Can progression of valvar aortic stenosis be predicted accurately?

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Can Progression of Valvar Aortic Stenosis Be Predicted Accurately? Cornelia Piper, MD, Rito Bergemann, MD, Hagen D. Schulte, MD, Reiner Koerfer, MD, and Dieter Horstkotte, MD Departments of Cardiology, and Thoracic and Cardiovascular Surgery, Heart Center North Rhine-Westphalia, Ruhr University of Bochum, Bad Oeynhausen, Institute for Medical Outcome Research, Lo¨rrach, and Department of Thoracic and Cardiovascular Surgery, Heinrich-Heine University, Du¨sseldorf, Germany

Background. It was the aim of the present study to elaborate criteria for the assessment of rapid hemodynamic progression of valvar aortic stenosis. These criteria are of special importance when cardiac surgery is indicated for other reasons but the established criteria for aortic valve replacement are not yet fulfilled. Such aspects of therapeutic planing were mostly disregarded in the past so that patients had to undergo cardiac reoperation within a few years. Methods. Hemodynamic, echocardiographic, and clinical data of 169 men and 88 women with aortic stenosis, aged 55.2 ⴞ 15.7 years at their first and 63.4 ⴞ 15.6 years at their second cardiac catheterization, were analyzed. Results. The progression rate of aortic valve obstruction was found to be dependent on the degree of valvar calcification ([VC] scoring 0 to III) and to be exponen-

tially correlated with the aortic valve opening area (AVA) at initial catheterization. Neither age nor sex of the patient nor etiology of the valvar obstruction significantly influence the progression of aortic stenosis. If AVA decreases below 0.75 cm2 with a present degree of VC ⴝ 0, or AVA of 0.8 with VC of I, AVA of 0.9 with VC of II, or AVA of 1.0 with VC of III, it is probable that aortic stenosis will have to be operated upon in the following years. Conclusions. The present data indicate that for clinical purposes and planning of valvar surgery the progression of asymptomatic aortic stenosis can be sufficiently predicted by the present aortic valve opening area and the degree of valvar calcification. (Ann Thorac Surg 2003;76:676 – 80) © 2003 by The Society of Thoracic Surgeons

A

tive complication rates of simultaneous aortic valve replacement plus coronary artery bypass grafting or mitral valve surgery are usually lower than the overall perioperative risk of a second intervention at a later time. It is the aim of this study to analyze factors that may be appropriate to predict the progression of AS. As a database we used patients with mild to moderate AS at the time of their first cardiac catheterization who had at least a second invasive hemodynamic evaluation including assessment of transaortic pressure gradient, transaortic flow, and calculation of the aortic valve opening area.

ortic valve stenosis (AS) is a constantly progressing disease [1–3] as the turbulent blood flow causes chronic damage of the valvar endocardium [4]. Inflammatory, immunologic, or metabolic processes as well as an enhanced expression of proteins that accelerate valve calcification (eg, osteopontin) have been linked with an exceptionally rapid progression of aortic valve obstruction [5– 8]. Assessment of the natural history of yet mild to moderate AS is of special importance if cardiac surgery or catheter interventions are indicated at a time when the established criteria for aortic valve surgery are not given [9]. Therapeutic decision making (eg, surgical revascularization versus catheter intervention) is also influenced by the expected interval at which AS will become symptomatic and aortic valve surgery indicated. Such aspects of a prospective disease management are often ignored with the consequence that an increasing number of patients have to be reoperated on, often within a few years (Fig 1) [7, 10, 11]. Morbidity and mortality after aortic valve replacement have markedly decreased in recent years [3]. Periopera-

Accepted for publication March 20, 2003. Address reprint requests to Dr Piper, Department of Cardiology, Heart Center North Rhine-Westphalia, Ruhr University of Bochum, Georgstr. 11, D-32545 Bad Oeynhausen, Germany; e-mail: [email protected].

© 2003 by The Society of Thoracic Surgeons Published by Elsevier Inc

Patients and Methods Progression of AS was analyzed in 257 consecutive patients who had at least two cardiac catheterizations. Aortic valve stenosis was mild to moderate at the first catheterization indicated to assess a suspected coronary artery disease (n ⫽ 233; 90.7%) or to evaluate nonaortic valve lesions (n ⫽ 24; 9.3%). Mean age of the 169 men (65.8%) and 88 women was 55.2 ⫾ 15.7 years (range, 12 to 82) at that time and 63.4 ⫾ 15.6 years (range, 14 to 91) at the time of the second catheterization. Forty-eight patients underwent more than two cardiac catheterizations. From the patient’s history and echocardiographic findings, AS was most likely degenerative in 158 cases (61.4%) whereas the revised Jones criteria suggested a 0003-4975/03/$30.00 PII S0003-4975(03)00566-6

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Fig 1. Recurrent surgery for progressive aortic stenosis in 57 patients (22.2%) at the University of Du¨sseldorf during a 10-year period (1981 to 1992). (cath ⫽ catheterization.)

rheumatic etiology in 41 patients (16.0%). In 37 of these patients (90.2%) a concomitant mild mitral valve lesion was present. A bicuspid valve was imaged echocardiographically in 31 (12.1%) and the etiology remained unclear in 37 patients (10.5%). Hemodynamic severity of AS was assessed by the aortic valve opening area (AVA). The AVA was calculated according to the Gorlin formula [12] utilizing the mean transaortic pressure gradient (dp) and the transaortic volume flow (AFlow). The dp was measured continuously from the simultaneous recordings of the left ventricular and the aortic pressure curves by computerized planimetric integration. Cardiac output, stroke volume, and AFlow (mL/s) were calculated by the Fick technique [13] with oxygen consumption measured paramagnetically [14]. In patients with atrial fibrillation, AFlow and dp were taken as an average of measurements from 10 successive cycles. The degree of valvar calcification was classified from cineangiographic films using the following grading: grade 0 ⫽ no evidence of calcification, grade I ⫽ spot-like (⬍ 3 mm) calcification; grade II ⫽ multiple calcium plaques larger than 3 mm; grade III ⫽ extensive calcifications of the valvar annulus or the semilunar cusps or both [15].

Statistical Analyses Data are given as mean ⫾ SD and with ranges if appropriate. The statistical analyses were initiated by a factor analysis using SAS software 6.12 (SAS Insight). The progression of AS was calculated for each individual patient as a difference of AVA at the initial (t0) and the subsequent examination (t1) [⌬AVA ⫽ AVA(t1) ⫺ AVA(t0)]. Age, AVA, and degree of valvar calcification at the time of the first catheterization, progression of calcification between the first and second catheterization, etiology of the valve lesion, sex of the patient, and time interval between the two (in 48 patients more than two) consecutive invasive investigations were used as variables for the multiple linear regression analysis [16, 17].

In a second analysis the degree of calcification was used as an explanatory nominal scaled variable. The confidence intervals for the progression were calculated using the Monte Carlo simulation. A random sample of the patient data set was used for this simulation. The model function applied a variation of the coefficients within the range mean ⫾ 1.96 ⫻ SEM. The results of 100 simulation runs with 100 patients for each run were then used for regression analyses and calculation of the 95% confidence intervals (CI) [16].

Results During follow-up 57 patients of the study cohort (22.2%) had to be operated on for progressive AS. The mean interval between the initial catheterization and valve surgery was 67.2 ⫾ 31.6 months (median, 57.4; range, 8 to 141; Fig 1). In all 57 patients dp at the initial catheterizaTable 1. Analysis of Different Patient-Related and LesionRelated Factors on Possibility of Assessing Progression of Aortic Stenosis Factors Etiology of aortic stenosis Patient age at first examination Sex Time interval between the consecutive examinations Degree of aortic valve opening area at first examination Degree of aortic valve calcification NS ⫽ nonsignificant.

Regression Coefficient

Level of Significance

—

NS

—

NS

— ␤ ⫽ 0.0558 ⫾ (0.0073)

NS p ⫽ 0.0001

␤ ⫽ 0.4496 ⫾ (0.1398)

p ⫽ 0.0013

␤ ⫽ 0.7969 ⫾ (0.1980)

p ⬍ 0.0001

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Table 2. Influence of Degree of Aortic Valve Calcification Determined by Fluoroscopy on Progression of Aortic Stenosis Degree of Aortic Valve Calcification

Regression Coefficient

Level of Significance

0 degree/III degree I degree/III degree II degree/III degree

␤ ⫽ ⫺0.7969 ⫾ (0.1980)–1.0704 ⫾ (0.1375) ␤ ⫽ ⫺0.4536 ⫾ (0.0793)–1.0704 ⫾ (0.1375) ␤ ⫽ ⫺0.1807 ⫾ (0.0798)–1.0704 ⫾ (0.1375)

p ⫽ 0.0001 p ⫽ 0.0001 p ⫽ 0.0235

tion was more than 25 mm Hg (range, 27 to 42 mm Hg) and AVA less than 1.0 cm2 (range, 0.96 to 0.75 cm2). Aortic valve obstruction developed exponentially over time (Table 1). Multiple regression analysis identified neither sex, age at the time of the initial invasive examination, nor etiology of AS as independent predictors of the progression of valvar obstruction, while both AVA (p ⫽ 0.0013) and degree of valvar calcification (p ⬍ 0.0001) were strong predictors for a rapid progression. Patients with extensive (grade III) calcifications of the annulus or cusps demonstrated a much faster decrease of their AVA than patients without calcification (p ⫽ 0.0001), spot-like calcifications (grade I; p ⫽ 0.0001), or plaque calcifications (grade II; p ⫽ 0.0.4; Table 2). Progression of AS was most precisely predicted by the AVA at the time of the initial catheterization (Table 3). The mean intervals until manifestation of severe AS (AVA ⱕ 0.65 cm2) were 20 years (CI: 7 to ⬎20) for noncalcified valves with AVA more than 1.0 cm2 at the initial catheterization and 7 years (CI: ⬍1 to 17) years if initial AVA was 0.75 cm2 or more. Patients with severe (grade III) valve calcification had a much more rapid progression and presented with the same end point after 7 years (CI: ⬍1 to 13.5) instead of 20 years and within 1 year (CI: ⬍1 to ⬍ 1) instead of 7 years respectively (Table 3). The multiple linear regression analysis allowed predicting the progress of chronic AS with sufficient accuracy for clinical purposes, if AVA and the degree of valvar calcification were known. The progression can also be described by a mathematic formula (Appendix).

tion. If the actual aortic valve area and the degree of calcification are known, the hemodynamic progression of the lesion is predictable. However confidence intervals are wide, indicating large interindividual differences. Earlier serial echocardiographic investigations have demonstrated an annual increase of the mean transaortic pressure gradient by 6.3 to 8.3 mm Hg and an annual decrease of the aortic valve opening area by 0.14 cm2 [1] but were not able to show an exponential increase of the pressure gradients over time as the transaortic flow was disregarded in this study [18]. Serial hemodynamic measurements presented in this study clearly demonstrate the exponential progression of AS (see Appendix), which is in accordance with the typical natural course of the diseaese characterized by a long “asymptomatic” period and a rapid clinical deterioration after a crucial degree of obstruction is exceeded [2, 10, 11]. Furthermore it has been recognized earlier that valve obstruction accelerates parallel to the degree of valvar calcification [3, 8, 19, 20]. Histomorphologic studies of stenosed aortic valves have demonstrated that the degree of valvar calcification is positively correlated to age, blood pressure, and serum cholesterol [21–23]. A close correlation between valve calcification and progression of valvar obstruction was nicely shown in our patients: The median interval until a significant AS had developed was three times shorter (7 years) in patients with severe calcification compared with patients who had no calcification (more than 20 years) if the AVA was 1.0 cm2 at the initial catheterization and 7 times shorter (1 versus 7 years) in patients with initial AVA of 0.75 cm2 (Table 3).

Comment Our analysis of the progression of valvar AS based on serial hemodynamic measurements demonstrate that valve obstruction increases exponentially—not linearly— and accelerates parallel to the degree of valvar calcifica-

Prognosis The perioperative mortality for single aortic valve replacement has recently been reported to be in the range of 0.5% to 1.7% for patients aged less than 70 years and

Table 3. Time to Aortic Valve Stenosis Progressiona Initial AVA AVAt0:0.75 AVAt0:0.8 AVAt0:0.9 AVAt0:1.0

VC 0 t t t t

⫽ ⫽ ⫽ ⫽

7a (⬍1a–17a) 13a (2a–⬎20a) 17.5a (4.5a–⬎20a) ⬎20a (7a–⬎20a)

VC Ist Degree t t t t

⫽ ⫽ ⫽ ⫽

⬍1a (⬍1a– 8a) 6.5a (⬍1a–15a) 11a (4.5a–⬎18a) 15a (5.5a–⬎20a)

VC IInd Degree t t t t

⫽ ⫽ ⫽ ⫽

⬍1a (⬍1a–5a) 1.5a (⬍1a–9a) 6.5a (⬍1a–13a) 10a (3a–17.5a)

VC IIIrd Degree t t t t

⫽ ⫽ ⫽ ⫽

⬍1a (⬍1a–⬍1a) ⬍1a (⬍1a– 6a) 3a (⬍1a–9.5a) 7a (⬍1a–13.5a)

a Time interval (mean [t] with 95% confidence interval) in years (a) until a mild to moderate aortic valve stenosis (AS) progresses to a significant stenosis (aortic valve opening area [AVA] ⱕ 0.65 cm2). These time intervals depend on the initial (t0) AVA and the degree of valvar calcification (VC) at t0 (n ⫽ 257).

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Table 4. Comparison of Perioperative Mortality Ratesa Operation Isolated CABG Single AVR Age ⬍ 70 years Age ⬎ 70 years Simultaneous AVR ⫹ CABG Age ⬍ 70 years Age ⬎ 70 years AVR after CABG

Perioperative (30-Day) Mortality 2.85% [24]b 3.3% [24] 0.5–1.7% [25–28] 2.5–10.3% [25,27,28] 6.0% [24] 1.7–5.7% [26 –29] 0.9% [27] 14.3–19.4% [26] 14 –30.4% [29 –31]

a

Comparison of perioperative mortality after isolated coronary artery bypass grafting (CABG), single aortic valve replacement (AVR), simultab neous operation (CABG ⫹ AVR), and AVR after CABG. Numbers in brackets are reference numbers.

2.5% to 10.3% for patients aged more than 70 years. For isolated coronary artery bypass grafting (CABG) perioperative mortality is about 2.85% and for simultaneous operation (aortic valve replacement plus CABG) 0.9% to 19.4%. Perioperative mortality for aortic valve replacement after previous CABG surgery is significantly higher (14% to 30.4%) than that of the combined intervention (Table 4). This experience favors a simultaneous operation and aortic valve replacement even in patients with moderate AS instead of two consecutive interventions. An AVA of 0.65 cm2 or less indicates severe valve obstruction [10]. If left ventricular systolic function is not compromised, AVA of 0.65 cm2 or less corresponds to a peak aortic jet velocity (PVa) ⬎ 4 m/s. Even for asymptomatic patients with such a degree of AS, a poor prognosis has been demonstrated [32, 33]. In many clinical situations it may be important to estimate the interval until a patient with an AVA between 1.0 and 0.75 cm2 will develop a severe valve obstruction. Our data show that this interval is 20 years (CI: 7 to ⬎20) if the actual AVA is 1.0 cm2 and the valve is not calcified but only 7 years (CI: ⬍1 to 17) if the initial AVA is 0.75 cm2. Accordingly aortic stenosis is supposed to become an indication for surgery within 5 to 7 years if AVA is 0.75 cm2 or less and the valve is not calcified (VC of 0), if AVA is 0.8 cm2 or less with VC of I, if AVA is 0.9 cm2 or less with VC of II, or if AVA is 1.0 cm2 or less with VC of III.

Conclusion Our data show that in our patients with moderate to severe aortic stenosis the progression of valvar aortic stenosis can be sufficiently predicted by the present aortic valve opening area and the degree of valvar calcification. This finding enables making a more rational decision in favor of a simultaneous intervention with aortic valve replacement plus CABG or plus mitral valve surgery, if cardiac surgery is primarily performed for coronary artery disease or for other cardiac reasons. We advise a simultaneous aortic valve replacement if AVA decreases below 0.75 cm2 and the valve is not calcified (VC of 0), or below 0.8 cm2 with VC of I, below 0.9 cm2 with VC of II, or below 1.0 cm2 with VC of III.

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References 1. Brener SJ, Duffy CJ, Thomas JD, Stuart 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. 2. Horstkotte D, Loogen F. The natural history of aortic valve stenosis. Eur Heart J 1988;9(Suppl E):57–64. 3. Iung B, Drissi MF, Michel PL, et al. Prognosis of valve replacement for aortic stenosis with or without coexisting coronary heart disease: a comparative study. J Heart Valve Dis 1993;2:430 –9. 4. Yoganathan AP. Fluid mechanics of aortic stenosis. Eur Heart J 1988;9(Suppl E):13–17. 5. Juvonen J, Laurila A, Juvonen T, et al. Detection of chlamydia pneumoniae in human non-rheumatic stenotic aortic valves. J Am Coll Cardiol 1997;29:1054 –9. 6. O’Brien KD, Kusistor J, Reichenbach DD, et al. Osteopontin is expressed in human aortic valvular lesions. Circulation 1995;92:2163–8. 7. Olsson M, Dalsgaard CJ, Haegerstand A, Roesenquist M, Ryden L, Nilsson J. Accumulation of T-lymphocytes and expression of interleukin-2-receptors in non-rheumatic stenotic aortic valves. J Am Coll Cardiol 1994;23:1162–70. 8. Wagner S, Selzer A. Patterns of progression of aortic stenosis: a longitudinal hemodynamic study. Circulation 1982;65: 709 –12. 9. Antunes MJ. The dilemma of moderate aortic valve disease in patients subjected to coronary artery bypass grafting. J Heart Valve Dis 2002;11:710 –2. 10. Hoff S, Walter M, James S, Bender H Jr. Safety of remote aortic valve replacement after prior coronary artery bypass grafting. Ann Thorac Surg 1996;61:1689 –92. 11. Horstkotte D, Piper C, Wiemer M, Schulthei␤ HP. Diagnostic approach and optimal treatment of aortic valve stenosis. Herz 1998;23:434 –40. 12. Gorlin R, Gorlin G. Hydraulic formula for calculation of area of stenotic mitral valve, other cardiac valves and control circulatory shunts. Am Heart J 1951;41:1. ¨ ber die Messung des Blutquantums in den Herz13. Fick A. U ventrikeln. Sitz Ber Phys-Med Ges 1870;16:1. 14. Pauling R, Wood RE, Sturdivant J. An instrument for determinating the partial pressure of oxygen in gas. Science 1946;103:318. 15. Pomerance A. Pathogenesis of aortic stenosis and its relation to age. Br Heart J 1972;34:569 –74. 16. Rawlings JO. Applied regression analysis. A research tool. Pacific Grove, CA: Wadsworth and Brooks/Cole Advanced Books and Software, 1988. 17. Weisberg S. Applied linear regression. New York: Wiley & Sons, 1985. 18. Ford L, Feldman T, Chiu Y, Carroll J. Hemodynamic resistance as a measure of functional impairment in aortic valvular stenosis. Circ Res 1990;66:1–7. 19. Eitz T, Kleikamp G, Minami K, Gleichmann U, Ko¨ rfer R. Aortic valve surgery following previous coronary artery bypass grafting. Impact of calcification and leaflet movement. Int J Cardiol 1998;64:125–30. 20. Turina J, Hess O, Sepulcri F, Krayenbu¨ hl HP. Spontaneous course of aortic valve disease. Eur Heart J 1987;8:471–83. 21. Campbell M. Calcific aortic stenosis and congenital bicuspid aortic valves. Br Heart J 1968;30:606 –16. 22. Rajamannan NM, Subramaniam M, Springe M, et al. Atorvastatin inhibits hypercholesterolemia-induced cellular proliferation and bone matrix production in the rabbit aortic valve. Circulation 2002;105:2660 –5. 23. Lindross M, Kupari M, Valvanne J, et al. Factors associated with calcific aortic valve degeneration in the elderly. Eur Heart J 1994;15:865–70. 24. Kalmar P, Irrgang E. Cardiac surgery in Germany during 2000. Thorac Cardiovasc Surg 2001;49:33– 8. 25. Chocron S, Etievent JP, Viel JF, et al. Aortic valve replace-

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680

26. 27. 28. 29.

30. 31. 32.

PIPER ET AL PROGRESSION OF AORTIC STENOSIS

ment in the elderly: a comparative assay of potential risk factor modification. J Heart Valve Dis 1995;4:268 –75. Hoppe U, Sechtem U, Erdmann E. Operationsindikation bei asymptomatischer hochgradiger Aortenstenose. Dtsch Med Wschr 1994;119:1630 –6. Kleikamp G, Minami K, Breymann T, et al. Aortic valve replacement in octogenarians. J Heart Valve Dis 1992;1:196 – 200. Schwarz F, Metentzidou K, Giokoglu K, Reifart N, Preusler W, Sto¨ rger H. Ergebnisse nach prothetischem Klappenersatz. Dtsch Med Wschr 1991;116:327–30. Fighali S, Avendan˜ o 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. Collins JJ, Aranki SF. Management of mild aortic stenosis during coronary artery bypass graft surgery. J Card Surg 1994;9(Suppl 1):45–7. Odell J, Mullany C, Schaff H, Orszulak T, Daly R, Morris J. Aortic valve replacement after previous coronary artery bypass grafting. Ann Thorac Surg 1996;62:1424 –30. Hering D, Piper C, Horstkotte D. Clinical course of 100 consecutive “asymptomatic” patients with moderate or severe aortic stenosis [Abstract]. Eur Heart J 2001;22(Suppl): 492.

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33. Otto CM, Burwash IG, Legget ME, et al. Prospective study of asymptomatic valvular aortic stenosis: clinical, echocardiographic, and exercise predictors of outcome. Circulation 1997;95:2262–70.

Appendix Exponential Equation to Calculate Progression of Aortic Stenosis AVA共 t 兲 ⫽ e共 ␤ 共0兲⫹ ␤ 共0共i兲兲兲 · e共 ␤ 共1兲 · AVA 共t0兲兲 · e共 ␤ 共2兲 · t兲 · 关cm2 兴 , where AVA(t) is the decrease of the aortic valve opening area at the time t; i is the fluoroscopically determined degree of aortic valve calcification; (␤(0(i))) is the coefficient for the degree of valve calcification; (AVA(t0)) is the coefficient for the initial aortic valve opening area at the time 0; and (t) is the coefficient for the time t given in years. Furthermore, estimated values and standard deviations for the coefficients are as follows: ␤(0): the estimated value 1.0704, SEM: 0.1375, p ⫽ 0.0001. ␤(1): the estimated value 0.4496, SEM: 0.1398, p ⫽ 0.0013. ␤(2): the estimated value 0.0558, SEM: 0.0073, p ⫽ 0.0001. SEM ⫽ standard error of the mean.

INVITED COMMENTARY This work addresses a clinical situation, which, in view of the increasing age and comorbid disorders of the surgical candidate, is not infrequently met in our present practice. It is true that, in most instances, and certainly in patients with concomitant coronary artery disease, heart catheterization will remain mandatory before the first operation. However, noninvasive techniques like echocardiography and probably very soon MRI will get preeminence in preoperative diagnosis, especially if the necessity of selective coronary angiography decreases with time. As detailed by the authors in their answer to the reviewer’s comments, adequately performed echocardiographic assessment of aortic stenosis may result in identical or at least comparable findings, provided that the degree of valvular calcification is evaluated as well. Another important point is the ability to detect early exhaustion of myocardial adaptation. Early stages of left ventricle maladaptation to chronic pressure overload are characterized by a reduced contractility reserve that manifests only during a stress test. In order to assess myocardial adaptation in clinically asymptomatic patients with suspected moderate aortic stenosis, exercise examination such as radionuclid ventriculography or stress echocardiography is necessary. It is quite interesting that the authors have been able to determine that the etiology of aortic stenosis and the age

© 2003 by The Society of Thoracic Surgeons Published by Elsevier Inc

of the patient at first catheterization yield no significant influence on the progression of aortic stenosis. The conclusion of this remarkable work certainly will enable the surgeon to make a more clear-cut choice when facing such a patient. Personally, I would certainly agree to apply these rules even it might result in a few “unnecessary” concomitant aortic valve replacements. As stressed by the authors, the increased risk of a concomitant aortic valve replacement simply cannot be compared with that of a reoperation for aortic valve replacement later. I congratulate the authors for their contribution to clarify a most controversial medical indication. In the few borderline cases where the decision still will remain difficult, I shall certainly think of measuring the potentially reduced contractility reserve via an exercise test using MRI or echocardiography. Robert A. Dion, MD Department of Cardiothoracic Surgery Leids Universitair Medisch Centrum Thoraxchirurgie K6S Albinusdreef 2-Leiden PB 9600 NL-2300 RC Leiden the Netherlands e-mail: [email protected]

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