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Ann Thorac Surg 1999;68:1573-1577
© 1999 The Society of Thoracic Surgeons

Original Articles

Sinus of valsalva aneurysm or fistula: management and outcome

Thomas J. Takach, MDa, George J. Reul, MDa, J. Michael Duncan, MDa, Denton A. Cooley, MDa, James J. Livesay, MDa, David A. Ott, MDa, O.H. Frazier, MDa

a Department of Cardiovascular Surgery, Texas Heart Institute, Houston, Texas, USA

Address reprint requests to Dr Cooley, Department of Cardiovascular Surgery, Texas Heart Institute, PO Box 20345, Houston, TX 77225-0345

Presented at the Thirty-fourth Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 26–28, 1998.


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. Few large or long-term series exist regarding the management of patients with sinus of Valsalva aneurysms or fistulas (SVAFs).

Methods. Between 1956 and 1997, 129 patients presented with a ruptured (64 cases; 49.6%) or nonruptured (65 cases; 50.4%) SVAF. The patients included 88 men and 41 women, with a mean age of 39.1 years. Associated findings included a history of endocarditis (42 cases; 32.6%), a bicuspid aortic valve (21 cases; 16.3%), a ventricular septal defect (15 cases; 11.6%), and Marfan’s syndrome (12 cases; 9.3%). Operative procedures included simple plication (61 cases; 47.3%), patch repair (52 cases; 40.3%), aortic root replacement (16 cases; 12.4%), and aortic valve replacement/repair (75 cases; 58.1%).

Results. There were five in-hospital deaths (3.9%): four due to preexisting sepsis and endocarditis and one that followed dehiscence of the repair in a patient with Marfan’s syndrome. Two patients (1.6%) had strokes during the early postoperative period. The survivors were followed up for 661.1 patient-years (5.3 years/patient). The following late complications occurred: prosthetic valve malfunction (5 cases; 3.9%), prosthetic valve endocarditis (3 cases; 2.3%), SVAF recurrence (2 cases; 1.6%), thrombosis (1 case; 0.8%), and anticoagulation-related bleeding (1 case; 0.8%).

Conclusions. Resection and repair of SVAF entails an acceptably low operative risk and yields long-term freedom from symptoms. Early, aggressive treatment is recommended to prevent endocarditis or lesional enlargement, which causes worse symptoms and necessitates more extensive repair.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
The literature contains few large or long-term series concerning patients with sinus of Valsalva aneurysms or fistulas (SVAFs). A sinus of Valsalva aneurysm was first described in 1839 [1]. However, successful treatment of a ruptured sinus of Valsalva aneurysm was not accomplished until the mid-1950s, when Morrow and colleagues [2] and Bigelow and Barnes [3] independently used hypothermia and inflow occlusion to repair this lesion. In 1956, three groups [4–6], each working separately, used cardiopulmonary bypass to perform open repairs. Since that time, this method has been the one most commonly used.

Sinus of Valsalva aneurysms occur infrequently. In 1914, Smith documented seven of them (0.09%) in a study of 8,138 postmortem examinations [7]. According to three recent studies from major medical centers, the incidence is between 0.14% and 0.96% in patients undergoing open heart surgical procedures [8–10]. At our institution, the incidence is less than 0.15% in open heart surgery patients.

This report summarizes our 40-year experience with SVAFs. It examines the clinicopathologic spectrum of these lesions, as well as operative indications, immediate outcomes, and long-term postoperative results.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
We reviewed the hospital records and postoperative clinical charts of 129 consecutive patients with 149 SVAFs treated at our institution between April 1956 and January 1997. When necessary, supplemental information was obtained from the patient’s private cardiologist and family.

The series included 88 men (68.2%) and 41 women (31.8%), whose average age at operation was 39.1 years (range 2 to 74 years). With respect to New York Heart Association functional status, 8 patients were in class I (asymptomatic), 62 were in class II, 33 were in class III, and 26 were in class IV. Easy fatigability, dyspnea, chest pain, and palpitation or tachycardia were the most common symptoms. Sixteen patients had a sudden onset of symptoms, all associated with a ruptured aneurysm; in 8 patients, the rupture occurred during or after an episode of bacterial endocarditis. The remaining patients had a gradual onset and progression of symptoms. A "machinery-type" murmur along the left sternal border was documented in 20 patients, all of whom had a fistula from the aorta to the right ventricle. On chest roentgenography, cardiac enlargement was evident in 43 patients, and was most pronounced when associated with aortic insufficiency. Cineangiography was performed in 120 cases, with visualization of the aneurysm or fistula in 93 patients. Table 1 shows the location of the lesions, which involved the right coronary sinus in 78 patients, the noncoronary sinus in 50 patients, and the left coronary sinus in 21 patients. Of the 65 patients (50.4%) whose aneurysm had not ruptured, 14 had two dilated aortic sinuses. A fistula was present in 64 patients (49.6%), either as part of a ruptured aneurysm or as a simple fistulous tract without aneurysmal dilatation. In 6 patients, two fistulous tracts were present.


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  		Table 1. Anatomy of Aneurysms or Fistulas of the Sinus of Valsalva (n = 149) in 129 Patients

 
Aneurysms that ruptured tended to follow specific patterns. More than 97% of all ruptured aneurysms originated in either the right coronary sinus (47; 67.1%) or the noncoronary sinus (21; 30.0%). Aneurysms that originated in the noncoronary sinus tended to rupture into the right atrium (11; 16%). Aneurysms that originated in the right coronary sinus tended to rupture into the right atrium (9; 13%) or right ventricle (35; 50%).

Associated findings included a ventricular septal defect (15 cases; 11.6%), a bicuspid aortic valve (21 cases; 16.3%), a history of endocarditis (42 cases; 32.6%). Marfan’s syndrome (12 cases; 9.3%), infundibular pulmonary stenosis (5 cases; 3.9%), moderate to severe aortic insufficiency (57 cases; 44.2%), isolated aortic stenosis (5 cases; 3.9%), and combined aortic stenosis and aortic insufficiency (12 cases; 9.3%). Fourteen patients (10.9%) had sepsis and/or active bacterial endocarditis at the time of initial presentation.

Operative procedures included simple plication (61 cases; 47.3%) (Fig 1), patch repair (52 cases; 40.3%) (Figs 1 and 2), aortic root replacement (16 cases; 12.4%), and aortic valve replacement/repair (75 cases; 58.1%) (Fig 1). Prosthetic aortic root replacement, followed by reimplantation of the coronary arteries, was undertaken in patients with a dilated annulus and multiple sinus involvement in whom simple plication or patch repair was not possible.



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  		Fig 1. Primary repair options for sinus of Valsalva aneurysms. (A) Noncoronary sinus of Valsalva aneurysm extending into the right atrium. (B) Examination of aortic valve cusps. (C1) If the orifice is small, primary closure may be performed with interrupted sutures. (C2) If the orifice is large or if direct repair distorts the aortic leaflets, a Dacron patch is applied.

 


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  		Fig 2. Exposure (A) and excision (B) of the aneurysmal sac. Alternative repair options include a purse-string closure (C) or Dacron patch repair. If a ventricular septal defect is present (inset), patch repair via a ventriculotomy is preferred.

 
The long-term survivors were followed up for 661.1 patient-years (mean 5.1 years/patient). Life-table analysis was used to obtain an actuarial long-term survival curve. Statistical analysis was performed with SAS software (Statistical Analysis Systems Institute, Cary, NC).


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
Perioperative adverse events included five in-hospital deaths (3.9%): four (3.1%) that were secondary to preexisting sepsis and endocarditis, and one (0.8%) that followed dehiscence of the primary repair in a patient with Marfan’s syndrome. Two patients (1.6%) had strokes but completely recovered their neurologic function before being discharged from the hospital. All 124 survivors were symptom free at hospital discharge.

The late follow-up period totaled 661.1 patient-years (5.3 years/patient). Either partial (68/129; 52.7%) or complete (61/129; 47.3%) follow-up was available for each patient. Late complications (Table 2) were primarily related to the presence of a prosthetic valve or Marfan’s syndrome. Both recurrent lesions were associated with dehiscence after simple plication and with periprosthetic valve leakage. In each case, repeat repair and valve replacement provided long-term relief of symptoms. Neither recurrence involved Marfan’s syndrome or endocarditis.


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  		Table 2. Late Events

 
There were 23 known deaths, nine of which were due to a myocardial infarction or congestive heart failure. Three deaths followed aortic aneurysm rupture or dissection, and two were secondary to stroke. One death each was caused by intracerebral hemorrhage (anticoagulation-related), acute renal failure, trauma, systemic lupus erythematosus, and sepsis. In four cases, the cause of death was unknown. Figure 3 shows the actuarial survival rate, over time, for all survivors. The first patient in the series, who underwent successful correction of a fistula from the right coronary sinus to the right ventricle in 1956, died 12 years later of fulminating vegetative endocarditis.



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  		Fig 3. Actuarial survival rate over time.

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
Because of the relative infrequency of SVAFs, investigators have not accurately determined the natural history of these lesions. Abbott [11] and Edwards and Burchell [12] have provided evidence of a congenital etiology. They have suggested that the lesion is due to a structural deficiency in the media related to the development of the distal bulbar septum [11, 12]. Others have described an "acquired" etiology, marked by degeneration of the media secondary to syphilis [7], infection [13], atherosclerosis [14], or cystic medial necrosis [15].

Sawyers and associates [16] documented a mean survival period of 3.9 years in patients with untreated ruptured sinus of Valsalva aneurysms. This finding supports the need for early surgical intervention in this subgroup. For symptomatic, nonruptured aneurysms, the management is also clear: right ventricular outflow tract obstruction, infection, malignant arrhythmias, or acute ostial coronary artery obstruction mandates surgical intervention [12, 17–19]. Optimal management of an asymptomatic, nonruptured aneurysm, however, is less clear, owing to the absence of a precise natural history.

In our series, 1 patient with an asymptomatic noncoronary sinus aneurysm (Fig 4A) and trace aortic insufficiency refused surgery because, as a Jehovah’s Witness, he wished to avoid blood transfusion. Four years later, he had severe aortic insufficiency, dilatation of the aortic annulus, and extension of the aneurysm to the right and left aortic sinuses (Fig 4B). A condition that might originally have been treated with patch closure of the aneurysm now required aortic root replacement and reimplantation of the coronary arteries. This case suggests that sinus of Valsalva aneurysms may expand, causing more severe symptoms and requiring more extensive corrective procedures. In contrast, Martin and colleagues [20] followed up a nonruptured, asymptomatic aneurysm for more than 19 years. This lesion neither expanded nor caused clinical symptoms.



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  		Fig 4. Enlargement of a sinus of Valsalva aneurysm over time. (A) Cineangiogram with dilated noncoronary sinus (arrow). (B) Computed tomographic scan, performed on the same patient 4 years later, showing a dilated aortic root (arrow). The aneurysm had enlarged to involve both the right and left coronary sinuses. It necessitated replacement of the aortic root and reimplantation of the coronary arteries.

 
The specific etiology of a given sinus of Valsalva aneurysm may be difficult to determine, and the interrelationship between the various pathologic processes may affect the long-term outcome. Bacterial endocarditis of the aortic valve may cause aortic medial necrosis secondary to infection and lead to aneurysm formation [21]. Progression of the disease process may result in a dilated annulus and deformed aortic valve cusps that are increasingly predisposed to recurrent endocarditis [22–25]. On the other hand, a congenital lack of continuity between the aortic media and annulus fibrosis may initiate aneurysm formation [12], leading to local turbulence, laminar flow separation, or dilatation of the annulus and deformity of the valve cusps. Again, each process may increase the predisposition to bacterial endocarditis [22, 23].

This study suggests that the outcome may be improved if operation is undertaken in the absence of bacterial endocarditis. Four (80%) of our five operative deaths were related to the effects of preexisting sepsis and active bacterial endocarditis. Early, aggressive operative treatment may decrease the likelihood of bacterial endocarditis.

In summary, our salutary operative results, as well as those of other authors [21, 26], suggest that treatment of SVAF is associated with an acceptably low operative risk and long-term freedom from symptoms. An early, aggressive approach is recommended to prevent the development of worse symptoms and more extensive disease.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

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  7. Smith W.A. Aneurysm of the sinus of Valsalva, with report of 2 cases. JAMA 1914;62:1878.
  8. Mayer J.H., III, Holder T.M., Canent R.V. Isolated nonruptured sinus of Valsalva aneurysm. J Thorac Cardiovasc Surg 1975;69:429-432.[Abstract]
  9. Heydorn W.H., Nelson W.P., Fitterer J.D., et al. Congenital aneurysm of the sinus of Valsalva protruding into the left ventricle. J Thorac Cardiovasc Surg 1976;71:839-845.[Abstract]
  10. Chu S.H., Hung C.R., How S.S., et al. Ruptured aneurysms of the sinus of Valsalva in Oriental patients. J Thorac Cardiovasc Surg 1990;99:288-298.[Abstract]
  11. Abbott M.E. Clinical and developmental study of a case of ruptured aneurysm of the right anterior aortic sinus of Valsalva, leading to communication between the aorta and base of the right ventricle, diagnosed during life, opening in anterior interventricular septum (probably bulbar septal defect). Malignant endocarditis. In: Osler W., ed. Contributions to medical and biological research. New York: Paul B. Hoeber, 1919:899-914.
  12. Edwards J.E., Burchell H.B. The pathological anatomy of deficiencies between the aortic root and the heart, including aortic sinus aneurysms. Thorax 1957;12:125-139.
  13. Shumacker H.B., Jr Aneurysms of the aortic sinuses of Valsalva due to bacterial endocarditis, with special reference to their operative management. J Thorac Cardiovasc Surg 1972;63:896-902.[Medline]
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