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Ann Thorac Surg 1996;62:1424-1430
© 1996 The Society of Thoracic Surgeons


Original Article: Cardiovascular

Aortic Valve Replacement After Previous Coronary Artery Bypass Grafting

John A. Odell, FRCSEd, Charles J. Mullany, MD, Hartzell V. Schaff, MD, Thomas A. Orszulak, MD, Richard C. Daly, MD, James J. Morris, MD

Division of Cardiothoracic Surgery, Mayo Clinic and Foundation, Rochester, Minnesota

Accepted for publication June 17, 1996.


    Abstract
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background. As the population ages, an increasing number of patients with previous coronary artery bypass grafting (CABG) will require subsequent aortic valve replacement (AVR). This study examined outcome of AVR after previous CABG and reviewed possible indications for valve replacement at the time of initial myocardial revascularization.

Methods. Between March 1975 and December 1994, 145 patients had AVR after previous CABG. Sixty-three patients (43%) had their initial CABG elsewhere. Reoperation for AVR was the second cardiac procedure in 137 patients and the third in 8. Redo CABG with AVR was done in 66 (46%). There were 118 men and 27 women. The mean age at CABG was 64 ± 7.9 years; for AVR this was 71 ± 7.6 years.

Results. In 2 young patients accelerated calcific aortic stenosis occurred in the setting of renal failure. Significant aortic stenosis did not appear to be addressed at initial CABG in 3 patients. Transaortic valvular gradient, as measured by cardiac catheterization, increased by 10.4 ± 7.0 mm Hg/y. Twenty-four patients (16.6%) died. The mortality for AVR alone or for AVR + redo-CABG was 15 of 125 patients (12%). For patients having more complicated procedures, the mortality was 9 of 20 (45%). Nine patients (6.2%) suffered a postoperative cerebrovascular accident. Low preoperative ejection fraction measured by echocardiography, sternal reentry problems, complexity of operation, and prolonged cross-clamp and bypass times were significant factors associated with mortality. Age at AVR, interval between operations, the extent of underlying native coronary artery disease, the state of the previously placed bypass conduits, and methods of myocardial preservation were not significant predictors of operative mortality. On multivariate analysis there was only one significant value: prolonged cross-clamp time.

Conclusions. Aortic valve replacement after previous CABG is associated with a mortality that is higher than that seen after repeat CABG or repeat AVR. It seems prudent, therefore, to use liberal criteria for AVR in those patients who require coronary revascularization and who, at the same time, have mild or moderate aortic valve disease.


    Introduction
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
As the population ages, an increasing number of individuals who have undergone previous coronary artery bypass grafting (CABG) are presenting with significant aortic stenosis. A major question is whether the aortic valve was diseased at the initial procedure and, if so, whether it should have been replaced at that time. This is particularly relevant because of the sometimes considerable technical difficulties that may be encountered at the second cardiac surgical procedure. Moreover, a number of recent reports [13] have indicated a significant operative mortality that may be associated with this reoperative procedure. To evaluate this problem further, we have reviewed our experience of patients undergoing aortic valve replacement (AVR) after previous CABG.


    Material and Methods
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
The Mayo Clinic cardiac surgical data base was reviewed for patients who underwent AVR after previous CABG. One hundred seventy-nine patients having procedures between March 1975 and December 1994 were identified. However, 34 patients were excluded from analysis: 32 patients had undergone previous aortic valve decalcification, 1 patient had had a septal myectomy and repair of a damaged aortic leaflet at the time of CABG, and 1 patient underwent AVR in a transplanted heart. This patient had undergone two previous coronary artery bypass procedures. The preoperative, operative, and postoperative records of the remaining 145 patients (118 men [81%] and 27 women [19%]) were reviewed. Where appropriate, variables are expressed as the mean ± standard deviation except as otherwise noted. Differences in hemodynamic values noted at the time of CABG and at the time of AVR, as well as differences in mortality, were tested for statistical significance by the {chi}2 test for categoric variables and by the rank sum test for continuous variables. A multivariate analysis using logistic regression was done on variables found significant by univariate analysis. Procedures were regarded as less complex if AVR was done either alone, with an outflow tract-enlarging procedure (annulus or root enlargement or septal myectomy), or combined with CABG. Other complicated combined procedures were regarded as more complex.


    Results
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Sixty-three patients (43%) had their initial CABG elsewhere, and the data on these patients were often incomplete. When available, they were included in the analysis. All patients had previous CABG (Table 1Go). Five patients had two previous myocardial revascularization procedures, one of which was a right coronary endarterectomy together with a Vineberg procedure. One patient had CABG followed 12 years later by replacement of the ascending aorta for dissection. Seven patients had mitral and tricuspid procedures before CABG and, in 3 of these patients, previous valvular procedures had been undertaken. Therefore, reoperation for AVR was the second cardiac procedure in 137 patients and the third in 8.


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Table 1. . Previous Procedures in 145 Patients Undergoing Aortic Valve Replacement After Previous Coronary Artery Bypass Grafting
 
Preoperative clinical variables are listed in Table 2Go. The mean age at CABG was 64 ± 7.9 years, and the mean age at AVR was 71 ± 7.7 years. Two patients had the aortic valve inspected at the time of initial CABG. In the intervening period to AVR, 5 patients had a total of 10 percutaneous aortic balloon valvuloplasties. Three of these were done in a short period before AVR, when the patients had pulmonary edema and required intraaortic balloon support [4]. Four patients had five percutaneous coronary angioplasty procedures before AVR.


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Table 2. . Clinical Charactistics of 145 Patients Undergoing Aortic Valve Replacement After Previous Coronary Artery Bypass Grafting
 
Most patients had either senile (calcific) or bicuspid aortic valve disease (Table 3Go). There were 6 patients with aortic dissections. Clinical features of aortic stenosis were present in 100 patients, aortic regurgitation in 15, and mixed aortic valve disease in 30. The mitral valve was free of functional abnormality in 121 patients, 3 patients had features of mitral stenosis, and 21 had evidence of mitral regurgitation. The tricuspid valve was normal in 139 patients, 1 patient had tricuspid regurgitation, and there were features of mixed tricuspid valve disease in 5 patients.


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Table 3. . Valve Pathology in 145 Patients Undergoing Aortic Valve Replacement After Previous Coronary Artery Bypass Grafting
 
Progression of Aortic Stenosis
In reviewing the clinical details at the time of initial CABG, an abnormality of the aortic valve was recognized in many patients, but the extent of aortic valve disease was not thought severe enough to warrant AVR. Twenty-seven patients had an abnormality of the aortic valve described as either thickening, sclerosis, mild calcification, or mild to moderate stenosis. Using two-dimensional echocardiography with Doppler, 7 of these patients were documented as having gradients between 3 and 36 mm Hg. In 3 patients mild aortic regurgitation was noted. At cardiac catheterization before initial CABG, 11 patients had no gradient and 47 patients had documented gradients varying between 3 and 46 mm Hg. In 2 patients the aortic valve was inspected at the time of CABG, but not thought sufficiently diseased to warrant AVR.

To assess progression of the disease, the change in gradient between two similar investigational techniques (cardiac catheterization or two-dimensional echocardiography), when this was performed, was divided by the time interval between the procedures. Details of this group are summarized in Table 4Go, but are limited by the substantial number of procedures done elsewhere (32 of 60 patients, 53%). The average increase in gradient in 39 patients (measured at cardiac catheterization) was 10.4 ± 7.0 mm Hg/y (Table 4Go).


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Table 4. . Transvalvular Gradients Before Coronary Artery Bypass Grafting and Aortic Valve Replacement in 45 Patients
 
The clinical notes of 60 patients undergoing AVR within 5 years of CABG were reviewed to determine whether the abnormality of the aortic valve existed at the time of initial CABG. In 2 young patients, accelerated calcific aortic stenosis may have occurred because of the presence of renal failure. One patient had received two previous renal transplants and 1 patient was on chronic dialysis. The diagnosis of significant aortic stenosis was missed or ignored in 3 patients. One patient had a murmur and a calcified valve on two-dimensional echocardiography. However, left ventriculography and measurement of transvalvular gradients were not performed, presumably because the patient had one kidney. The second patient had a murmur, electrocardiographic evidence of left ventricular hypertrophy, a mean echocardiographic gradient of 26 mm Hg, and a calculated aortic valve area of 1.1 cm2. Six months later the calculated aortic valve area was 0.53 cm2. In the third patient the right coronary artery was dissected during cardiac catheterization and urgent revascularization may have precluded full investigation of the aortic valve.

Surgical Procedure
EXPOSURE AND BYPASS.
The majority of patients (143) underwent redo sternotomy. Reentry problems occurred in 23 patients (16%). Two patients had arrest during anesthesia. Damage to the following structures occurred during dissection or on reopening: previously inserted grafts, 13 patients; right atrium, 2; innominate vein, 3; pulmonary artery, 1; aorta, 1; and right ventricle, 1. Two patients underwent left thoracotomy and placement of a left ventricular–aortic conduit. In these patients the pulmonary artery was used for venous drainage and the external iliac artery or femoral artery for arterial return. The ascending aorta was cannulated in 120 patients, the femoral artery in 24, and the iliac artery in 1. Total bypass time was 126 ± 52 minutes (range, 0 to 300 minutes), and cross-clamp time was 73 ± 30 minutes (range, 0 to163 minutes).

MYOCARDIAL PROTECTION.
Most patients were managed with moderate hypothermia (24.3 ± 4.6°C; range, 18 to 37°C). One patient underwent deep hypothermia and circulatory arrest. Myocardial protection depended on anatomic findings at operation and the surgeon's preference. Seventy-five patients received crystalloid cardioplegia and 68 received blood cardioplegia. Antegrade cardioplegia was administered in a variety of ways. In patients with aortic stenosis, it was usually given into the aortic root initially and then later into the native coronary ostia and previously inserted grafts. A number of old vein grafts were transected, or small venotomies were made, to provide access for cardioplegic cannulas. Cardioplegic solution was also administered into newly inserted grafts. Occasionally, to gain access to the old ostia, a trapdoor-type incision was made in the ascending aorta to expose, by everting the aorta, the ostia of the old grafts. In the 37 patients with 42 patent internal thoracic arteries, the pedicles were occluded with a bulldog clamp in 13 patients. The artery was left perfusing in 14 patients. Details of internal thoracic artery management in 10 patients was not recorded. In patients with aortic regurgitation, cardioplegic solution was usually infused directly into the native and graft ostia after the aorta was opened.

OPERATIVE PROCEDURES.
One hundred forty-three patients underwent AVR and 2 patients had left ventricular apical aortic conduits placed. The majority of patients (85 of 145, 59%) received tissue valves (Table 5Go). One patient had a portion of the ascending aorta replaced for atheromatous disease. One patient with endocarditis had a pericardial patch closure of an aortic root abscess. Enlargement of the aortic annulus and root using a pericardial patch was performed in 16 (11%) of the patients. A septal myectomy was done in 6 patients. Additional valvular procedures are listed in Table 5Go.


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Table 5. . Operative Procedures in 145 Patients Undergoing Aortic Valve Replacement After Previous Coronary Artery Bypass Grafting
 
Redo CABG was undertaken in 66 patients. The mean number of grafts was 1.5 ± 0.8 (range, 1 to 4). In addition to long saphenous veins, the left internal thoracic artery was used in 12 patients; the basilic vein was used in 1 patient, and 8 patients had revision of proximal stenotic vein grafts. One patient with an internal thoracic artery and a proximal narrowing had this converted to a free graft.

Hospital Mortality
Twenty-four (17%) patients died within 30 days of operation or during the same hospitalization. In the less complex group of patients who underwent AVR alone (7 of 59) or AVR + CABG (8 of 66), the operative mortality was 15 of 125 patients (12%). In the more complex group 9 of 20 patients (45%) died.

The most common cause of death was low cardiac output (18 of 24, 75%). Ten of these patients could not be weaned from bypass. The remaining 8 patients died later of multiorgan failure, also associated with low cardiac output. Of the remaining 6 patients, 2 died suddenly on the 7th and 11th postoperative days (presumably attributable to an acute arrhythmia); both patients with ventricular aortic conduits died, one of a ruptured aorta on day 25 and the other with Wegener's granulomatosis, diabetes mellitus, and multiorgan failure; 1 patient died of a right ventricular laceration at sternal reentry; and another died of bacterial endocarditis.

A large number of preoperative and operative variables were studied to determine risk factors for operative death (Table 6Go). However, because of a large amount of missing data, particularly pre-CABG data, many of these variables have not been listed. On univariate analysis, factors predictive of operative mortality were prolonged cross-clamp time (p = 0.003) and bypass time (p = 0.005), complex operation (p = 0.001), ejection fraction less than 0.45 on echocardiogram (p = 0.03), and reentry problems (p = 0.07). There was a trend toward a higher mortality in women and in patients with heart failure or in whom no left internal thoracic artery was used at the original operation. Methods of myocardial protection or the state of previously placed vein grafts did not influence operative mortality. On multivariate analysis done with a full model, stepwise model, and backward model using logistic regression there was only one significant value: cross-clamp time.


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Table 6. . Operative Mortality in 145 Patients Undergoing Aortic Valve Replacement After Previous Coronary Artery Bypass Grafting
 
Hospital Morbidity
Postoperative complications are listed in Table 7Go. Fifty-nine (44%) of patients had an uncomplicated postoperative course. An intraaortic balloon pump was used in 27 (19%); 10 of these patients died. Nine (6.2%) patients suffered a perioperative cerebrovascular accident.


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Table 7. . Postoperative Complications in 145 Patients Undergoing Aortic Valve Replacement After Previous Coronary Artery Bypass Graftinga
 

    Comment
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
As the population ages, symptomatic aortic valve disease, particularly aortic stenosis, is becoming a more frequent clinical problem requiring surgical management. Moreover, as cardiac revascularization has become so common, many elderly patients now presenting for AVR have had previous CABG. An important issue in these patients is whether the aortic valve was significantly diseased at the time of initial operation and whether, if so, it should have been replaced. Because the symptoms of angina pectoris and exertional dyspnea are common to both aortic stenosis and coronary artery disease, careful clinical examination and evaluation need to be performed in all patients in whom surgical revascularization is anticipated. In those patients suspected of having aortic valve disease, hemodynamic evaluation by either two-dimensional echocardiography with Doppler or cardiac catheterization, or both procedures, must be undertaken. It has been generally accepted that valve replacement in patients with aortic stenosis, even in hemodynamically significant stenosis, can safely be delayed until symptoms occur [5, 6]. In addition, patients with asymptomatic coronary artery disease should have these vessels grafted at the time of AVR [7]. However, it is not clear how patients who have mild aortic valve disease and who primarily require surgical revascularization should be managed. It is clear that the majority of our patients fell into this category. The dilemma has been addressed by others [8] who believed that aortic valve repair (mainly decalcification) for minimally or moderately diseased aortic valves was an option that could delay the inevitable development of severe aortic stenosis. Unfortunately, the long-term results of aortic valve decalcification have been poor [9]. Measurement of transvalvular gradients at operation and aortic valve inspection may help resolve this dilemma, particularly when the surgeon finds the aortic valve disease more severe than expected. However, the reverse is usually the case, and these two maneuvers do not usually satisfactorily clarify the issue.

Is is clear from several studies [1015] that aortic stenosis will progress at a rate of 5 to 10 mm Hg/y [1, 11, 12], with a concomitant decrease of aortic valve area of approximately 0.08 to 0.1 cm2/y [1, 10, 12, 15]. However, it is difficult to predict for an individual patient [10, 15]. Faggiano and colleagues [10] found no significant relationship between the rate of progression and clinical features such as age, sex, duration of follow-up, and symptomatic status. However, patients with reduced left ventricular function had a higher rate of progression [10]. Wagner and Selzer [14] found similar results and hypothesized that a reduction in left ventricular performance will reduce the aortic valve opening force. Others [15, 16] have found that development of symptoms identified patients with a higher rate of progression. Peter and colleagues [11] compared patients with a rapidly progressive stenosis, as defined by an increase in the maximum pressure gradient greater than 10 mm Hg/y, with patients progressing at a slower rate. Patients progressing rapidly were significantly older and more often had concomitant coronary artery disease than patients with slowly progressive aortic stenosis. Because both coronary artery disease and degenerative aortic stenosis are similar degenerative processes associated with cell proliferation and calcification of vascular tissue, this may reflect a similar aging process affecting blood vessels and valvular tissue. Similarly, diabetes and hypercholesterolemia have been associated with the prevalence of aortic stenosis, suggesting a role for these factors in both coronary artery disease and aortic stenosis [11]. In the context of coronary artery disease, where symptoms may be similar to those of aortic valve disease and myocardial function may be depressed because of ischemia or previous ischemic events, the difficulties of using these modalities as markers of progression or underlying severity of aortic stenosis is obvious.

A hypothetical 70-year-old patient with an initial aortic valve area of 1.4 cm2, a mean gradient of 14 mm Hg, and triple-vessel disease requiring surgical revascularization may have a 5-year expected survival of 87% [17, 18]. After 5 years, the aortic stenosis may have progressed to a critical stage with a mean gradient greater than 60 mm Hg and an aortic valve area of 0.7 cm2. Although we cannot predict with certainty the ultimate outcome for any individual patient, we believe that an aggressive approach to the aortic valve at initial CABG should be followed. Although aortic valve decalcification was previously considered applicable to such patients with mild aortic stenosis undergoing CABG, the results of this procedure have been disappointing [9]. In our experience, a significant number of these patients have returned for subsequent reoperation. These patients were not included in our analysis as the purpose of this study was to review those patients in whom the aortic valve disease was either missed or ignored at initial operation or in whom significant aortic valve disease had developed subsequent to CABG.

We are not able to determine from our data what thresholds should be used to determine AVR in patients undergoing CABG. Factors such as age, urgency of operation, left ventricular function, body surface area, and sex most probably should be considered and individualized before concomitant AVR. An aggressive approach should apply to the young patient with good left ventricular function undergoing elective revascularization. The underlying aortic valve pathology may also influence the decision whether to replace the aortic valve at the time of CABG. Progression of rheumatic or congenital aortic stenosis [19] may be slower than that of degenerative valvular disease, particularly in the older age group with associated coronary artery disease. However, others [19] may argue that valve replacement at the time of CABG is the correct option because of the progressive nature of the abnormal congenital bicuspid aortic valve.

The risk of AVR after previous CABG is not inconsiderable. Avendano and colleagues [3], in an abstract, reported a mortality of 18%. However, in this series 37% of the patients had had previous AVR as well as CABG. After exclusion of previous valve replacement and aortic dissection patients, these same investigators had a mortality of 14% [2]. Collins and co-workers [1] also reported a significant mortality of 18%. Because most of the deaths reported by Fighali and colleagues [2] and the deaths seen in our series were related to complications of low cardiac output, myocardial protection would seem to be of major importance. Patients requiring AVR after previous CABG are particularly at risk because of older age and the presence of left ventricular hypertrophy and myocardial ischemia due to severe coronary artery disease, as well as graft disease. The higher mortality in patients with poor ejection fraction, as well as heart failure, would appear to confirm this. Additional problems include that of reentry, ability to deliver cardioplegia, and management of previously placed grafts. In an effort to place the mortality in perspective we have listed in Table 8Go the mortality for primary and reoperation for AVR with and without CABG. As much as possible, results include those published from our own institution; where our results are not available, recently published results of large series from other institutions or from The Society of Thoracic Surgeons data base are included.


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Table 8. . Comparison of Mortality for Aortic Valve Replacement and Coronary Artery Bypass Grafting in Various Clinical Situations
 
We believe that a combination of techniques are required to provide optimal cardiac protection. These include moderate hypothermia, left ventricular venting, topical cooling, and a combination of antegrade and retrograde cardioplegia. The use of retrograde cardioplegia is most probably a major advance in the current practice, although we do not have any firm data to confirm this in our patients. The management of the patent internal thoracic artery graft is controversial. Ideally, this should be dissected free and clamped during aortic cross-clamping. However, on occasion this may be extremely difficult because of dense pericardial adhesions. In those instances, deep hypothermia and topical cooling is appropriate. Our data would suggest that patients with a patent internal thoracic artery graft had a lower mortality than those patients without such a graft.

The decision to place a mechanical versus a bioprosthetic valve should be dictated by the usual criteria. Although most of our patients received a bioprosthetic valve, we believe that the indications to use a mechanical valve should be more liberal, because of their greater durability and less need for subsequent reoperation. On the other hand, there is some evidence that porcine xenografts last longer in patients with coronary artery disease [23].

Limitations of this study include its retrospective nature and the fact that details of the earlier operation of CABG in many of the patients who had this procedure elsewhere are missing. Many investigations, particularly echocardiography, were performed during a period of evolution and were not uniformly obtained, making analysis difficult. We would have liked to have given thresholds of determining AVR in patients undergoing CABG. However, to be more specific we would need to know the denominator, that is, the number of patients with mild aortic stenosis who have had CABG who are in the community and who do or do not require AVR. This study is considerable and needs to be done. Because of few events, the multivariate models are considered to be unstable and therefore lack power and are unreliable.

In conclusion, in determining whether the patient with mild aortic valve disease having CABG should have the aortic valve replaced, the following should be considered: (1) the natural history of degenerative aortic valve disease; (2) complications of an implanted prosthetic valve; (3) the natural history of a patient having CABG; (4) the risk of primary AVR + CABG; and, most important, (5) the risk of reoperation for AVR in a patient who is now older after previous CABG.

The definitive study of the efficacy of a surgical procedure is a prospective, randomized trial, and it may be argued that this is necessary before making any conclusions regarding whether the patient with mild aortic valve disease should or should not have the aortic valve replaced at the time of CABG. We and others have demonstrated that there is substantial risk with AVR after previous CABG. Therefore, we believe that a prospective, randomized trial is unnecessary. Most of the mortality and morbidity of the procedure are associated with complex operations, low ejection fraction, and low cardiac output, all of which suggests that myocardial preservation is of critical concern. These patients at reoperation are extremely heterogeneous with a wide spectrum of native coronary and graft disease, variations in vessel operability, and different degrees of aortic stenosis and ventricular hypertrophy. In our analysis, although techniques and methods of cardioplegic delivery did not influence mortality, myocardial preservation clearly needs to be individualized. In most cases systemic hypothermia with a combination of retrograde and antegrade blood cardioplegia would appear to be the best option.

The natural history of degenerative aortic valve disease is progressive, and it is reasonable to assume that the gradient will increase by approximately 10 mm Hg/y. Present generation bioprosthetic [24] and mechanical valves in the older patient demonstrate excellent long-term results with a low morbidity. Therefore, it appears logical to recommend that the threshold for AVR in patients requiring CABG should be lowered because the subsequent risk of reoperation for AVR is higher and outweighs the risk of a prosthetic valve and its subsequent complications.


    Acknowledgments
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
The assistance of Cathy Schleck and Duane Ilstrup of the Department of Biostatistics with statistical analysis and Kathy Distad with the typing of the manuscript is gratefully appreciated.


    Footnotes
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Address reprint requests to Dr Odell, Mayo Clinic Jacksonville, 4500 San Pablo Rd, Jacksonville, FL 32224.


    References
 Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Collins JJ, Jr, Aranki SF. Management of mild aortic stenosis during coronary artery bypass graft surgery. J Cardiac Surg 1994;9:145–7.[Medline]
  2. Fighali SF, Avendano A, Elayda MA, et al. Early and late mortality of patients undergoing aortic valve replacement after previous coronary artery bypass graft surgery. Circulation 1995;92(Suppl 2):163–8.[Abstract/Free Full Text]
  3. Avendano A, Fighali SF, Elayda MA, et al. Early and late mortality of aortic valve replacement after a previous coronary artery bypass graft surgery [Abstract]. Circulation 1994;90(Suppl 1):587.
  4. Smedira NG, Ports TA, Merrick SH, Rankin JS. Balloon aortic valvuloplasty as a bridge to aortic valve replacement in critically ill patients. Ann Thorac Surg 1993;55:914–6.[Abstract]
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  6. Hossack KF, Neutze JM, Lowe JB, Barratt-Boyes BG. Congenital valvular aortic stenosis: natural history and assessment for operation. Br Heart J 1980;43:561–73.[Abstract/Free Full Text]
  7. Mullany CJ, Elveback LR, Frye RL, et al. Coronary artery disease and its management: influence on survival in patients undergoing aortic valve replacement. J Am Coll Cardiol 1987;10:66–72.[Abstract]
  8. Shapira N, Lemole GM, Fernandez J, et al. Aortic valve repair for aortic stenosis in adults. Ann Thorac Surg 1990;50:110–20.[Abstract]
  9. Freeman WK, Schaff HV, Orszulak TA, Tajik AJ. Ultrasonic aortic valve decalcification: serial Doppler echocardiographic follow-up. J Am Coll Cardiol 1990;16:623–30.[Abstract]
  10. Faggiano P, Ghizzoni G, Sorgato A, et al. Rate of progression of valvular aortic stenosis in adults. Am J Cardiol 1992;70:229–33.[Medline]
  11. Peter M, Hoffmann A, Parker C, Luscher T, Burckhardt D. Progression of aortic stenosis. Role of age and concomitant coronary artery disease. Chest 1993;103:1715–9.[Abstract/Free Full Text]
  12. Brener SJ, Duffy CI, Thomas JD, Stewart WJ. Progression of aortic stenosis in 394 patients: relation to changes in myocardial and mitral valve dysfunction. J Am Coll Cardiol 1995;25:305–10.[Abstract]
  13. Cheitlin MD, Gertz EW, Brundage BH, Carlson CJ, Quash JA, Bode RS. Rate of progression of valvular aortic stenosis in the adult. Am Heart J 1979;98:689–700.[Medline]
  14. Wagner S, Selzer A. Progression of aortic stenosis: a longitudinal hemodynamic study. Circulation 1982;65:709–12.[Free Full Text]
  15. Otto CM, Pearlman AS, Gardner CL. Hemodynamic progression of aortic stenosis in adults assessed by Doppler echocardiography. J Am Coll Cardiol 1989;13:545–50.[Abstract]
  16. Roger VL, Tajik AJ. Progression of aortic stenosis in adults: new insights provided by Doppler echocardiography [Review]. J Heart Valve Dis 1993;2:114–8.[Medline]
  17. ACC/AHA Task Force Report. Guidelines and indications for coronary artery bypass graft surgery. J Am Coll Cardiol 1991;17:543–89.[Medline]
  18. Rowe MH, Mullany CJ, White AL, Wilson AC, Clarebrough JK. Early and late survival after coronary artery surgery. Med J Aust 1989;150:682–93.[Medline]
  19. Beppu S, Suzuki S, Matsuda H, Ohmori F, Nagata S, Miyatake K. Rapidity of progression of aortic stenosis in patients with congenital bicuspid aortic valves. Am J Cardiol 1993;71:322–7.[Medline]
  20. Sundt TM, Rasmi N, Wong K, Radley-Smith R, Khaghani A, Yacoub MH. Reoperative aortic valve operation after homograft root replacement: surgical options and results. Ann Thorac Surg 1995;60:S95–S100.[Medline]
  21. Clark RE. The STS cardiac surgery national database: an update. Ann Thorac Surg 1995;60:1376–81.[Abstract/Free Full Text]
  22. He G, Acuff TE, Ryan WH, He Y, Mack MJ. Determinants of operative mortality in reoperative coronary artery bypass grafting. J Thorac Cardiovasc Surg 1995;110:971–8.[Abstract/Free Full Text]
  23. Angell WW, Pupello DF, Bessone LN, et al. Influence of coronary artery disease on structural deterioration of porcine bioprostheses. Ann Thorac Surg 1995;60:S276–81.[Medline]
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