Download Valvular Replacement for Patients with Aortic Stenosis and Severe

Original Article
Acta Cardiol Sin 2005;21:21-7
Valvular Heart Disease
Valvular Replacement for Patients with Aortic
Stenosis and Severe Left Ventricular Dysfunction
Chung-Pin Liu, Ron-Bin Hsu,1 Shi-Zhe Hua and Yi-Lwun Ho
Background and Purpose: The 2-year survival of patients with aortic stenosis (AS) and congestive heart failure is
less than 10% under medical treatment. On the other hand, the surgical risk of aortic valve replacement (AVR) also
increases for patients with AS and severe left ventricular (LV) dysfunction. The aim of this study was to evaluate the
risk and benefit of AVR for such patients.
Methods: From May 1999 to April 2003, 8 consecutive patients with AS and severe LV dysfunction (ejection
fraction [EF] £ 30%) underwent aortic valve replacement in National Taiwan University Hospital. The myocardial
protection was initially achieved with antegrade perfusion and maintained with continuous retrograde cold blood or
crystalloid cardioplegia. The indication for aortic valve replacement was severe AS, which was defined as an aortic
valve area of £ 1.0 cm2 or a maximum pressure gradient of ³ 50 mmHg assessed by Doppler echocardiography. The
mean age was 67 ± 9 years; and 7 of 8 patients suffered from severe exertional dyspnea (functional class III-IV of
New York Heart Association). Respiratory failure developed in 5 patients prior to surgery.
Results: The perioperative (30-day) mortality was 0%. During a mean follow-up period of 32 ± 18 months (range
16-61 months), the survival rate was 75%. The clinical symptoms of heart failure improved at least one functional
class in all patients. The mean change of LVEF was an increase of 26 ± 18 EF units (p = 0.005), and the mean
reductions of LV end-systolic dimension and LV end-diastolic dimension were 16 ± 8 (p = 0.001) and 11 ± 8 mm (p =
0.005), respectively.
Conclusions: The surgical risk was acceptable for AVR in patients with AS and severe LV dysfunction.
Improvements in symptoms, heart size and LV systolic function were observed in most patients.
Key Words:
Aortic stenosis · Valvular replacement · Left ventricular dysfunction · Left ventricular
remodeling
INTRODUCTION
ventricular (LV) pressure lead to decreases in stroke
volume and ejection fraction (EF) that contribute to LV
dysfunction. 1,2 Furthermore, irreversible systolic dysfunction may be caused by myocardial fibrosis due to
LV hypertrophy or superimposed myocardial infarction.3
Severe AS with congestive heart failure carries a poor
prognosis, with a 2-year survival less than 10% under
medical treatment.4 The surgical risk of aortic valve replacement (AVR) also increases for patients with AS
and severe LV dysfunction.5-7 Many patients are often
denied surgical treatment, especially the elderly. 8 AS
with severe LV dysfunction was also an indication for
heart transplantation in the past.9 However, with recent
improvements in myocardial protection and design of
In patients with aortic stenosis (AS), increases in left
Received: August 12, 2004
Accepted: November 17, 2004
Departments of Internal Medicine (Division of Cardiology) and
1
Surgery, National Taiwan University Hospital and National Taiwan
University College of Medicine, No. 7, Chung-Shan South Road,
Taipei 100, Taiwan.
Address correspondence and reprint requests to: Dr. Yi-Lwun Ho,
Division of Cardiology, Department of Internal Medicine, National
Taiwan University Hospital and National Taiwan University College
of Medicine, No. 7 Chung-Shan South Road, Taipei 100, Taiwan.
Tel: 886-2-2312-3456 ext. 2328; Fax: 886-2-2396-6013;
E-mail: [email protected]
21
Acta Cardiol Sin 2005;21:21-7
Chung-Pin Liu et al.
valve prosthesis, the outcome of AVR for such patients
is of great interest. There have been only a few papers
about this issue.10,11 Therefore, we conducted the present
study to (1) evaluate the surgical risk and survival of
such patients after AVR; (2) assess the effects of AVR
on the regression of heart size, improvement of heart
failure symptoms and LV function in such patients.
equation using time-velocity integral (TVI) of the aorta
and left ventricular outflow tract (LVOT) as follows:
AVA = (AreaLVOT ´ TVI LVOT)/TVIAorta.16
Surgical procedure
All of the operations were conducted by a single
surgeon (RB Hsu). Aortic valve replacement was performed in a standard manner with median sternotomy,
cardiopulmonary bypass and aortic cross-clamp. Interrupted mattress sutures of 2-0 Ticron were used with
Teflon felts. Myocardial protection was initially
achieved with antegrade perfusion of the coronary artery and maintained with continuous retrograde cold
blood or crystalloid cardioplegia of the coronary sinus.17 The temperature of the cardioplegia was maintained at 4 °C. After excision of the aortic valve,
careful debridement of the annular calcium was performed if necessary. Bioprosthesis was used in patients
with old age (> 65 years-old) or high risk of bleeding
tendency. 18 One patient received simultaneous mitral
valve replacement due to severe mitral stenosis in addition to aortic stenosis. The largest prosthesis that could
be fitted was implanted.19 Lifelong anticoagulant treatment was administered to the patients with a mechanical
prosthesis.
MATERIAL AND METHODS
Patients
We identified all the patients with AS and severe LV
dysfunction (LVEF £ 30%) who underwent AVR in National Taiwan University Hospital between 1999 and
2003. The indication for aortic valve replacement was
severe AS, which was defined as an aortic valve area
(AVA) of £ 1.0 cm2 or a maximum pressure gradient of ³
50 mmHg assessed by Doppler echocardiography.12 Preoperative LVEF was determined by echocardiography
and radionuclide angiography. All patients received coronary angiography prior to surgery. The medical records
were reviewed, including preoperative clinical data,
echocardiographic results, coronary artery anatomy and
operative data. The functional classes of the patients
were evaluated preoperatively and one month later after
surgery.
Statistical analysis
The clinical data collected from the patients were listed
individually, including preoperative and postoperative findings. All results were expressed as mean ± standard
deviation. Continuous variables between groups before and
after AVR were compared by paired-t test. p < 0.05 was
considered as significant.
Echocardiography
Standard echocardiographic assessment was performed
within 30 days before AVR and at a mean interval of 6
months after surgery without knowledge of this study. The
LVEF was determined by area length method.13 Measurements of posterior wall thickness, interventricular septal
thickness, left ventricular end-diastolic and end-systolic
dimensions were made according to the criteria of the
American Society of Echocardiography.14
The LV outflow tract area was calculated from the
diameter of the outflow tract (area = diameter2 ´ 0.785),
assuming a circular geometry. The velocity of the LV
outflow tract was obtained by pulsed-wave Doppler
echocardiography from the apical four-chamber view,
and the maximum pressure gradient across aortic valve
was calculated from the peak Doppler velocity by the
modified Bernoulli equation (pressure gradient = 4 ´ velocity 2 ). 15 The AVA was calculated by the continuity
Acta Cardiol Sin 2005;21:21-7
RESULTS
Clinical characteristics (Tables 1 and 2)
Eight consecutive patients fulfilled the entrance
citeria and were included in the analysis. There were 5
of 8 patients with LV hypertrophy on electrocardiography. Five patients (62.5%) were ventilator-dependent
due to respiratory failure, and six patients (75%) received intravenous infusion of inotropic agents prior to
AVR. Seven patients suffered from severe exertional
dyspnea (functional class III-IV of New York Heart As22
Aortic Stenosis and Left Ventricular Dysfunction
Table 1. Preoperative clinical data
Pt
No.
Age (yr) Significant
AVA MPG LVEF LVIVS LVPW
Ventilator NYHA
AR
/gender comorbidity Rhythm
use
class grading (cm2) (mmHg) (%)
(mm) (mm)
1
2
3
57/F
78/F
51/M
4
5
6
7
8
65/M
75/M
75/M
65/M
67/M
COPD, DM
Nil
MS
CAD, DM,
HTN
HTN
CAD, Pul TB
Nil
Nil
LVESD
(mm)
LVEDD
(mm)
AF
AF
AF
Yes
Yes
Yes
IV
IV
IV
2
3
2
0.9
0.7
0.6
53
85
132
18
11
20
14
12
12
14
12
14
49
57
56
55
61
62
AF
NSR
NSR
NSR
NSR
Yes
No
Yes
No
No
IV
III
IV
II
III
1
1
0
3
0
0.6
0.5
0.9
0.8
0.6
83
102
50
46
76
16
27
25
26
14
10
15
11
9
14
10
12
11
10
14
63
48
57
75
71
68
54
64
91
76
AR = aortic regurgitation, (0: nil, 1: mild, 2: moderate, 3: moderate-to-severe, 4: severe); AF = atrial fibrillation; CAD = coronary artery
disease; COPD = chronic obstructive pulmonary disease; DM = diabetes mellitus; F = female; HTN = hypertension, LVEDD = left
ventricular end-diastolic dimension; LVEF = left ventricular ejection fraction; LVESD = left ventricular end-systolic dimension; LVIVS
= left ventricular interventricular septal thickness; LVPW = left ventricular posterior wall thickness; M = male; MPG = maximum
pressure gradient; MS = mitral stenosis; NSR = normal sinus rhythm; NYHA = New York Heart Association; Pt = patient; Pul TB =
pulmonary tuberculosis.
Table 2. Surgical and postoperative data
Pt
No.
Aortic prosthesis type CPB time ACC time Cardioplegia Weaning NYHA PPG LVEF LVIVS LVPW LVESD LVEDD Follow-up
(trademark), size (mm)
(min)
(min)
type
days
class (mmHg) (%) (mm) (mm) (mm) (mm) (month)
1
2
3
4
5
6
7
8
bioprothesis (CPE), 23
bioprothesis (CPE), 21
bioprothesis (CPE), 21
bioprothesis (CPE), 21
bioprothesis (CPE), 23
mechanical (Sorin), 23
mechanical (St Jude), 25
mechanical (Sorin), 23
119
113
170
132
109
144
66
120
73
60
109
66
68
57
57
65
blood
blood
crystalloid
blood
blood
crystalloid
crystalloid
crystalloid
75
3
6
13
3
6
1
3
III
I
I
II
II
I
I
II
30
18
32
32
29
11
19
17
57
54
69
48
48
34
26
25
14
10
11
11
15
10
10
13
14
10
13
11
13
8
14
13
37
33
28
37
38
49
59
64
50
45
46
47
51
59
71
73
15
40
61
33
55
17
22
16
CPB = cardiopulmonary bypass; CPE = Carpentier-Edwards; ACC = aortic cross-clamp, LVEDD = left ventricular end-diastolic dimension;
LVEF = left ventricular ejection fraction; LVESD = left ventricular end-systolic dimension; LVIVS = left ventricular interventricular septal
thickness; LVPW = left ventricular posterior wall thickness; NYHA = New York Heart Association; PPG = prosthetic valve pressure gradient.
days). Mean intubation period after AVR was 5 ± 4 days
except for one patient (pt No. 1), for whom ventilator
weaning was hindered by chronic obstructive pulmonary
disease. It took 75 days for that patient to be weaned
from ventilator.
The mean follow-up period was 32 ± 18 months
(ranged from 15 to 61 months). Two patients died during
the follow-up period. One of the patients (pt No. 1) suffered from prolonged weaning (75 days) mentioned
previously and had received tracheostomy. However, infective endocarditis with septic lung occurred 15 months after
AVR and she expired due to profound shock. The other patient (pt No. 4) recovered well after surgery. Unfortunately,
tracheostenosis with upper airway obstruction occurred 3
sociation). LV dilatation was noted in all patients; the
mean LV end-diastolic dimension (LVEDD) was 66 ±
12 mm and the LV end-systolic dimension (LVESD)
was 60 ± 10 mm. The maximum pressure gradients
across aortic valve ranged from 46 to 132 mmHg, with a
mean of 78 ± 29 mmHg. The mean LVEF was 20 ± 6%
and the mean AVA was 0.7 ± 0.2 cm2. Four patients had
atrial fibrillation and two patients had coronary artery
disease. Because there were no critical coronary lesions,
we did not perform any simultaneous coronary artery
bypass grafting during operation of AVR.
Outcome
No patient died within the perioperative period (30
23
Acta Cardiol Sin 2005;21:21-7
Chung-Pin Liu et al.
DISCUSSION
months postoperatively. He received tracheostomy and
died of pneumonia 33 months after AVR.
Most patients showed a significant increase in
LVEF and a decrease of LVEDD. The mean change of
LVEF was an increase of 26 ± 18 EF units (p = 0.005)
(Figure. 1), and the mean reductions of LVESD and
LVEDD were 16 ± 8 (p = 0.001) and 11 ± 8 mm (p =
0.005). The symptoms improved at least one functional
class in all patients (Figure. 2). The maximal pressure
gradient of the prosthetic valve was 23.5 ± 8.2 mmHg,
with a significant decline from the baseline (p = 0.001).
However, there was no significant change of wall thickness.
Under medical treatment, the average survival of AS
with congestive heart failure is only 1.5 years.20 Unfortunately, the surgical risk of AVR increases significantly in
the presence of LV dysfunction. 21,22 The decision of
AVR for patients with severe AS and LV dysfunction has
been a medical dilemma. The high proportion of severe
heart failure symptoms and ventilator use in such patients often shifted the surgical decision from AVR to
heart transplantation in the past. In 1997, Connolly et al.
reported a series of AVR for patients with AS and an
LVEF £ 35%. The operative mortality was 9% and
5-year survival was 58%.23 Thereafter, clinical studies of
AVR for patients with severe AS and LV dysfunction
have increased.24,25
Very old age (> 80-year-old), renal impairment and
coronary artery disease have been related to worsen
prognosis of AVR for such patients.26 Our patients were
relatively younger (mean age 67 ± 9 years) and their renal functions were not severely impaired. The prevalence
of coronary artery disease was also low in our patients.
In addition, we used continuous retrograde cardioplegia
during operation. Improved surgical outcomes in aortic
valve surgery using this cardiac protection method were
reported increasingly.27,28 Compared with previous reports, these factors contributed to the lower peri-operative
mortality in the present study.
Long-term mortality occurred in 2 patients during
follow-up period, and both patients died of non-cardiac
causes. About 31% of late deaths have been reported to
result from non-cardiac causes.23 Our data was compatible with the previous study. Similar to the result of
Powell et al.,10 no relationship was found between LVEF
and patient survival. In our study, both the 2 mortality
cases had successful LV remodeling (LVEDD decreased
from 55 mm to 50 mm in pt No. 1 and 68 mm to 47 mm
in pt No. 4) and systolic function improvement (LVEF
increased from 18% to 57% in pt No. 1 and 16% to 48%
in the pt No. 4). On the other hand, underlying pulmonary conditions (such as chronic obstructive pulmonary
disease and tracheostenosis) of the patients should be
considered as distinctive risk factors for AVR in such patients.
In severe AS, the chronic pressure overload was compensated by hypertrophy of the LV. The cardiac output
Figure 1. Left ventricular ejection fraction (LVEF) before (preop) and
after (postop) aortic valve replacement. Solid horizontal line indicates
mean EF; hatched box indicates one standard deviation; vertical line
indicates highest and lowest values.
Figure 2. Changes of preoperative (preop) and postoperative (postop)
New York Heart Association (NYHA) functional class.
Acta Cardiol Sin 2005;21:21-7
24
Aortic Stenosis and Left Ventricular Dysfunction
and LVEF were maintained initially. However, when the
wall stress exceeds the compensating mechanism, the LV
function declines and the chamber size becomes enlarged.29,30 There was once a suspicion of the reversibility
of myocardial contractility in patients with AS and severe
systolic dysfunction. In our study, not only the symptoms
and LVEF improved, but also the LV size decreased in
most patients after AVR. There was one patient (pt No. 7)
who had improved clinical symptoms without improvement of LVEF. The possible explanation is the significant
decrease of LV size (LVESD from 91 to 71 mm and
LVESD from 75 to 59 mm), implying improved LV
stretch and LV end-diastolic pressure. The successful LV
remodeling encourages further surgical intervention for
such patient group.31,32
Our study had several limitations. First, the patient
number in this study was small. Second, the follow-up
period was not long enough. Third, a lack of control
group was also a drawback.
7.
8.
9.
10.
11.
12.
13.
CONCLUSIONS
14.
The surgical mortality was acceptable in patients with
AS and severe LV dysfunction. Heart failure symptoms,
heart size, and LV contractility improved postoperatively.
Given the substantial potential clinical benefit, patients
with AS and severe LV dysfunction might be considered
as candidates for AVR.
15.
16.
17.
REFERENCES
1. Ross J Jr. Afterload mismatch in aortic and mitral valve disease:
implications for surgical therapy. J Am Coll Cardiol 1985;5:
811-26.
2. Huber D, Grimm J, Koch R, et al. Determinants of ejection
performance in aortic stenosis. Circulation 1981;64:126-34.
3. Wisenbaugh T, Booth D, DeMaria A, et al. Relationship of
contractile state to ejection performance in patients with chronic
aortic valve disease. Circulation 1986;73:47-53.
4. Horstkotte D, Loogen F. The natural history of aortic valve
stenosis. Eur Heart J 1988;9(Suppl E):57-64.
5. Smith N, McAnulty JH, Rahimtoola SH. Severe aortic stenosis
with impaired left ventricular function and clinical heart failure:
results of valve replacement. Circulation 1978;58:255-64.
6. Hwang MH, Hammermeister KE, Oprian C, et al. Preoperative
identification of patients likely to have left ventricular dysfunction
18.
19.
20.
21.
22.
25
after aortic valve replacement: participants in the Veterans
Administration Cooperative Study on Valvular Heart Disease.
Circulation 1989;80(3, pt 1):I65-76.
Verheul HA, van den Brink RBA, Bouma BJ, et al. Analysis of
risk factors for excess mortality after aortic valve replacement. J
Am Coll Cardiol 1995;26:1280-6.
Bouma BJ, van den Brink RBA, Verheul HA, et al. To operate or
not on elderly patients with aortic stenosis: the decision and its
consequences. Heart 1999;82:143-8.
McCarthy PM. Aortic valve surgery in patients with left
ventricular dysfunction. Semin Thorac Cardiovasc Surg 2002;
14(2):137-43.
Powell DE, Tunick PA, Rosenzweig BP, et al. Aortic valve
replacement in patients with aortic stenosis and severe left
ventricular dysfunction. Arch Intern Med 2000;160:1337-41.
Bevilacqua S, Gianetti J, Ripoli A, et al. Aortic valve disease with
severe ventricular dysfunction: stentless valve for better recovery.
Ann Thorac Surg 2002;74:2016-21.
Bonow RO, Carabello B, De leon AC, et al. ACC/AHA guidelines
for the management of patients with valvular heart disease. J Am
Coll Cardiol 1998;32(5):1486-588.
Schiller NB, Shah PM, Crawford M, et al. Recommendations for
quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee
on Standards, Subcommittee on Quantitation of Two-dimensional
Echocardiograms. J Am Soc Echocardiogr 1989;2:358-67.
Sahn DJ, DeMaria K, Kisslo J, et al. Recommendation regarding
quantitation in M-mode echocardiography: results of a survey of
echocardiographic measurements. Circulation 1978;58:1072-7.
Nishimura RA, Miller FA Jr, Callahan MJ, et al. Doppler echocardiography: theory, instrumentation, technique, and application.
Mayo Clin Proc 1985;60:321-43.
Harrison MR, Gurley JC, Smith MD, et al. A practical application
of Doppler echocardiography for the assessment of severity of
aortic stenosis. Am Heart J 1988;115:622-8.
Buckberg GD, Beyersdorf F, Alen BS, et al. Integrated myocardial
management: background and initial application. J Card Surg
1995;10:68-89.
Lin FY, Yu HY, Ho YL, et al. Long-term evaluation of CarpentierEdwards porcine bioprosthesis for rheumatic heart disease. J
Thorac Cardiovasc Surg 2003,126:80-9.
Morris JJ, Schaff HV, Mullany CJ, et al. Determinants of survival
and recovery of left ventricular function after aortic valve
replacement. Ann Thorac Surg 1993;56:22-9.
Hakki A-H, Kimbiris D, Iskandrian AS, et al. Angina pectoris and
coronary artery disease in patients with severe aortic valvular
disease. Am Heart J 1980;100:441-9.
O’Toole JD, Geiser EA, Reddy PS, et al. Effect of preoperative
ejection fraction on survival and hemodynamic improvement
following aortic valve replacement. Circulation 1978;58:1175-84.
Galloway AC, Colvin SB, Grossi EA, et al. Ten-year experience
with aortic valve replacement in 482 patients 70 years of age or
older: operative risk and long-term results. Ann Thorac Surg
Acta Cardiol Sin 2005;21:21-7
Chung-Pin Liu et al.
1990;49:84-93.
23. Connolly HM, Oh JK, Orszulak TA, et al. Aortic valve
replacement for aortic stenosis with severe left ventricular
dysfunction: prognostic indicators. Circulation 1997;95:2395-400.
24. Otto CM. Timing of aortic valve surgery. Heart 2000;84:211-8.
25. Carabello BA. Aortic stenosis. N Engl J Med 2002;346(9):
677-82.
26. Gilbert T, Orr W, Banning AP. Surgery for aortic stenosis in
severely symptomatic patients older than 80 years: experience in
a single UK centre. Heart 1999;82(2):138-42.
27. Flameng WJ, Herijgers P, Dewilde S, et al. Continuous retrograde
blood cardioplegia is associated with lower hospital mortality
after heart valve surgery. J Thorac Cardiovasc Surg 2003;125(1):
121-5.
28. Nomoto T, Komeda M. Combined surgery for valvular and
ischemic heart disease. Nippon Geka Gakkai Zasshi. J Japan Surg
Society 2001;102(4):348-52.
Acta Cardiol Sin 2005;21:21-7
29. Douglas PS, Reichek N, Hackney K, et al. Contribution of
afterload, hypertrophy and geometry to left ventricular ejection
fraction in aortic valve stenosis, pure aortic regurgitation and
idiopathic dilated cardiomyopathy. Am J Cardiol 1987;59:
1398-404.
30. Dineen E, Brent BN. Aortic valve stenosis: comparison of
patients with to those without chronic congestive heart failure.
Am J Cardiol 1986;57:419-22.
31. Pela G, Canna GL, Metra M, et al. Long-term changes in left
ventricular mass, chamber size and function after valve
replacement in patients with severe aortic stenosis and depressed
ejection fraction. Cardiology 1997;88:315-22.
32. Gelsomino S, Morocutti G, Frassani R, et al. Early recovery of left
ventricular function after stentless versus stented aortic valve
replacement for pure aortic stenosis and severe cardiac dysfunction.
Semin Thorac Cardiovasc Surg 2001;13(4 Suppl 1):120-8.
26
Original Article
Acta Cardiol Sin 2005;21:21−7
主動脈瓣狹窄併發嚴重左心室功能不良患者之
主動脈瓣膜置換手術
劉中平 許榮彬 1 花世哲 何奕倫
台北市 國立台灣大學附設醫院 心臟內科 心臟外科1
背景 主動脈瓣狹窄患者併發心臟衰竭後的兩年存活率不及百分之十；此外，進行外科手
術的風險也會增加。本研究的目的是要評估主動脈瓣膜置換手術在這樣的病患的風險與效
益。
方法 從 1999 年 5 月至 2003 年 4 月，共有連續 8 名主動脈瓣狹窄併發嚴重左心室功能不
良 (心臟射出分率小於 30%) 的患者在台大醫院接受主動脈瓣膜置換手術。心肌保護的方
式是初始順流灌注，繼之以連續的逆流冷血液或電解質溶液灌注。手術的適應症為嚴重主
動脈瓣狹窄，定義是主動脈瓣面積 ≦ 1 cm2 或是以都卜勒氏超音波量測的最大壓力差 ≧
50 mmHg。平均病患年齡為 67 ± 9 歲，其中有七位病患有嚴重的運動性呼吸困難 (New York
Heart Association functional class III-IV)，有五位在手術前已經呼吸衰竭。
結果 手術後短期內 (30 天) 的死亡率為 0%。在追蹤期間內 (平均 32 ± 18 月) 的存活率
為 75%，所有病患心臟衰竭的症狀都獲得改善。平均心臟射出分率進步 26 ± 18 單位 (p 值 =
0.005)，左心室收縮和舒張末期直徑分別縮小 16 ± 8 (p 值 = 0.001) 和 11 ± 8 mm (p 值 =
0.005)。
結論 主動脈瓣狹窄併發嚴重左心室功能不良患者進行主動脈瓣膜置換手術之風險是可以
接受的。本研究大部分的病患獲得了症狀、心臟大小及左心室收縮功能之改善。
關鍵詞：主動脈瓣狹窄、瓣膜置換手術、左心室功能不良、左心室改造。
27