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Ann Thorac Surg 2000;70:1466-1470
© 2000 The Society of Thoracic Surgeons

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Original articles: cardiovascular

Ruptured sinus of valsalva aneurysm: early recurrence and fate of the aortic valve

^a Division of Cardiovascular Surgery, The Toronto General Hospital, Toronto, Ontario, Canada
^b The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada

Address reprint requests to Dr Williams, Division of Cardiovascular Surgery, The Hospital for Sick Children, 555 University Ave, Suite 1525, Toronto, ON M5G-1X8, Canada
e-mail: bill.williams{at}mailhub.sickkids.on.ca

Presented at the Thirty-sixth Annual Meeting of The Society for Thoracic Surgeons, Fort Lauderdale, FL, Jan. 31–Feb. 2, 2000.

	Abstract

Top Abstract Introduction Material and methods Results Comment References

 
Background. We reviewed our experience with congenital ruptured sinus of Valsalva aneurysms (RSVA) to determine patterns of early recurrence and the fate of the aortic valve (AV).

Methods. Over a 28-year period, RSVA was identified in 34 patients, (mean age 31.6 years). Primary closure of the RSVA was performed in 10 patients, and a patch employed in 24. Aortic insufficiency was present in 24 patients. AV replacement (AVR) was performed in 5 patients; AV repair in 6.

Results. Follow-up of 9.2 ± 8.3 years (6 months to 24 years) was complete in all but 2 patients. Five early fistula recurrences (in 4 patients) correlated with primary rather than patch closure (p < 0.03). Kaplan-Meier survival at 10 years is 90 ± 7%. Freedom from reoperative AVR at 10 years is 83 ± 9%. Late AVR was performed in 6 patients for progressive aortic insufficiency due to bicuspid valve (n = 3), cusp disease of affected sinus (n = 2), or aortic root dilatation (n = 2).

Conclusions. Patch closure of the RSVA should be routinely employed. A bicuspid valve may be associated with the late need for AVR.

	Introduction

Top Abstract Introduction Material and methods Results Comment References

 
Congenital ruptured sinus of Valsalva aneurysm (RSVA) is a rare lesion that usually originates in the right or noncoronary aortic sinus and communicates with a cardiac chamber, frequently right sided, producing an aorto-cardiac fistula. Associated cardiac abnormalities are common, including aortic valve (AV) regurgitation and ventricular septal defect (VSD) [1].

Reports vary on the techniques employed to repair the fistulous connection [2–12]. Operative approaches used include primary/buttressed closure of the defect, or patch closure with various materials [4–13]. In some instances, complete replacement of the affected sinus may be necessary [14]. Furthermore, reports vary on the feasibility of aortic valve repair and the frequency with which AV replacement (AVR) is indicated at initial operation [5, 9–11]. We reviewed our experience with RSVAs to determine if early recurrence of the RSVA is associated with primary rather than patch closure of the defect, and the fate of the AV.

	Material and methods

Top Abstract Introduction Material and methods Results Comment References

 
Patients
The Hospital for Sick Children (1982 to 1998) and Toronto General Hospital (1990 to 1998) databases were searched for all patients with diagnosis of sinus of Valsalva aneurysms. Only those patients with congenital ruptured sinus of Valsalva aneurysms were included. Patients with nonruptured sinus of Valsalva aneurysms, Marfan’s syndrome, medionecrosis, a history of previous aortic root surgery, or trauma were excluded. When possible, elastic defeciency in the aortic wall was confirmed on histopathology. A retrospective review of inpatient charts and office/clinic follow-up records of patients with RSVAs who met these criteria were reviewed for pertinent details. Follow-up was also obtained by telephone contact of patients, or their primary care physicians or families.

RSVA was identified in 34 patients, 19 men and 15 women, with a mean age of 31.6 years (range 7 to 57 years). Fourteen patients were Asian. Thirty of 34 patients were symptomatic (dyspnea, palpitations, fatigue, pain). Eight patients presented with acute onset symptoms and 4 patients were asymptomatic. Upon presentation, endocarditis was identified in 7 patients due to the following organisms: Staphylococcus aureus (n = 1), S epidermidis (n = 1), Streptococcus viridans (n = 1), S mutans (n = 1), S intermedius (n = 1), S species (n = 1), culture negative (n = 1). After a 4- to 6-week course of intravenous antibiotics, all but 1 patient had negative blood cultures before operation. New York Heart Association (NYHA) classification was as follows: I, 7; II, 10; III, 14; and IV, 3. The pulmonary-to-systemic shunt ratio was available in 30 patients and averaged 2.6:1, with a range of 1.7 to 3.8. Postoperative and/or follow up echocardiography was obtained in 27 patients (79%).

Operative findings and associated lesions
The origin of the aorto-cardiac fistula was the right sinus of Valsalva in 27 patients (79%), the noncoronary sinus of Valsalva in 6 (18%), and the left coronary sinus of Valsalva in 1 (3%). In 23 (68%) patients, the sinus of Valsalva aneurysm ruptured into the right ventricle (RV). The right atrium (RA) was the second most common exit chamber (n = 11, 33%). In 2 patients, the aneurysm fistulized into the left ventricle. In 1 patient, the aneurysm eroded into the interventricular septum. The sinus of Valsalva aneurysm ruptured into multiple exit chambers in 2 patients. One patient had a right sinus of Valsalva aneurysm that ruptured into the RV, RA, and left ventricle (LV). In another patient, a right sinus of Valsalva aneurysm ruptured into both the RA and RV.

Associated lesions are shown in Table 1. A ventricular septal defect (VSD) was present in 18 patients. In 14, the defect was subarterial, while in 4, it was perimembranous. Of the 14 Asian patients in this series, 9 had a VSD (subarterial, 7; perimembranous, 2). Aortic insufficiency (AI) was present in 24 (70%) patients (mild, 14; moderate, 7; severe, 3). Of the 24 patients with AI, 15 had a VSD. Seven patients had a bicuspid AV.

Operative technique
Primary closure of the RSVA was performed in 10 patients. A Dacron or pericardial patch was employed in the remaining 24 patients. Eighteen patients had ventricular septal defects. Buttressed closure of the VSD was performed in 8 patients, and in 10 a patch was employed. Primary closure of the RSVA or VSD (if present) was preferred when the defect was small (<4 mm) and included pledgetted support.

Aortic valve replacement was deemed necessary in 5 patients where repair was apparently not feasible at the time for the following indications: severe AI in 2 patients, cusp disease in 2 patients, and persistent infection in 1. In 3 patients, the affected sinus was replaced with a patch. Three mechanical and two bioprosthetic valves were used.

Aortic valve repair was achieved in 6 patients by the following techniques: cusp suspension/valvuloplasty (n = 2) [15, 16], valvotomy for commissural fusion of bicuspid valve (n = 2), and aortic annuloplasty (n = 2) [14]. Repair of associated anomalies is listed in Table 2.

	Results

Top Abstract Introduction Material and methods Results Comment References

 
Early outcomes
There were no perioperative deaths. Two patients required mediastinal exploration for bleeding. In none of the 24 patients who had patch closure of the ruptured sinus of Valsalva was there a recurrence of the fistula. Four patients had five early recurrences of the aorto-cardiac fistula (twice in 1 patient). Recurrence of the RSVA did not correlate with presence of endocarditis. All 4 had primary closure (with or without pledget support) of the fistula. Recurrence of the fistula correlated with primary versus patch repair (p < 0.03 Fisher’s exact, calculated using five events).

In 1 patient, a combined aortic and mitral valve replacement, VSD closure, and primary closure of a ruptured right sinus of Valsalva aneurysm was complicated postoperatively by aortic prosthetic valve dehiscence, recurrence of the RSVA, and hemolysis. At reoperation, patching of the sinus with reimplantation of a prosthetic valve was performed. On 3-year follow-up, the patient is in NYHA class I. The second patient had undergone AVR, patch closure of a membranous VSD, and primary closure of a right sinus of Valsalva aneurysm, which ruptured into the RA and RV. Postoperatively, the patient suffered recurrence of the RSVA and aortic valve dehiscence. At reoperation, the aortic sinus was patched and the prosthetic valve replaced. This patient required a pacemaker 1 year later and has since been lost to follow-up. In the third patient, buttressed closure of a ruptured right sinus of Valsalva aneurysm was complicated by early recurrence of the fistula requiring reoperative patch repair. The patient did well until 7 years later when he developed severe angina from combined bicuspid aortic valve stenosis and coronary artery atherosclerotic occlusive disease. He expired during reoperative AVR and coronary artery bypass grafting. Finally, in the fourth patient, a small ruptured sinus of Valsalva aneurysm was closed primarily with pledgetted support. In addition, an elongated, prolapsing noncoronary aortic cusp was resuspended. On the sixth postoperative day, the patient was returned to the operating room for repeat, direct closure of the defect. A second recurrence of the fistula led to patch closure of the defect and bioprosthetic aortic valve replacement. Thirteen years later, the patient is well.

Late morbidity and mortality
Follow-up was available in all (94%) but 2 patients, and ranged from 8 months to 24 years (mean 9.2 ± 8.3 years). Kaplan-Meier survival at 10 years is 90 ± 7% (Fig 1). Kaplan-Meier freedom from reoperative AVR at 10 years is 83 ± 9% (Fig 2). Cox regression analysis revealed that the presence of VSD or AI, initial AVR or its dehiscence, initial AV repair, endocarditis, or bicuspid AV did not have a statistically significant relationship to late need for reoperative AVR or survival. The presence of a bicuspid AV was marginally related to late need for AVR (Fisher’s exact, p = 0.085; Cox regression, p = 0.14).

View larger version (11K): [in this window] [in a new window]   Fig 1. Kaplan-Meier survival curve. Numbers of patients at risk are given above the abscissa. Survival is expressed as percent ± SE.

View larger version (10K): [in this window] [in a new window]   Fig 2. Freedom from reoperative AVR expressed along the ordinate as percent ± SE. Numbers of patients at risk given above the abscissa.

In two patients, pacemaker insertion was necessary for atrioventricular block, in 1 patient at 24 years and the other at 14 months postoperatively. The patient in whom the sinus of Valsalva aneurysm ruptured into the interventricular septum did not require a pacemaker.

Late AVR (Fig 3) was necessary in 6 patients for progressive AI due to insufficient (and stenotic) bicuspid valve (n = 3), calcific/degenerative cusp disease of the affected sinus of a tricuspid valve (n = 2), or aortic root dilatation/aneurysm (n = 2). The mean interval from repair of the RSVA to reoperative AVR is 10.8 years (range 3 to 23 years).

View larger version (13K): [in this window] [in a new window]   Fig 3. Fate of the AV. AI is present in 70% of patients. Approximately 20% of patients with AI required initial AVR. Another 25% had undergone AV repair. Late reoperative AVR was necessary in 25% of all patients at a mean of 10.8 years after initial RSVA repair. (AI = aortic insufficiency; AV = aortic valve; AVR = aortic valve replacement; VSD = ventricular septal defect.)

	Comment

Top Abstract Introduction Material and methods Results Comment References

 
Congenital ruptured sinus of Valsalva aneurysm is a rare lesion [1]. It is produced by mural deficiencies or outpouchings of an aortic sinus that perforate into a cardiac chamber resulting in an aorto-cardiac fistula. The fistula develops either as a "windsock" deformity or simple fistulous connection.

The natural history of the lesion depends on the size of the shunt, presence of associated defects, or endocarditis, all of which accelerate development of symptoms and timing of presentation. Increased pulmonary blood flow produces left ventricular volume overload, right ventricular hypertension, and ultimately, congestive heart failure [1–13]. Presence of the lesion is usually an indication for repair. However, there are documented cases of RSVAs with small, asymptomatic shunts, no associated lesions, and normal right sided size/pressures that have been left unrepaired for up to 15 years (unpublished data, Toronto General Hospital, cardiovascular surgery database).

Clinical presentation is usually within the third decade of life, but can range from infancy to seventh decade. In our series, patients ranged from 7 to 57 years of age. The lesion is five times more common in Asians [1, 6, 9]. Various reports indicate a male preponderance in Asians, and a relatively even gender distribution among Caucasians [1, 6, 9–13]. In our series, 14 patients were of Asian descent, 2 of whom were women, and overall, men were 1.3 times more commonly affected than women.

Upon presentation, approximately 80% to 85% of patients are symptomatic with dyspnea, pain, palpitations, or fatigue. About 3 of 4 will have gradual onset, while the other 1 of 4 will have acute onset of their symptoms. In our series, 88% were symptomatic at the time of presentation, and 27% presented acutely. Approximately 10% of patients will present with infectious endocarditis caused by streptococcus, staphylococcus, klebsiella, hemophilus, or HACEK (Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) group organisms [1, 9–11]. Seven patients (20%) in our series had a history of endocarditis caused by predominantly streptococcal or staphylococcal organisms. Although histopathologic confirmation of elastic defeciency within resected specimens was obtained when possible, it is conceivable that fistula development was due to a primary infectious etiology in few cases.

The right coronary sinus is most commonly affected, followed by the noncoronary sinus. Rupture of the aneurysm most commonly occurs into the right ventricle followed by the right atrium [1–13]. Embryologically, it is postulated that congenital aortic sinus aneurysms result from incomplete fusion of the distal bulbar septum and truncal ridges, which separate the primitive bulbis cordis and truncus arteriosus [18, 19]. Pathological and clinical reports concur that isolated congenital left aortic sinus aneurysms are exceedingly rare. The proposed developmental explanation for such an observation is that only two sinuses can participate in partitioning of the primitive exit tube of the heart [18].

The histopathological etiology of the lesion is a deficiency of normal elastic tissue between the media of the aorta and the aortic annulus. Autopsy studies have shown that the deficiency of elastic tissue between the annulus and aortic media extends an average of 4 to 5 mm beyond the apparent rupture hole [20]. This anatomic substrate raises issues about optimal technique for closure of the defect.

Barragry and associates reported 15- to 30-year follow-up on 14 patients undergoing repair of ruptured congenital sinus of Valsalva aneurysm [4]. Three patients had recurrences of the fistula after direct closure and required reoperation. A total of 5 patients had direct closure of the defect. The finding suggests that primary closure of the defect is associated with recurrence of RSVA. Similarly, a report from the Mayo Clinic on outcome of surgical repair of the ruptured sinus of Valsalva aneurysm in 31 patients identified 3 patients who had early recurrence of the fistula [13]. All 3 had primary closure of the defect. Although the finding was not statitically significant, the authors favor closing "thin" or "large" RSVAs with a patch. An early report from the Texas Heart Institute favors tailoring the operative repair to the type of fistulous connection that it is present. The authors recommend patch repair of a perforated "windsock" aneurysm and note that a simple tract can often be closed primarily with interrupted mattress sutures [5]. In a series of 53 patients from Hong Kong, Au and associates used patch to repair 10 ruptured sinuses of Valsalva [9]. In 40 patients, pledgetted support was used, and no recurrent fistulas were identified. The authors propose that patching the sinus is not always necessary, and that frequently a buttressed closure may be sufficient. Our experience suggests that primary rather than patch closure of the defect is associated with a significantly higher incidence of recurrence. Despite selective, buttressed closure of small defects in 10 patients, 4 of them had five early recurrences of the fistula. In the remaining 24 patients in whom patch closure was employed, no recurrences were observed. The development of recurrent fistula, however, was not related to a history of endocarditis.

Although Au and associates [9] reported no recurrences of fistula, 3 patients did experience aortic prosthetic valve dehiscence. In each case, the aneurysm was directly closed against the sewing ring of the valve and no patch was applied to the sinus. All 3 patients died after dehiscence of the aortic prosthesis. Although each patient did suffer from endocarditis, the authors found that by multivariate analysis only aortic valve prosthetic dehiscence was a significant determinant of survival. Pericardial patching of attenuated sinus and annular tissue, especially in view of infection, could potentially prevent AVR dehiscence [14]. In our series, 5 patients had undergone initial AVR, 2 of whom suffered AVR dehiscence. Neither patient had patch replacement of the aortic sinus, and 1 had endocarditis. None of the patients who had AVR with concomittant patching of the associated aortic sinus had dehiscence of the aortic prosthesis.

Associated lesions are common in patients with congenital, ruptured sinus of Valsalva aneurysm [1]. Aortic regurgitation occurs in 30% to 75% of patients, and ventricular septal defects, either subarterial or perimembranous, occur with a comparable incidence of 30% to 50%. AI is usually due to cusp prolapse of the affected sinus. The mechanisms by which cusp prolapse occurs include loss of annular support of the affected sinus, Venturi effect of the involved cusp with resultant retraction into the sinus of Valsalva and prolapse into the left ventricular outflow tract, and presence of VSD that results in loss of infundibular support of right coronary cusp with conal VSDs. With prolonged AI and cusp prolapse, turbulence at the free margin results in cusp retraction, thickening, and deformation (fibrosis or calcification). Most published reports indicate that the AV requires replacement in 50% to 80% [4, 5, 9, 10, 13] of patients who present with concomittant AI. Au and associates report an initial AVR rate of over 50% in patients with AI [9]. In the Texas Heart Institute series, 80% of patients with AI had undergone AVR [5]. Choudhary and associates report [10] AI was present in 45 out of 92 patients with ruptured sinus of Valsalva aneurysms. Twenty-one (47%) had AVR and only 6 (13%) had aortic valve repair. In our series, AI was present in 70% of patients. In only 20% of these patients was AVR performed. In another 25%, repair was performed by cusp resuspension, aortic annuloplasty, or valvotomy. The repair was durable, and need for reoperative AVR was not related to a history of endocarditis or presence of a VSD or bicuspid AV in a statistically significant manner, although the numbers in this series are small for statistical value. Other studies [13] have shown a trend towards late failure of the valve repair in the presence of VSD in related groups of patients. The presence of bicuspid aortic valve has not been associated with need for late AVR. Although our study is clearly limited by the small sample size, there was a trend to late AV repair failure in the presence of bicuspid AV.

	References

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