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Ann Thorac Surg 1996;61:1693-1697
© 1996 The Society of Thoracic Surgeons

Original Article: Cardiovascular

Management of Asymptomatic Mild Aortic Stenosis During Coronary Artery Operations

Andrew C. Fiore, MD, Marc T. Swartz, BA, Keith S. Naunheim, MD, Debra A. Moroney, BSN, David A. Canvasser, MD, Lawrence R. McBride, MD, Pamela S. Peigh, MD, George C. Kaiser, MD, Vallee L. Willman, MD

Division of Cardiothoracic Surgery, St. Louis University Health Sciences Center and St. Mary's Health Center, St. Louis, Missouri


   Abstract
Top
 Footnotes
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background. Management of asymptomatic mild aortic stenosis at the time of coronary artery bypass grafting (CABG) remains controversial. We have retrospectively analyzed a cohort of patients requiring aortic valve replacement (AVR) subsequent to CABG and compared their operative morbidity and mortality with that of a group receiving CABG and AVR simultaneously at the first operation.

Methods. Analysis is drawn from 28 patients who required AVR 8 ± 4 years subsequent to CABG (group A) and 175 patients receiving AVR along with CABG at the primary operation (group B). Groups were similar with respect to age, sex, risk factors for cardiac disease, extent of coronary artery disease, left ventricular function, New York Heart Association class, aortic valve area, number of grafts, and size of prosthesis inserted.

Results. Patients having AVR subsequent to CABG had a significantly prolonged aortic cross-clamp time and global myocardial ischemic time and incurred a twofold increase in operative mortality. The actuarial survival at 10 years was not significantly different between cohorts. In the 28 patients in group A, the aortic valve area during the period between operations decreased 0.05 mm2/y.

Conclusions. The operative mortality and morbidity of a second operation for AVR is high, but there is no significant difference in survival at 10 years. In at least a portion of patients having mild aortic stenosis at the time of CABG there will be progression of the stenosis necessitating reoperation at a later date.


   Introduction
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 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
See also page 1697.

A small number of patients with coronary artery disease who require myocardial revascularization have coexisting asymptomatic mild aortic valve stenosis. The optimal management of these patients remains controversial. Some authors have recommended aortic valve replacement (AVR) at the time of myocardial revascularization [1]. They argue that natural history studies demonstrate mild aortic stenosis usually progresses to a critical stage within 5 years and the risk of reoperation in this now older patient with patent coronary artery bypass grafts is substantially increased. On the other hand, critics of this position believe that prophylactic AVR for mild aortic stenosis in a patient whose primary symptoms are coronary insufficiency unjustifiably increases the operative mortality as well as the risk of subsequent valve-related events, and such patients should not have valve replacement until hemodynamically significant aortic stenosis develops.

To help resolve these issues we have analyzed our experience with reoperative AVR performed after previous myocardial revascularization and compared the results with data from patients receiving simultaneous valve replacement and coronary artery bypass grafting (CABG).


   Material and Methods
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Acknowledgments
 References
 
Between 1980 and 1994, 28 patients had AVR subsequent to CABG (group A) at a mean 8 ± 4 years (range, 2 months to 16 years) whereas 175 patients (group B) underwent a primary operation for AVR and CABG. None of the patients in group A were considered to have hemodynamically significant aortic stenosis at the time of the initial coronary revascularization. One patient did have aortic valve decalcification at the first operation. Twenty-one patients had repeat CABG at the follow-up second operation. Variables reported in this group were recorded before the valve replacement (ie, second procedure).

Clinical data obtained from hospital records included age, sex, body surface area, and the presence of concomitant medical problems such as smoking, diabetes mellitus, and hypertension. New York Heart Association functional class, history of myocardial infarction, prior valve procedure, and prior CABG were also recorded. Angina was graded using the Canadian Cardiovascular Society classification.

Cardiac catheterization findings recorded included number of diseased vessels (defined as >=50% obstruction of the luminal diameter in any plane on coronary angiography) and left ventricular function as quantitated by left ventricular score (abnormal segmental wall motion scoring system used by the Coronary Artery Surgery Study) [2]. Left ventricular end-diastolic pressure and peak-to-peak systolic gradient across the aortic valve at first and subsequent catheterizations were also recorded. The interval between initial and second catheterization was noted. The aortic valve area was calculated by the Hakki formula. Aortic stenosis was considered mild when the aortic valve area was 1.0 cm2 or greater, moderate when the area was less than 1.0 cm2 but greater than 0.7 cm2, and severe when the area was 0.7 cm2 or less. Progression of aortic stenosis was considered to have occurred after stenosis increased from mild to moderate, mild to severe, or moderate to severe on the basis of the calculated aortic valve area.

Operative variables included the size of the prosthesis implanted, concomitant CABG, global ischemic time, and total cardiopulmonary bypass time.

The general conduct of all surgical procedures was similar. The operations were performed jointly by university faculty and surgical residents using a membrane oxygenator, moderate systemic hypothermia (28°C), and hemodilution. Median sternotomy was undertaken in all patients, with mediastinal dissection being conducted as extensively as possible before heparinization. Cardiopulmonary bypass was established using ascending aortic and dual-stage right atrial cannulation. The left ventricle was routinely vented through the right superior pulmonary vein. Myocardial preservation consisted of cold intermittent potassium blood cardioplegia delivered antegrade or retrograde every 20 minutes and supplemented with topical myocardial cooling. After aortic clamping, coronary artery bypass grafts were performed. Proximal and distal anastomoses were routinely performed under a single cross-clamp. Suture placement for AVR consisted of interrupted pledgeted horizontal mattress sutures placed from above downward to evert the annulus. Sodium warfarin therapy was initiated within 3 days of valve implantation to maintain the international ratio at 2.5 to 3.0 times control.

Postoperative complications recorded included low cardiac output (defined as a cardiac index <2.L • min-1 • m-2 or the need for intravenous inotropic drugs or intraaortic balloon pump support for more than 24 hours postoperatively), reoperation for bleeding, renal failure requiring dialysis, perioperative myocardial infarction (defined by the presence of new Q waves on the electrocardiogram or cardiac enzyme analysis), respiratory insufficiency (defined as the need for reintubation or mechanical ventilatory support for more than 48 hours), and the presence of new postoperative ventricular or atrial arrhythmias. Cardiac cause of death was defined as death due to myocardial infarction, cardiac arrest, fatal ventricular arrhythmia, or sudden unexplained death. Operative mortality was defined as any death during hospitalization or within 30 days of the surgical procedure.

Follow-up was complete in 182 hospital survivors with 910 patient-years. The total follow-up was 306.8 patient-years in group A and 603.2 patient-years in Group B.

Data were analyzed with the Statview Four statistical software package (Brainpower, Inc, Calabasas, CA). A {chi}2 test or Fisher's exact test was used to determine significance for discrete variables. Continuous variables were compared by an unpaired two-tailed Student's t test. A p value of less than 0.05 was considered significant.

Actuarial survival curves were computed by the method of Berksen and Gage [3] and compared using a log rank analysis. Patients having CABG followed by AVR had their actuarial survival calculated from the time of valve replacement. Mean values are expressed as plus or minus the standard deviation except as noted.


   Results
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 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Acknowledgments
 References
 
Clinical and Operative Profile
Both groups were similar with respect to the risk factors for heart disease except for the presence of diabetes mellitus being more frequent in group A. The extent of coronary artery disease and the frequency of preoperative myocardial infarction were similar (Table 1Go). The majority of patients in both cohorts had mild left ventricular dysfunction and similar degrees of aortic stenosis at the time of valve replacement (Table 2Go).


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  		Table 1. . Patient Characteristics
 

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  		Table 2. . Cardiac Catheterization Data
 
Twenty-one of 28 patients (75%) in group A required concomitant repeat myocardial revascularization at the time of valve replacement. In both groups the size of the prosthesis and the number of bypass grafts inserted were similar. Patients in group A were undergoing redo procedures and not unexpectedly incurred a significantly greater global myocardial ischemic and extracorporeal circulation time (Table 3Go). A mechanical prosthesis was used more frequently than a porcine valve in both cohorts, but the difference was not significant (group A: mechanical, 79%, porcine, 21%; group B: mechanical, 62%, porcine, 38%).


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  		Table 3. . Operative Data
 
Interval Change in Aortic Valve Stenosis and Valve Anatomy
Patients with mild aortic stenosis requiring myocardial revascularization as their initial procedure had a preoperative peak gradient of 26 ± 10 mm Hg and a valve area of 1.05 ± 0.2 cm2. In this group, subsequent AVR was performed at a mean of 8 ± 4 years (range, 2 months to 16 years). At the time of valve replacement the peak pressure gradient had increased to 61.3 ± 26 mm Hg and the valve area had decreased to 0.69 ± 0.12 cm2 (p < 0.05). The interval change in valve area and gradient was 0.05 mm2/y and 6.5 mm Hg/y, respectively. Linear regression analysis did not demonstrate a relationship between stenosis severity and interval to AVR (valve area: F = 0.368, not significant; valve gradient: F = 0.599, not significant).

The anatomy of the excised aortic valve and the mean rate of gradient progression was as follows: congenital bicuspid (4 patients), 10.6 ± 5 mm Hg/y; degenerative (19 patients), 5.9 ± 7.6 mm Hg/y; and rheumatic (5 patients), 3.9 ± 2.3 mm Hg/y.

Patients undergoing simultaneous myocardial revascularization with AVR had a preoperative peak pressure gradient and valve area of 53.2 ± 24 mm Hg and 0.73 ± 0.21 cm2 respectively. This degree of aortic stenosis was not significantly different from that of those patients in group A (see Table 2Go).

Hospital Mortality and Morbidity
There were 21 patients (group A = 5, 18%; group B = 16, 9.1%; not significant) who died in the hospital. The most common cause of death was cardiac (group A = 3, 11%; group B = 5, 2.8%). Four patients, 2 in each group, died within the first 24 hours postoperatively of low cardiac output. The remaining 8 hospital deaths (all in group B) were caused by multiorgan system failure (3 patients), mediastinal infection (2 patients), cerebrovascular accident (2 patients) and postoperative bleeding (1 patient).

Postoperative complications occurred with a significantly greater frequency in those patients having AVR following myocardial revascularization (Table 4Go). Valve replacement in this group was performed as a reoperation, and not unexpectedly reexploration for bleeding in this population increased twofold. This cohort had recurrent coronary artery disease, as 75% of these patients required repeat myocardial revascularization. The incidence of myocardial infarction, ventricular ectopy, and low cardiac output, complications frequently associated with ischemic heart disease, was increased in this group, the latter two achieving statistical significance. In addition, patients in group A had a significantly greater requirement for prolonged ventilatory support.


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  		Table 4. . Postoperative Complications
 
Late Mortality
Late death occurred in 60 patients (group A = 3, 13%; group B = 57, 37%; not significant). The causes of late death are summarized in Table 5Go. Figure 1Go depicts the actuarial survival of the two cohorts. At 5 years, the actuarial survival was 70% for all patients. At 10 years, there is a trend toward greater survival advantage in those patients in whom valve replacement had been delayed, but the difference did not achieve statistical significance.


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  		Table 5. . Causes of Late Death
 


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  		Fig 1. . Ten-year actuarial survival of both cohorts beginning at the time of aortic valve replacement (AVR). Hospital deaths are included. (CABG = coronary artery bypass grafting; NS = not significant.)

 

   Comment
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Acknowledgments
 References
 
A small number of patients who require myocardial revascularization will present with coexisting mild asymptomatic aortic stenosis. The dilemma faced by the surgeon is whether to replace the aortic valve "prophylactically" at the time of revascularization or follow up these patients with the realization that some may require future reoperation for AVR. This latter alternative may potentially increase mortality and morbidity at the time of subsequent AVR but avoids the risk of chronic anticoagulation in the instance of mechanical valves and the risk of reoperation due to degeneration of bioprostheses.

We emphasize that our review does not provide information on the incidence of need for subsequent valve replacement in the category under consideration, ie, concomitant mild aortic stenosis and coronary artery disease requiring reoperation. Our review does confirm that in at least a portion of such cases, the valve stenosis progresses and reoperation causes a burden of increased risk. This observation has been reported by Collins and associates [4]. They demonstrated a 23.5% operative mortality for reoperative AVR after CABG compared with 7.6% for reoperative AVR without CABG and 6.6% for primary AVR with CABG. The reasons for this high mortality are multifactorial. At the time of reoperation the patients are older and the procedure takes longer. Age, prolonged bypass time, and prolonged cross-clamp time are the strongest independent predictors of mortality after AVR [5]. Patients requiring AVR subsequent to CABG have progressive native and graft coronary atherosclerosis, which may need to be addressed at reoperation. Twenty-one of 28 patients (75%) in our study required repeat myocardial revascularization. Embolization of atherosclerotic materials through diseased saphenous vein grafts at reoperation is associated with ventricular arrhythmias and low cardiac output, complications we observed with a significantly increased frequency in group A. If a patient has had an internal thoracic artery bypass graft, this vessel must be dissected without injury and its flow controlled to administer antegrade-retrograde cardioplegia. In our series, damage to the internal thoracic artery at reentry was associated with one perioperative death. Myocardial protection can be suboptimal in such patients secondary to increased concentric hypertrophy, which predisposes to greater myocardial damage during prolonged global ischemia.

Because the risk of reoperation is high, several investigators have advocated valve repair at the time of myocardial revascularization [6, 7]. Advocates of this position argue this technique can alleviate valve stenosis and delay the need for valve replacement without increasing operative risk during myocardial revascularization [8]. Decalcification using mechanical debridement with a rongeur or ultrasonic devices has been reported, but the outcome has been disappointing [9–11]. Although valves appear functional initially, they undergo scarring, which results in restenosis and regurgitation within 1 to 5 years in a significant percentage of cases. There are several variables affecting the results of mechanical debridement that remain to be clarified (eg, anatomy of the valve, pathology of the valve, and the energy setting of the ultrasonic device). Currently, we believe the published data for aortic valve decalcification do not support this technique [12–14].

The progressive nature of valvar aortic stenosis as assessed by clinical symptoms, Doppler echocardiography, and cardiac catheterization is well established [15–17]. In this report the incremental increase in valve stenosis is similar to that reported by Wong and associates [1]. However, the rate of valve stenosis could not be correlated with the interval to valve replacement. This suggests that progression of aortic stenosis is multifactorial and could be related to valve anatomy, the presence of coexisting coronary artery disease, or progressive leaflet calcification. Davies and co-authors [18] noted the progression rate was not related to age, sex, or initial observed gradient, but rather to valve anatomy and degree of calcification. Rheumatic valve pathology was associated with less calcification and slower rates of progressive aortic stenosis [18]. Wagner and Selzer [19] found that degenerative trileaflet valves progress faster and had the highest calcification rates, whereas congenital bicuspid valves fell in between rheumatic and degenerative pathology. In our report, progressive aortic stenosis was more rapid in congenital bicuspid and slowest for rheumatic valves. These observations have been confirmed by Horstkotte and Loogen [20]. They hypothesized that dystrophic calcification may be a marker of greater tissue stress, leaflet immobility, and collagen damage, which could be responsible for rapid deterioration of the bicuspid valve.

Proponents of prophylactic AVR in this setting argue it prevents the risk of sudden death reported at 3% to 5% [21]. We believe this is not justified as the operative risk of AVR-CABG is higher and the procedure does not prevent this complication, especially in the presence of coronary artery disease. In our series, sudden unexplained death occurred early and late in both cohorts.

Finally, one may argue that placement of a prosthesis (mechanical or bioprosthetic) in a patient with asymptomatic mild aortic stenosis subjects the patient to the cumulative risk of valve-related complications and valve-related death, which is significant. The mean interval between the CABG and AVR procedures was 8 years. Valve-related morbidity 8 years after operation is 25% to 30% for mechanical and 15% to 20% for bioprosthetic valves [22–24]. The patients in this report bear witness to the gravity of such valve-related morbidity. Twenty-one of 57 late deaths (37%) in the CABG with AVR group were valve related.

We recognize that a significant negative feature of this study is our comparison group (CABG with AVR), which is not a true control patient population, as their concomitant procedure was not a reoperation. The ideal control group would be those patients with asymptomatic mild aortic stenosis who come to CABG and are subsequently observed. Unfortunately we have no follow-up information on this cohort. However, the demographic, hemodynamic, and operative characteristics of our two cohorts are similar. Furthermore, their survival is calculated in an actuarial manner with 100% follow-up, which we believe supports the conclusions reached.

In conclusion, patients who present for myocardial revascularization and have asymptomatic mild aortic valve stenosis should undergo CABG. The increased operative risk of valve replacement and the potential for subsequent valve-related complications (15% to 20% in 5 years) are significant and do not justify prophylactic AVR. Those patients in whom significant aortic valve stenosis subsequently develops after myocardial revascularization have an increased operative mortality at the time of reoperative AVR. The information currently available does not support aortic valve debridement using mechanical or ultrasonic techniques.


   Acknowledgments
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
References
 
We gratefully acknowledge Terri Wriley for her expert technical assistance with manuscript preparation.


   Footnotes
Top
 Footnotes
Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Presented at the Forty-second Annual Meeting of the Southern Thoracic Surgical Association, San Antonio, TX, Nov 9-11, 1995.

Address reprint requests to Dr Fiore, Department of Cardiothoracic Surgery, St. Mary's Health Center, 6420 Clayton Rd, St. Louis, MO 63117.


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

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