Asian Cardiovasc Thorac Ann 2008;16:361-365
© 2008 Asia Publishing EXchange Ltd
Surgery for Sinus of Valsalva Aneurysm: 27-Year Experience with 100 Patients
Fei Yan, MD,
Qiang Huo, MD,
Jun Qiao, MD,
Vakeli Murat, MD,
Song-Feng Ma, MD
Department of Cardiac Surgery The First Affiliated Hospital Xinjiang Medical University Urumqi, China
For reprint information contact: Fei Yan, MD Tel: 86 13609 908376 Fax: 86 991 436 2601 Email: yfheart{at}gmail.com, Department of Cardiac Surgery, The First Affiliated Hospital, Xinjiang Medical University, Urumqi 830054, China.
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ABSTRACT
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Sinus of Valsalva aneurysm is a rare anomaly. This study was designed to assess the long-term outcome of surgical repair of sinus of Valsalva aneurysm and factors influencing the prognosis. From August 1980 to August sinus of Valsalva aneurysm repair. Ventricular septal defect (42) and aortic regurgitation (34) were the most frequent coexisting anomalies. An approach via the involved chamber was used in 60 patients, aortotomy in 5, and a combined approach in 35. Either direct (43) or patch (57) closure was used to repair the defect. Aortic valve replacement was required in 14 patients, and 8 needed valvuloplasty. Eighty patients were followed up for 15.6 ± 3.9 years. There were 3 hospital deaths and 2 late deaths. New York Heart Association functional class improved significantly after surgery. Actuarial survival was 94% at 10 years, and 90% at 15 years. Surgical treatment of sinus of Valsalva aneurysm is safe and effective, but late progressive aortic regurgitation is still a risk during long-term follow-up, and early aggressive measures are recommended.
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INTRODUCTION
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Sinus of Valsalva aneurysm (SVA) occurs infrequently, with an incidence of 0.14% to 3.5% in patients undergoing open heart surgical procedures.1 Males are 3- to 4-times more often affected than females, and the incidence of ruptured SVA is higher in Asian (1.2%–4.94%) than in Western populations (0.5%–1.5%).1–3 In recent years, improvements in diagnostic techniques have resulted in increasing numbers of these patients undergoing surgical repair. A variety of surgical methods have been described, with good results.2–10 However, few large or long-term series have been reported. We reviewed our 27-year experience of SVA in 100 patients to assess the long-term outcome of surgical repair and the factors influencing the prognosis.
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PATIENTS AND METHODS
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From August 1980 to August 2007, 100 patients (67 males and 33 females) with SVA underwent surgical repair, which comprised 1.5% of the 6,543 open heart operations performed in the First Affiliated Hospital of Xinjiang Medical University. The mean age of patients at repair was 31 ± 12 years (range, 14 to 57 years). At the time of admission, 90 patients were symptomatic; 55 of them presented with acute onset of symptoms. Major symptoms were dyspnea in 86, palpitations in 57, fatigue in 53, chest pain in 18, syncope in 2, and fever in 2; 32 were in New York Heart Association (NYHA) functional class III and IV. A continuous "machinery-type" murmur was heard at the left sternal border in 85 patients. Preoperative systemic pulse pressure ranged from 40 to 150 mm Hg (mean, 70 ± 20 mm Hg). Chest radiography findings included an increased cardiothoracic ratio of 0.53 ± 0.07 (range, 0.45–0.79) with various degrees of pulmonary plethora. Electrocardiographic findings were normal in 15 patients, 54 had left ventricular hypertrophy, 15 had right ventricular hypertrophy, 9 had biventricular hypertrophy, and 1 had right bundle branch block. SVA was diagnosed by echocardiography in 92 patients. In the other 8 patients, it was found during surgery for other heart diseases.
Surgical repair was performed through a median sternotomy under cardiopulmonary bypass with moderate hypothermia in all cases. The left ventricle was vented. Before inducing ventricular fibrillation, the aorta was cross-clamped and cardioplegia was infused. When the aortic valve was competent and the aneurysm was long enough, the fistula was clamped before cardioplegia was administered. Otherwise, cardioplegia was infused directly into the coronary ostia via an aortotomy. Cold crystalloid cardioplegia was used for myocardial protection in 82 patients, and cold blood cardioplegia in 18. The mean aortic cross-clamp time was 43 ± 23 min (range, 16–111 min), and the mean cardiopulmonary bypass time was 71 ± 31 min (range, 24–164 min). Operations were carried out through the chamber of termination in 60 cases (right atrium in 20, right ventricle in 40), aortotomy in 5, or a combined approach (right atrial, right ventricular, main pulmonary artery, and aortic) in 35. The origins of the ruptured SVA and the cardiac chambers into which rupture occurred are summarized in Table 1
. Single or multiple holes were found, measuring 0.75 ± 0.22 cm (range, 0.2–2.5 cm) and 1.85 ± 0.32 cm (range, 1.0–3.5 cm) in diameter, respectively. Unruptured SVA was discovered in 6 patients. After excising the aneurysmal tissue, the defect in the sinus of Valsalva was repaired by direct suture closure in 43 patients (pledgetted interrupted sutures in 41, continuous suture in 2), and by patch closure in 57 in whom the diameter of the defect exceeded 0.8 cm. Coexisting cardiac lesions and corresponding procedures in 64 patients are listed in Table 2. Forty-two patients had a ventricular septal defect (VSD), of which 32 were subarterial. The VSD was closed with a patch in 27 cases where the VSD diameter exceeded 1.0 cm. Among the 34 patients with aortic regurgitation (AR), 25 had VSD, 5 had a bicuspid aortic valve, and 2 had infectious endocarditis.
The patients were followed up at our outpatient department. Telephone calls were made, and questionnaires were sent to the patients for data collection when necessary. Heart function was appraised according to echocardiograms and reported symptoms. Student’s t test was used for statistical analysis, and values of p < 0.05 were considered significant. Data are presented as mean ± standard deviation. Time-related analyses of survival was estimated by the Kaplan-Meier method using SPSS version 11.0 software (SPSS, Inc., Chicago, IL, USA).
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RESULTS
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There were 3 hospital deaths (mortality, 3%) due to acute renal failure, low cardiac output syndrome, and massive blood loss secondary to deep sternal wound infection. Postoperative complications included skin wound infection in 4 patients, arrhythmia in 4, and 2 patients each had a minor residual VSD shunt, right pneumothorax, and acute left heart failure. Mean duration of postoperative hospital stay was 9 ± 4 days (range, 2–31 days). All 97 survivors were symptom-free at hospital discharge. Of the 97 survivors, 80 (82%) were followed up for 15.6 ± 3.9 years (range, 1 month to 25 years). Two late postoperative deaths occurred. One patient who had undergone SVA patch repair and aortic valve replacement, died of anticoagulant-related cerebral embolism 2 years after the operation. Another who had SVA suture repair, VSD patch repair, and aortic valve replacement, had periprosthetic valve leakage 1 year after the operation and died as a result of progressive heart failure at 3 years postoperatively, with no reoperation due to economic circumstances. Postoperatively, AR worsened in 6 patients. The NYHA class progressed from II to III in 2 patients who had SVA repair and aortic valvuloplasty, and 4 with mild AR and SVA repair only, deteriorated from class I to II. Two patients with a minor residual VSD were in NYHA class II with no further treatment. All survivors were found to be in NYHA class I III. NYHA class at the last follow-up is shown in Table 3. The mean NYHA class improved significantly after surgery. Actuarial survival was 94% at 10 years, and 90% at 15 years (Figure 1).
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DISCUSSION
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SVA is a rare cardiac anomaly that may be either congenital or acquired. The morphology of congenital SVA was described by Edward and colleagues11 in 1957, who showed the absence of normal elastic tissue in the media between the aortic sinus and the hinge line of the aortic annulus. The cause of the SVA is believed to be incomplete fusion of the distal bulbar septum, resulting in aneurysm formation when subjected to a prolonged period of high pressure. Most studies, including ours, found that the right coronary sinus is most frequently affected, followed by the noncoronary sinus. Rupture of the aneurysm most often occurs into the right ventricle, followed by the right atrium, and rarely into the left ventricle, pulmonary artery, or interventricular septum.2,3,5–10,12–14 The left coronary cusp does not usually arise from the bulbar septum, as do the right and noncoronary cusps, thus explaining the rarity of ruptured left SVA. It is infrequently associated with acquired diseases such as endocarditis, atherosclerosis, syphilis, or aortic dissection.15
Sawyers and colleagues16 documented a mean survival period of 3.9 years in patients with untreated ruptured SVA. This intervention in this subgroup. Surgical intervention is also mandatory in cases of unruptured SVA with VSD, AR, or both, or a huge SVA causing mitral valve incompetence, right ventricular outflow obstruction, and myocardial ischemia.17–19 Associated lesions are common in patients with congenital SVA; AR occurs in 17% to 75%, and VSD occurs with a comparable incidence of 30% to 50%.15 When a VSD is present, AR usually results from a prolapsed aortic cusp. Without a VSD, AR usually arises from other aortic valve abnormalities, including bicuspid valve. With prolonged AR and cusp prolapse, turbulence at the free margin results in cusp retraction, thickening, and deformation (fibrosis or calcification), which then preclude adequate aortic valve repair and necessitate valve replacement.5 Aortic valve replacement is required in 20% to 58% of patients with SVA who present with concomitant AR.3,6,9,10 In our series, grade 1 or higher AR occurred in 34% of patients and in 42% of those with VSD; 14 required aortic valve replacement.
Three main operative approaches have been described for correction of SVA: through the cardiac chamber into which the aneurysm has ruptured, by opening the aortic root only, or by a combined approach.7,9,10,20 Our current strategy is to use the involved chamber in simple SVA without concomitant VSD or AR, and to use a combined approach for a large SVA, or SVA concurred with VSD and/or AR. In patients with uncertain associated lesions, the involved chamber approach can be used first, and an aortotomy may be added if necessary. Some reports have recommended closing both small and large SVAs with a patch, whereas others found that patching is not always necessary and a buttressed closure may often be sufficient.6,9,10 We favor closing the SVA with a patch when the diameter of the defect exceeds 0.8 cm; smaller defects can be closed with pledged interrupted sutures. The principles of repairing a ruptured SVA include always placing the sutures in normal tissue, and using a patch large enough to reinforce the entire involved coronary sinus wall. One patch may be used to repair both the SVA and a coexisting VSD, if present. The hinge line of an involved aortic valve cusp should always be kept at its proper functional location on the patch. Aortic valve distortion should be avoided.
The operative results for SVA repair are excellent, as shown in this and other studies, with long-term survival rates of 90% ± 7% at 10 years and up to 90% at 20 years.8,9 The risks of recurrent fistula or VSD are reported to be minimal in the current era; however, some patients develop hemodynamically significant AR after repair of ruptured SVA, and recent literature reports that 0% to 30% of operative survivors required reoperation on the aortic valve because of deteriorating AR.6,9,10 Progressive AR is the crucial factor influencing prognosis.6,8 Our study also suggests that AR has an important influence on cardiac function postoperatively. Cardiac function decreased because of worsening AR in 2 patients who underwent aortic valvuloplasty and 4 with mild AR who were not treated during the operation. Therefore, with recent advances in myocardial protection and surgical techniques, we recommended that more aggressive measures be adopted for SVA. These include greater use of a combined approach to achieve optimal evaluation of lesions, more patch repairs to diminish the chance of recurrence, and more valve replacements in patients with moderate to severe AR. We conclude that surgical treatment of SVA is safe and effective, so ruptured SVA or unruptured SVA with VSD and/or AR should be repaired surgically as early as possible.
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ABSTRACT
INTRODUCTION
