J Thorac Cardiovasc Surg 1999;117:1157-1165
© 1999 Mosby, Inc.
SURGERY FOR ADULT CARDIOVASCULAR DISEASE |
MANUAL DEBRIDEMENT OF THE AORTIC VALVE IN ELDERLY PATIENTS WITH DEGENERATIVE AORTIC STENOSIS
Ernesto Weinschelbaum, MD,
Pablo Stutzbach, MD,
Martín Oliva, MD,
Javier Zaidman, MD,
Augusto Torino, MD,
Eduardo Gabe, MD
From the Departments of Cardiovascular Surgery and Medicine, Institute of Cardiology and Cardiovascular Surgery, Favaloro Foundation, Buenos Aires, Argentina.
Received for publication April 10, 1998. Revisions requested May 20, 1998. Revisions received March 1, 1999. Accepted for publication March 1, 1999.
Address for reprints: Ernesto Eduardo Weinschelbaum, MD, Department of Cardiovascular Surgery, Favaloro Foundation, Belgrano 1746, 1093 Buenos Aires, Argentina.
 |
Abstract
|
|---|
Objective: We prospectively analyzed the short- and long-term results of manual debridement of the aortic valve in elderly patients with severe degenerative aortic stenosis.
Methods: Between September 1988 and January 1997, 103 patients aged 73.7 ± 6 years with degenerative aortic stenosis underwent the manual debridement technique. All had symptoms (angina or dyspnea, or both). Peak systolic gradient was 89 ± 28 mm Hg. Forty-one patients (39.8%) had associated coronary artery disease necessitating revascularization.
Results: Follow-up time was 42 ± 21 months (range 3-98 months). The Kaplan-Meier estimated survival at 98 months was 50% (95% CI: 30%-70%). In-hospital mortality was 5.8% (6 patients), and late mortality was 21% (21 patients). No predictors of in-hospital mortality or of late mortality were detected. Nonfatal postoperative complications appeared in 25 patients (24%). At 8 years, freedom from endocarditis was 98% (95% CI: 95%-100%) and freedom from thromboembolic events was 99% (95% CI: 96%-100%). No patient required long-term anticoagulation as a result of the procedure. Fourteen patients (14%) required reoperation for aortic insufficiency (n = 5), restenosis (n = 8), and mitral regurgitation (n = 1). The probability of reoperation at 98 months was 23% (95% CI: 12%-35%).
Conclusion: Manual aortic valve debridement has low rates of in-hospital mortality, perioperative complications, and thromboembolic and infectious events and it offers freedom from anticoagulation. However, the incidence of restenosis and reoperation is high in the long term. It may therefore be regarded as an alternative in aged patients with favorable valve anatomy (no distortion and calcium deposits only on the aortic surface of the cusps), especially in those with a small aortic anulus, associated coronary artery disease, and/or contraindication for anticoagulation.
|
Introduction
|
|---|
Degenerative aortic stenosis is the most prevalent valvular disease in clinical practice.
1 Although aortic valve replacement has modified the prognosis of this disease, the use of mechanical valves is not free of infectious, thromboembolic, and hemorrhagic complications, the last being a consequence of long-term anticoagulation. 2-5 Even though biologic valves do not require long-term anticoagulation, they are not free of other complications observed with mechanical valves. In addition, biologic valves show structural damage from the seventh year after implantation, 3,5 and if the aortic root is small, an anulus-enlargement procedure should precede the placement of a biologic valve.
Aortic valve debridement appeared to be an alternative treatment for severe aortic stenosis, 6 but it was abandoned because of the high short- and long-term incidence of restenosis and aortic regurgitation, especially when the ultrasonic technique was used. 7,8
Few data have been published regarding manual aortic valve debridement in the elderly. 9 We thus aimed to assess short- and long-term results of manual debridement of the aortic valve as a treatment for degenerative aortic stenosis in aged patients with favorable anatomic conditions to perform this procedure (no valvular distortion and calcific lumps only on the aortic surface of the cusps), some of whom had a small aortic root with or without associated coronary artery disease.
|
Patients and methods
|
|---|
Between September 1988 and January 1997, 103 patients with degenerative aortic stenosis underwent manual debridement of the aortic valve. Mean age was 73.7 ± 6 years (range 65-87 years), and 57 patients (55%) were women. We selected some patients in whom the procedure was technically viable—patients with well preserved valvular architecture and calcium deposits only on the aortic surface of the cusps. Some of these patients had a small aortic root that would have necessitated prior enlargement of the outflow tract to allow placement of a bioprosthesis of at least 23 mm, and some others had combined coronary artery disease and moderate-to-severe aortic stenosis. Patients younger than 65 years, those with aortic stenosis of rheumatic etiology, and those having aortic regurgitation of more than 2+/4 were excluded from this technique and subjected to valve replacement. Table I shows the clinical features of the population. All patients underwent coronary angiography. In 41 patients (40%), significant coronary artery disease was documented.
Surgical technique
All patients underwent manual debridement of the aortic valve. The procedure was always done by the same surgeon, using No. 15 scalpel blades, dissecting forceps, and rongeur forceps. Removal of the calcium lumps from the fibrous matrix of the cusps was started with a slight torsion movement with a rongeur forceps. Thereafter, removal was completed by careful dissection with the use of delicate pickups until the lump remained adherent to the leaflet by a thin endothelial layer, which was finally cut with scissors. This maneuver was done with great care, because any piercing of the leaflet would have resulted in failure of the repair. Occasionally, the calcium deposits reached the valvular anulus and even the site of insertion of the cusps. If these deposits were lumps, they were removed by means of the technique just described, but if they were firm calcific plaques extending to the aortic wall, we removed them only if they restricted the movement of the cusps. The procedure was ended when all calcium was removed and the 3 cusps were mobile enough to contact the aortic wall, thus ensuring significant reduction of the gradient.
In patients undergoing myocardial revascularization, 1.9 grafts per patient were done. The internal thoracic artery was used in 30 patients (73%) and a free radial artery graft in 1 (2.3%).
In 2 patients (1.9%) with severe mitral regurgitation, annuloplasty with bovine pericardium was performed.
In 2 patients (1.9%), a minithoracotomy with a vertical incision through the third and fourth right costal cartilages was carried out, whereas in the others conventional thoracotomy was used.
Follow-up
Clinical and echocardiographic studies were performed in all patients just before discharge, at 6 months and 1 year after the operation, and every year thereafter. Hospital mortality was defined as death occurring within 30 days after the operation. During long-term follow-up the following events were assessed: death, reoperation, thromboembolism, infectious endocarditis of the treated valve, restenosis, and aortic regurgitation.
Peak transvalvular gradients, chamber diameters, the degree of aortic regurgitation, and left ventricular systolic function were assessed by means of Doppler echocardiography. Aortic regurgitation was classified as mild (1+/4), moderate (2+/4), moderate to severe (3+/4), and severe (4+/4).
Statistics
The estimates of the survival curves and their standard errors were computed by means of the Kaplan-Meier method and the Greenwood formula. We plotted a representation of the distribution of the survival time until reoperation, the cumulative incidence curve. 10,11 This plot has a simple meaning for both independent and dependent end points. If we call T the time until the first observed end point, the cumulative incidence function is defined as follows:
F (t) = P (the end point observed is reoperation and T 
t) = P (reoperation occurred by time t).
The log-rank test was used to assess differences between groups. Cox regression models were used for multivariate analysis.
Postoperative transvalvular gradients were modeled with a linear mixed model of the following form:
gij = (ß0 + ß1 tj+ ß 2 tj2 ) + (bi0 + bil t j + bi2 tj2) + 
ij
where gij is the observed gradient for the ith patient at time tj; ß0, ß1, and ß 2 are population polynomial coefficients, and bi = (b i0, bil, bi2) allows the coefficients to change for each patient. The vectors bi are assumed to be independent and normally distributed, with a mean value of zero and an arbitrary covariance matrix. The terms ij are independent normal errors. The procedure lme of S-Plus version 4.5 (MathSoft, Inc, Seattle, Wash) was used to fit this model.
|
Results
|
|---|
In 61 patients (59%) only aortic debridement was done. In 40 patients (39%) with associated coronary artery disease, aortic debridement plus myocardial revascularization was performed. In 2 patients (1.9%), debridement plus mitral valve repair was done, 1 of them also undergoing myocardial revascularization.
Two patients were excluded from the study because of unsuccessful debridement (valve perforation greater than 5 mm in both cases) and conversion to valve replacement.
The duration of extracorporeal circulation and aortic crossclamping was 65 ± 21 and 47 ± 17 minutes, respectively, in patients undergoing valvular debridement only and 95 ± 16 and 70 ± 16 minutes in those with combined myocardial revascularization and/or mitral valve repair.
In-hospital mortality
Overall in-hospital mortality was 5.8% (6 patients). Of the 61 patients undergoing only aortic valve debridement, 3 (4.9%) died. Three (7.1%) of 42 patients subjected to combined procedures died: 2 of these underwent myocardial revascularization, and 1 revascularization with combined mitral valve repair. In 3 patients the cause of death was of cardiac nature: ventricular tachycardia in 2 and cardiogenic shock in 1. The remaining 3 died of sepsis, stroke, and renal failure, respectively. Statistical analysis of the diverse clinical, angiographic, hemodynamic, and surgical variables did not identify any of them as a predictor of in-hospital mortality.
In-hospital morbidity
Nonfatal complications appeared in 25 patients (24%) (Table II), the most frequent being atrial fibrillation (11 patients, 11%). No patient had atrioventricular or intraventricular conduction disturbances necessitating implantation of a permanent pacemaker.
Follow-up
Mean follow-up time was 42 ± 21 months (range 3-98 months). Late mortality was 21% (21 patients), principally in those subjected to combined procedures.
The estimated survival at 4 and 8 years was 74% (95% CI: 64%-84%) and 50% (95% CI: 30%-70%) (Fig. 1). Patients undergoing only valve debridement had a higher Kaplan-Meier survival curve than those having valve debridement combined with coronary artery bypass grafting (80% vs 65% at 4 years and 60% vs 35% at 8 years; Fig. 2), but the difference is not statistically significant (P = .27). The causes of late mortality are listed in Table III. Cox regression analysis was unable to detect any predictor of late mortality.
View larger version (15K):
[in this window]
[in a new window]
|
Fig. 2 Comparison of the estimated survival for 2 groups of patients: with aortic valve debridement only and with aortic valve debridement combined with coronary artery bypass grafting (CABG).
|
|
At 11 months, 1 patient had a stroke and, although the cause could not be established, it was considered to be related to the valve. Stroke occurred in 2 more patients at 22 and 24 months. In these, stroke was attributed to carotid artery disease and the patients underwent carotid endarterectomy. In the 98-month follow-up period, freedom from thromboembolic events was 99% (95% CI: 96%-100%). No patient required anticoagulation because of the surgical procedure. In 3 patients, anticoagulation was indicated because of chronic atrial fibrillation. One patient had aortic valve endocarditis after erysipelas. In the 98-month follow-up period, freedom from endocarditis was 98% (95% CI: 95%-100%).
Gradients at the sixth postoperative month were much lower than those measured before the operation. It should be noticed that in all patients the gradient had decreased 6 months after the operation (Table IV).
In the long term, the gradient increased (P < .0001; Fig. 3). As seen, this increase is nonlinear, the rate of increase being greater during the first years. To see if this observation could be due to random variations, we adjusted a second-degree polynomial. The polynomial adjusted was as follows: mean gradient = 16.8 + 17.3 · time–1.26 · time2 (P value for the quadratic term < .0001). Therefore we conclude that the gradient does not have a linear relation with time, but its derivative decreases with time.
Table IV
shows that when 1 period is compared with the following period, almost all patients exhibit an increasing gradient. If, instead of comparing consecutive periods, the value observed in 1 year is compared with that observed 2 years earlier (not shown in Table IV), the gradient increases in all patients, without exceptions. When the measurement at 6 months is compared with that taken after 4 years, the mean variation for the 24 patients undergoing both measurements is 36.5 ± 13.4 mm Hg (range 15-61 mm Hg).
In the early patients of this series, aortic regurgitation was an important cause of reoperation. Table V shows the evolution of aortic regurgitation: after 6 months, the degree of aortic regurgitation had increased in 50 of 83 patients. In some patients, regurgitation continued to worsen for 1 year after the operation. Thereafter, almost no patient exhibited variations.
All patients had an improvement in functional class of dyspnea or angina (or both) at 6 months and, despite the increase in gradient, most patients remained free of symptoms, the exception being those who required reoperation (Table VI).
Reoperations
Fourteen patients (14%) had reoperations, 5 (5.1%) because of severe aortic regurgitation and 8 (8%) because of restenosis. In 1 patient (1%), reoperation was indicated because of severe mitral regurgitation, and during the same operation the aortic valve was replaced because of signs of recalcification. All reoperations were indicated because of the presence of symptoms. At 98 months of follow-up, 69% of the patients were free of reoperations (Fig. 4). The probability of reoperation at 4 and 8 years was 15% (95% CI: 6%-24%) and 23% (95% CI: 12%-35%), respectively (Fig. 5). During follow-up, reoperations necessitated by regurgitation showed a tendency to occur earlier than those necessitated by restenosis. After 3 years of follow-up, the only reason for reoperation was stenosis. Two patients died during reoperation.
|
Discussion
|
|---|
Several studies have demonstrated that a small-sized aortic bioprosthesis has an unfavorable hemodynamic performance with high residual transvalvular gradients. 12-14 Insertion of a larger valve requires prior root enlargement, but this prolongs the duration of the operation and may increase the operative risk in older patients. 15 Stentless aortic xenografts, which have appeared recently, have not yet been tested in the long term. 16
Aortic valve debridement is a surgical technique that has been questioned on the basis of the results reported. 7-9 However, some authors have suggested the usefulness of this method in elderly patients who have a small aortic anulus. 17 The anatomopathologic characteristics of these valves suggest that this technique may be useful to restore valvular motility and decrease the transvalvular gradient without inducing incompetence. The lesser degree of distortion with regard to other causes, the minimal leaflet retraction observed in most cases, and the fact that the commissures are preserved allow debridement of the valvular surface without distorting the original architecture. 18
In the present series, a low in-hospital mortality rate was observed, both for the patients subjected to the procedure alone and for those undergoing combined myocardial revascularization. Such rates are comparable with those reported for valve replacement, which range from 4.4% to 18%. 19-23 Other studies reporting the use of this technique are not strictly comparable with the present one because they include diverse causes and age groups. 6-8
The incidence of nonfatal postoperative complications was approximately 25%, significantly less than that reported in studies of valve replacement. Aranki and coworkers 21 reported a 48% incidence, 10% of which was directly related to the valve.
We did not observe any complication related to the valve, and no patient required anticoagulation associated with the procedure. In patients with biologic prostheses and no anticoagulation, Heras and colleagues 24 observed that the incidence of thromboembolic events between the first and tenth days after surgery was 41% per year and between the eleventh and ninetieth postoperative days, 3.6% per year. On the basis of these results and those of others, 5,25 the need for anticoagulation during the first 3 months after surgery was suggested. However, in elderly patients, the reported incidence of bleeding is 9% per patient-year. 15
Aortic valve replacement is associated with a 3.2% to 5.6% incidence of conduction disturbances necessitating permanent pacing. 26,27 In our series, no patient required implantation of a permanent pacemaker because of conduction disturbances induced by the procedure. Reduced trauma on the valvular anulus and the absence of sutures probably explain why conduction disturbances did not occur.
Survival at 4 and 8 months was similar to that observed in aged patients undergoing valve replacement with biologic prostheses. 19,28 Patients undergoing only valve debridement had higher survivals than those with combined myocardial revascularization. Similar results were reported by other authors. 29,30
Freedom from endocarditis and thromboembolic events in our experience was higher than that reported for similar time periods in patients receiving biologic prostheses. 22,23,31
Despite similar survivals and probably a lower incidence of infectious and thromboembolic events, in the long-term follow-up both the need for reoperations and the structural damage of the valve are higher in our experience higher with biologic prostheses. With biologic prostheses, freedom from reoperation at 10 years is approximately 76% to 91% and freedom from structural valve deterioration, 89% to 91%. 23,31
Since our technique is essentially manual, we believe that the higher overall incidence of reoperations in our series was influenced by suboptimal technique in the early patients. During the first 3 years, the main cause of reoperation was severe aortic regurgitation. It should be noticed, however, that this complication was prevalent in our early patients and did not occur again after the technique had been corrected. Late reoperations, on the other hand, are not attributable to technical problems, but to recalcification and restenosis.
Echocardiographic follow-up evidenced a progressive increase in peak gradient values and restricted valve motility. Two different types of outcomes were observed: valvular restenosis necessitating surgery rapidly developed within 3.5 years in 1 group; in others, the progression was slower, with milder increase of transvalvular gradient values. We were unable to detect preoperative values related to these types of progression.
Moderate-to-severe and severe residual valvular regurgitation (a complication related to the early cases) at 6 months was 11.3%. With ultrasound debridement, the reported development of severe and moderate aortic insufficiency at 9 months after surgery is 26% and 37%, respectively. 32 These differences with regard to our own results probably are due to the lesser scar effect generated by manual debridement.
Ninety-eight percent of the patients showed improvement in functional capacity in the postoperative study despite progressive increase of the transvalvular gradient. A dissociation was observed between the increase in transvalvular gradient and functional capacity, the latter remaining stable during follow-up. Despite its progressive increase, the transvalvular gradient was lower than the preoperative value. This could explain the dissociation between the increase in the gradient and the stability of the functional class.
|
Conclusion
|
|---|
Manual aortic valve debridement has low rates of in-hospital mortality, perioperative complications, and thromboembolic and infectious events, and no need for anticoagulation. However, it has a high incidence of restenosis and reoperation in the long term. It may therefore be said that this procedure is useful in aged patients with favorable valve anatomy (no distortion and calcium deposits only on the aortic surface of the cusps), especially those with a small aortic anulus, associated coronary artery disease, or contraindication for anticoagulation.
|
Acknowledgments
|
|---|
We thank Dr Alberto Crottogini from the Basic Sciences Research Institute (Favaloro Foundation) for helping in the preparation of the manuscript and Dra Marta García Ben for statistical assistance.
|
References
|
|---|
-
Wei JY. Heart disease in the elderly. Cardiovasc Med 1984;9:971-82.
-
Selzer A. Aortic valve stenosis. In: Kapoor AS, Sing BN, editors. Prognosis and risk in cardiovascular disease. 1st ed. Washington: Churchill Livingstone; 1994. p. 261-8 .
-
Akins CW. Mechanical cardiac valvular prostheses. Ann Thorac Surg 1991;52:161-72.[Abstract]
-
Magilligan DJ, Lewis JR, Stein P, Alam M. The porcine bioprosthetic heart valve: experience at 15 years. Ann Thorac Surg 1989;48:324-30.[Abstract]
-
Turina J, Turina M, Krayenbuehl HP. Cardiac bioprostheses in the 1990. Circulation 1993:88:775-81.
-
Mulder DG, Winfield ME. Valvuloplasty for acquired aortic stenosis. Ann Surg 1960;151:203-15.[Medline]
-
Enright LP, Hancock EW, Shumway NE. Aortic debridement: long-term follow-up. Surgery 1971;69:404-9.[Medline]
-
Craver JM. Aortic valve debridement by ultrasonic surgical aspirator: a word of caution. Ann Thorac Surg 1990;49:746-53. [Abstract]
-
Hill DG. Long-term results of debridement valvotomy for calcified aortic stenosis. J Thorac Cardiovasc Surg 1973;65:708-11. [Medline]
-
Kalbfleish JD, Prentice RL. The statistical analysis of failure time data. New York: John Wiley & Sons; 1980.
-
Gaynor JJ, Feuer EJ, Tan CC, Wu DH, Little CR, Straus DJ, et al. On the use of cause-specific failure and conditional failure probabilities: examples from clinical oncology data. J Am Stat Assoc 1993;88:400-9.
-
Wiseth R, Levang OW, Sande E, Tangen G, Skjaerpe T, Hatle L. Hemodynamic evaluation by Doppler echocardiography of small (21 mm) prostheses and bioprostheses in the aortic valve position. Am J Cardiol 1992;70:240-6.[Medline]
-
Bojar RM, Rastegar H, Payne DD, Mack CHA, Schawartz SL. Clinical and hemodynamic performance of the 19-mm Carpentier-Edwards porcine bioprosthesis. Ann Thorac Surg 1993;56:1141-7.[Abstract]
-
Kadir I, Izzat MB, Birdi I, Wilde P, Reeves B, Walsh C, et al. Hemodynamic performance of the 21-mm St Jude BioImplant prosthesis using dobutamine Doppler echocardiography. Am J Cardiol 1998;81:559-603.
-
Abdelnoor M, Hall KV, Nitter-Hauge S, Lindberg H, Øvrum E. Prognostic factors in aortic valve replacement associated with narrow aortic roots. Scand J Thorac Cardiovasc Surg 1986;20:227-32.[Medline]
-
Westaby S, Huysmans HA, Davis TE. Stentless aortic bioprostheses: compelling data from the Second International Symposium. Ann Thorac Surg 1998;65:235-40.[Abstract/Free Full Text]
-
Bojar RM. Adult cardiac surgery . Boston: Blackwell Scientific Publications; 1992. p. 167-79.
-
Isner JM, Chokshi SK, DeFranco A, Braimen J, Slovenkai GA. Contrasting histoarchitecture of calcified leaflets from stenotic bicuspid versus stenotic tricuspid aortic valves. J Am Coll Cardiol 1990;15:1104-8. [Abstract]
-
Ruygrok PN, Barratt-Boyes BG, Agnew TM, Coverdale HA, Kerr AR, Whitlock RM. Aortic valve replacement in the elderly. J Heart Valve Dis 1995;4:268-73.[Medline]
-
Flameng WJ, Herijgers P, Szécsi J, Sergeant PT, Daenen WJ, Scheys I. Deerminants of early and late results of combined valve operations and coronary artery bypass grafting. Ann Thorac surg 1996;61:621-8.[Abstract/Free Full Text]
-
Aranki SF, Rizzo RJ, Couper GS, Adams DH, Collins JJ, Gildea JS, et al. Aortic valve replacement in the elderly: effect of gender and coronary artery disease on operative mortality. Circulation 1993;88(Suppl):II17-23.
-
Borkon AM, Soule LM, Baughman KL, Baumgartner WA, Gardner TJ, Watkins L, et al. Aortic valve selection in the elderly patient. Ann Thorac Surg 1988;46:270-7.[Abstract]
-
Fann JI, Miller C, Moore KA, Mitchell RS, Oyer PE, Stinson EB, et al. Twenty-year clinical experience with porcine bioprostheses. Ann Thorac Surg 1996;62:1301-12.[Abstract/Free Full Text]
-
Heras M, Chesebro JH, Fuster V, Penny WJ, Grill DE, Bailey KR, et al. High risk of thromboemboli early after bioprosthetic cardiac valve replacement. J Am Coll Cardiol 1995;25:1111-9.[Abstract]
-
Israel DH, Sharma SK, Fuster V. Antithrombotic therapy in prosthetic heart valve replacement. Am Heart J 1994;127:400-11. [Medline]
-
Boughaleb D, Mansourati J, Genet L, Barra J, Mondine P, Blanc J. Permanent cardiac stimulation after aortic valve replacement: incidence, predictive factors and long-term prognosis. Arch Mal Coeur Vaiss 1994;87:925-30.[Medline]
-
STS National Cardiac Surgery Database 1995-1996. The Society of Thoracic Surgeons, 1997 (www.sts.org/outcomes/sts/ar97/ ar97mrbd.html).
-
Morris JJ, Schaff HV, Mullany CH Jr, Rastogi A, McGregor CHG, Daly RC, et al. Determinants of survival and recovery of left ventricular function after aortic valve replacement. Ann Thorac Surg 1993;56:22-30.[Abstract]
-
Bessone LN, Pupello DF, Hiro SP, Lopez-Cuenca E, Glattere MS, Ebra G. Surgical management of aortic valve disease in the elderly: a longitudinal analysis. Ann Thorac Surg 1988;46:264-9.[Abstract]
-
Lund O, Nielsen TT, Pilegaard HK, Magnussen K, Knudsen MA. The influence of coronary artery disease and bypass grafting on early and late survival after valve replacement for aortic stenosis. J Thorac Cardiovasc Surg 1990;100:327-37. [Abstract]
-
Akins CW, Caroll DL, Buckley MJ, Daggett WM, Hilgenberg AD, Austen WG. Late results with Carpentier-Edwards porcine bioprosthesis. Circulation 1990;82(Suppl):IV65-74.
-
Freeman WK, Schaff HV, Orszulak TA, Tajik AJ. Ultrasonic aortic valve descalcification: serial Doppler echocardiographic follow-up. J Am Coll Cardiol 1990;16:623-30.[Abstract]
Top
Abstract
Introduction
