, we performed direct closure in patients with VSD limited to the right ventricular outflow tract but not in patients with VSD extending to the perimembranous area or with malalignment VSD, or both. As a result, direct closure can be performed easily and safely by raising the lower edge of the VSD, even though the defect is large, when undertaken with precise orientation. We also found that direct closure actually improved coaptation of the aortic cusp. Recently, Yacoub and associates [9] described the results of their ideal means of total repair of VSD associated with a prolapsing aortic cusp through a transaortic approach alone. Consistent with their experience, we performed direct closure in 21 consecutive patients with a doubly committed subarterial VSD with or without mild AR. These patients had no residual VSD or progression of AR; the prolapsing cusp and mild AR disappeared, except in older patients; and no anatomic changes (distortion) in either the aortic or pulmonary annulus were found on follow-up echocardiography. Furthermore, postoperative murmur, which sometimes appears to result from the use of a patch, was not detected in any of the patients. Our findings suggest that direct closure for this type of VSD is safe and reliable in improving mild AR and that direct closure is more effective for younger patients in whom the prolapsing aortic cusp is mobile enough to be protruded. However, the present study is limited by the short duration of postoperative follow-up, and further long-term follow-up studies will be needed to ascertain the adequacy and usefulness of this method.
Ann Thorac Surg 1999;67:756 –9
References 1. Tatsuno K, Konno S, Ando M, Sakakibara S. Pathogenetic mechanisms of prolapsing aortic valve and aortic regurgitation associated with ventricular septal defect: anatomical, angiographic, and surgical considerations. Circulation 1973; 48:1028–37. 2. Tohyama K, Satomi G, Momma K. Aortic valve prolapse and aortic regurgitation associated with subpulmonic ventricular septal defect. Am J Cardiol 1997;79:1285–9. 3. Schmidt KG, Cassidy SC, Silverman NH, Stanger P. Doubly committed subarterial ventricular septal defects: echocardiographic features and surgical implications. J Am Coll Cardiol 1988;12:1538– 46. 4. Backer CL, Idriss FS, Zales VR, et al. Surgical management of the conal (supracristal) ventricular septal defect. J Thorac Cardiovasc Surg 1991;102:288–96. 5. Komai H, Naito Y, Fujiwara K, Noguchi Y, Nishimura Y, Uemura S. Surgical strategy for doubly committed subarterial ventricular septal defect with aortic cusp prolapse. Ann Thorac Surg 1997;64:1146–9. 6. Omoto R, Yokote Y, Takamoto S, et al. The development of real-time two-dimensional Doppler echocardiography and its clinical significance in acquired valvular disease, with special reference to the evaluation of valvular regurgitation. Jpn Heart J 1984;25:325– 40. 7. Spencer FC, Doyle EF, Danilowicz DA, Bahnson HT, Weldon CS. Long-term evaluation of aortic valvuloplasty for aortic insufficiency and ventricular septal defect. J Thorac Cardiovasc Surg 1973;65:15–31. 8. Kawashima Y, Danno M, Shimizu Y, et al. Ventricular septal defect associated with aortic insufficiency. Circulation 1973; 47:1057– 64. 9. Yacoub MH, Khan H, Stavri G, Shinebourne E, Radley-Smith R. Anatomic correction of the syndrome of prolapsing right coronary cusp, dilatation of the sinus of Valsalva, and ventricular septal defect. J Thorac Cardiovasc Surg 1997;113: 253– 61.
INVITED COMMENTARY Doctor Hisatomi and colleagues have addressed a very focused question, Is direct closure dangerous for treatment of doubly committed subarterial ventricular septal defect? They operated on 21 patients with conal ventricular septal defects, all of whom underwent direct closure of the ventricular septal defect with pledgeted sutures. Exposure was through the pulmonary artery, with the sutures tied at the base of the pulmonary valve. Indications for operation were aortic valve prolapse or aortic valve regurgitation, or both. There were no residual ventricular septal defects, and all patients had either reduction or nonprogression of their aortic insufficiency. They concluded that direct suture closure is safe and reliable for patients with doubly committed subarterial ventricular septal defects. The technique was particularly effective in younger patients (, 10 years of age), in that subgroup most children had no postoperative aortic regurgitation. The approach to the patient with a doubly committed subarterial (conal, supracristal) ventricular septal defect has evolved considerably in the past decade. Many of the features of the authors’ current review I strongly agree © 1999 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
with, including (1) aortic valve prolapse is an indication for operative intervention in these patients, (2) early ventricular septal defect closure results in preservation of the aortic valve; and (3) excellent results can be obtained by approaching the conal ventricular septal defect through the pulmonary artery. Since initially reviewing the manuscript I have had the opportunity in 1 patient to directly close a conal ventricular septal defect as described by the authors, and the technique worked well. However, I also had a recent experience with a patient with a larger conal ventricular septal defect in whom the direct closure technique was not successful. That patient had prolapse of both the right and the noncoronary cusps through the ventricular septal defect. In keeping with the report by Dr Hisatomi and colleagues, I proceeded with direct closure. This approach resulted in severe aortic valve insufficiency (by intraoperative transesophageal echocardiography), which was corrected by removing the direct closure sutures and then using a patch for the ventricular septal defect closure. This child left the hospital with only trivial aortic valve insufficiency. It is my opinion that a patient 0003-4975/99/$20.00 PII S0003-4975(99)00005-3
Background. We performed direct closure of doubly committed subarterial ventricular septal defects with aortic cusp prolapse. Postoperative echocardiographic studies showed that this method improved coaptation of the prolapsing aortic cusp, especially in patients with mild aortic regurgitation (AR). Methods. Twenty-one patients (mean age, 7.8 6 4.3 years; range, 2 to 18 years) with doubly committed subarterial ventricular septal defect underwent direct closure alone. Aortic valve prolapse was observed in all 21 patients, with mild AR found in 13 patients but not in the remaining 8. The site of the prolapsed aortic valve was in the right coronary cusp in all patients. We inserted an interrupted 4-0 or 5-0 polypropylene suture with a pledget from the lower margin of the ventricular septal defect to the pulmonary ring to increase protrusion of the prolapsed cusp by pushing it back and to improve coaptation of the aortic cusp. Results. The interval between surgical treatment and the last postoperative evaluation ranged from 3 to 24 months (median, 11 months). No residual ventricular
septal defect was detected in any patient. In the 8 patients who had aortic valve prolapse without AR preoperatively, no AR was found at follow-up. Of the 13 patients who had mild AR associated with aortic valve prolapse preoperatively, AR diminished in 7 and did not progress in the remaining 6. Furthermore, no anatomic changes in either the aortic or pulmonary annulus were found on follow-up echocardiography. In the group of 13 patients with mild preoperative AR, AR significantly persisted in patients who were more than 10 years old at operation (p < 0.05). Conclusions. Our findings suggest that direct closure for this type of ventricular septal defect is safe and reliable in improving mild AR and that direct closure is more effective for younger patients in whom the prolapsing aortic cusp is mobile enough to be protruded. However, further long-term follow-up studies will be needed to ascertain the adequacy and usefulness of the method.
R
Patients and Methods
ecently, the number of patients requiring aortic valve repair for aortic regurgitation (AR) associated with doubly committed subarterial ventricular septal defect (VSD) has markedly decreased because the mechanism of its occurrence is well understood, and patients are immediately referred for closure of the VSD when progression of prolapse of the aortic cusp or AR is detected [1–3]. Patch closure alone for this type of VSD, if the grade of the associated AR is mild or less, has been found to prevent further progression of AR in several recent postoperative follow-up studies [3–5]. In the present study, we used direct closure for this type of VSD to protrude the prolapsing cusp (to return the cusp to its normal position) and to diminish the AR rather than to prevent progression. We examined the results obtained by postoperative echocardiographic studies.
Accepted for publication Aug 6, 1998. Address reprint requests to Dr Hisatomi, Second Department of Surgery, Faculty of Medicine, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima City, 890-8520 Japan.
© 1999 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
(Ann Thorac Surg 1999;67:756 –9) © 1999 by The Society of Thoracic Surgeons
From November 1995, to October 1997, 21 patients with doubly committed subarterial VSD underwent operation. Patients ranged in age from 2 to 18 years (mean, 7.8 6 4.3 years). All but 3 patients, who were being treated with diuretic drugs and digitalis derivates, had no limitation of exercise preoperatively. Preoperative echocardiography and angiography were performed in all patients. Aortic valve prolapse was observed in all 21 patients; mild AR was found in 13 patients but not in the remaining 8. Pulmonary-to-systemic flow ratios ranged from 1.1 to 2.2 (mean, 1.4 6 0.3), and no other cardiac anomalies were observed in any of the patients. The operation was performed under moderate hypothermia with ascending aortic and bicaval cannulation, and hearts were arrested with antegrade infusion of blood cardioplegic solution after aortic cross-clamping. The pulmonary trunk was transversely incised approximately 1 cm above the pulmonary ring, and we were able to confirm that the principal location of the VSD was just beneath the pulmonary valve. The size of the defect, which was measured by the distance between the pulmonary ring and the lower margin of the defect, ranged 0003-4975/99/$20.00 PII S0003-4975(99)00004-1
Ann Thorac Surg 1999;67:756 –9
757
HISATOMI ET AL DIRECT CLOSURE OF SUBARTERIAL VSD
Table 1. Relation Between Presence of Residual Aortic Regurgitation and Age at Operation in 13 Patients With Mild Preoperative Aortic Regurgitation Age at Operation Postoperative AR
$ 10 y (n 5 6)
, 10 y (n 5 7)
Present (n 5 6) Absent (n 5 7)
83% (5) 14% (1)
17% (1) 86% (6)
AR 5 aortic regurgitation.
of AR by two-dimensional color Doppler flow imaging were based on the maximal distance reached by regurgitant blood flow images in the left ventricular outflow tract in the long-axis view [6]. Mild regurgitation was indicated by a regurgitant flow image localized in the subaortic region and corresponded to grade 11 AR according to the Sellers’ classification. Results are presented as mean 6 standard deviation. Correlations between the presence of residual AR and age at operation were analyzed by the Fisher’s exact test. A p value less than 0.05 indicated statistical significance.
Results
Fig 1. Direct closure performed through a transpulmonary approach. Top panel shows an interrupted polypropylene suture with a pledget inserted from the lower margin of the ventricular septal defect to the pulmonary ring. Bottom panel shows direct closure pushing the prolapsed sinus and cusp back, resulting in improved coaptation of the aortic cusp. (Ao 5 aorta; PA 5 pulmonary artery; IVS 5 interventricular septum.)
from 7 to 15 mm (median, 10 mm). The site of the prolapsed aortic valve was in the right coronary cusp in all patients. We inserted an interrupted 4-0 or 5-0 polypropylene suture with a pledget from the lower margin of the VSD to the pulmonary ring (Fig 1). The number of stitches varied from three to six. In some patients for whom orientation of the boundary between the prolapsed aortic cusp itself and the rim of the VSD was difficult, cardioplegic solution was infused to reveal the extent of the aortic cusp and to prevent its injury during repair. All patients were followed up carefully, and postoperative examination included color Doppler echocardiography (HDI 3000; Advanced Technology Laboratories Co, WA) in all patients. The criteria for assessing the severity
There were no early and late deaths in this series, and no patient has undergone reoperation. Postoperative complications occurred in only 1 patient who experienced pericardial effusion and was given aspirin for 2 weeks postoperatively. The interval between surgical treatment and the last postoperative evaluation ranged from 3 to 24 months (median, 11 months). All patients are now New York Heart Association functional class I. No residual VSD was detected in any patient. In the 8 patients who had aortic valve prolapse without AR preoperatively, no AR was found during follow-up study. In 7 of the 13 patients who had mild AR associated with aortic valve prolapse preoperatively, the AR diminished. In the remaining 6 patients, no AR occurred in 4, and AR lessened, becoming only slight in the subaortic area, in 2 patients, as determined by color Doppler flow imaging. Furthermore, no anatomic changes (distortion) in either the aortic or pulmonary annulus were found on follow-up echocardiography. In the group of 13 patients with mild preoperative AR (Table 1), AR significantly persisted in those who were older than 10 years at operation ( p 5 0.029).
Comment Since Spencer and associates [7] and Kawashima and colleagues [8] described the surgical procedure for patients with doubly committed subarterial VSD associated with AR, patch closure for this type of VSD has been considered the most reliable and definitive procedure for preventing residual VSD and disruption of the aortic annulus postoperatively. In 1991, Backer and colleagues [4] also suggested that direct closure appeared to have the risk of pulling the valve down to the septum and
758
HISATOMI ET AL DIRECT CLOSURE OF SUBARTERIAL VSD
making aortic valve insufficiency worse by producing a downward deflection of the aortic annulus and disruption of its commissural support, especially in doubly committed subarterial VSD. However, we performed direct closure in patients with VSD limited to the right ventricular outflow tract but not in patients with VSD extending to the perimembranous area or with malalignment VSD, or both. As a result, direct closure can be performed easily and safely by raising the lower edge of the VSD, even though the defect is large, when undertaken with precise orientation. We also found that direct closure actually improved coaptation of the aortic cusp. Recently, Yacoub and associates [9] described the results of their ideal means of total repair of VSD associated with a prolapsing aortic cusp through a transaortic approach alone. Consistent with their experience, we performed direct closure in 21 consecutive patients with a doubly committed subarterial VSD with or without mild AR. These patients had no residual VSD or progression of AR; the prolapsing cusp and mild AR disappeared, except in older patients; and no anatomic changes (distortion) in either the aortic or pulmonary annulus were found on follow-up echocardiography. Furthermore, postoperative murmur, which sometimes appears to result from the use of a patch, was not detected in any of the patients. Our findings suggest that direct closure for this type of VSD is safe and reliable in improving mild AR and that direct closure is more effective for younger patients in whom the prolapsing aortic cusp is mobile enough to be protruded. However, the present study is limited by the short duration of postoperative follow-up, and further long-term follow-up studies will be needed to ascertain the adequacy and usefulness of this method.
Ann Thorac Surg 1999;67:756 –9
References 1. Tatsuno K, Konno S, Ando M, Sakakibara S. Pathogenetic mechanisms of prolapsing aortic valve and aortic regurgitation associated with ventricular septal defect: anatomical, angiographic, and surgical considerations. Circulation 1973; 48:1028–37. 2. Tohyama K, Satomi G, Momma K. Aortic valve prolapse and aortic regurgitation associated with subpulmonic ventricular septal defect. Am J Cardiol 1997;79:1285–9. 3. Schmidt KG, Cassidy SC, Silverman NH, Stanger P. Doubly committed subarterial ventricular septal defects: echocardiographic features and surgical implications. J Am Coll Cardiol 1988;12:1538– 46. 4. Backer CL, Idriss FS, Zales VR, et al. Surgical management of the conal (supracristal) ventricular septal defect. J Thorac Cardiovasc Surg 1991;102:288–96. 5. Komai H, Naito Y, Fujiwara K, Noguchi Y, Nishimura Y, Uemura S. Surgical strategy for doubly committed subarterial ventricular septal defect with aortic cusp prolapse. Ann Thorac Surg 1997;64:1146–9. 6. Omoto R, Yokote Y, Takamoto S, et al. The development of real-time two-dimensional Doppler echocardiography and its clinical significance in acquired valvular disease, with special reference to the evaluation of valvular regurgitation. Jpn Heart J 1984;25:325– 40. 7. Spencer FC, Doyle EF, Danilowicz DA, Bahnson HT, Weldon CS. Long-term evaluation of aortic valvuloplasty for aortic insufficiency and ventricular septal defect. J Thorac Cardiovasc Surg 1973;65:15–31. 8. Kawashima Y, Danno M, Shimizu Y, et al. Ventricular septal defect associated with aortic insufficiency. Circulation 1973; 47:1057– 64. 9. Yacoub MH, Khan H, Stavri G, Shinebourne E, Radley-Smith R. Anatomic correction of the syndrome of prolapsing right coronary cusp, dilatation of the sinus of Valsalva, and ventricular septal defect. J Thorac Cardiovasc Surg 1997;113: 253– 61.
INVITED COMMENTARY Doctor Hisatomi and colleagues have addressed a very focused question, Is direct closure dangerous for treatment of doubly committed subarterial ventricular septal defect? They operated on 21 patients with conal ventricular septal defects, all of whom underwent direct closure of the ventricular septal defect with pledgeted sutures. Exposure was through the pulmonary artery, with the sutures tied at the base of the pulmonary valve. Indications for operation were aortic valve prolapse or aortic valve regurgitation, or both. There were no residual ventricular septal defects, and all patients had either reduction or nonprogression of their aortic insufficiency. They concluded that direct suture closure is safe and reliable for patients with doubly committed subarterial ventricular septal defects. The technique was particularly effective in younger patients (, 10 years of age), in that subgroup most children had no postoperative aortic regurgitation. The approach to the patient with a doubly committed subarterial (conal, supracristal) ventricular septal defect has evolved considerably in the past decade. Many of the features of the authors’ current review I strongly agree © 1999 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
with, including (1) aortic valve prolapse is an indication for operative intervention in these patients, (2) early ventricular septal defect closure results in preservation of the aortic valve; and (3) excellent results can be obtained by approaching the conal ventricular septal defect through the pulmonary artery. Since initially reviewing the manuscript I have had the opportunity in 1 patient to directly close a conal ventricular septal defect as described by the authors, and the technique worked well. However, I also had a recent experience with a patient with a larger conal ventricular septal defect in whom the direct closure technique was not successful. That patient had prolapse of both the right and the noncoronary cusps through the ventricular septal defect. In keeping with the report by Dr Hisatomi and colleagues, I proceeded with direct closure. This approach resulted in severe aortic valve insufficiency (by intraoperative transesophageal echocardiography), which was corrected by removing the direct closure sutures and then using a patch for the ventricular septal defect closure. This child left the hospital with only trivial aortic valve insufficiency. It is my opinion that a patient 0003-4975/99/$20.00 PII S0003-4975(99)00005-3