Download Progression of Aortic Stenosis

The Natural
History and Rate of
Progression of Aortic Stenosis*
Steven J. Lester, MD; Brett
and John Jue, MD
Heilbron, MD; Ken Gin, MD; Arthur Dodek, MD;
One ofthe challenges in clinical cardiology is to determine the optimal time of valve replacement
surgery in patients with aortic stenosis. To meet this challenge, one requires an accurate
knowledge of the natural history and rate of progression of the disease. This review will
summarize the natural history of aortic stenosis in terms of symptoms, mortality, and stenosis
progression. (CHEST 1998; 113:1109-14)
Key words: aortic stenosis; natural history; rate of progression
and effective
therapy,
although important
Surgical
for
inherent
stenosis, has
therapy
risks.1-3 addition
and
aortic
its
own
In
to operative morbidity
mor¬
tality,
surgery in essence replaces one disease pro¬
cess with another. The burden of aortic stenosis is
removed, but the patient is left with "prosthetic heart
valve disease." This latter disease is associated with a
risk of thromboembolism, endocarditis, prosthetic
valve failure, and hemorrhage if anticoagulation is
required. On average, the risk of a serious prosthetic
valve-related complication is estimated to be 1 to 2%
per year.4 The challenge is to determine the inflec¬
tion point at which surgical therapy will portend a
better prognosis compared with medical therapy. To
meet this challenge, one requires an accurate knowl¬
edge of the natural history of aortic stenosis treated
medically vs the risks and long-term outcome of
operative treatment. This review will summarize the
natural history of aortic stenosis in terms of symp¬
toms, mortality, and stenosis progression.
The Natural History
of
Aortic Stenosis
Much of our understanding of the natural history
of aortic stenosis is derived from clinical studies
performed in the era prior to the development of
cardiac catheterization and hence lacks hemody¬
namic information.5"10 In studies done subsequent to
our ability to derive invasive hemodynamic data and
replace valves, the clinical course of aortic stenosis
was often interrupted by valve replacement.1116 As a
*From the University of British Columbia (Dr. Lester), St. Paul's
and Dodek), and Vancouver General
Hospital (Drs. Heilbron
(Drs. Gin and Jue), Vancouver, British Columbia,
Hospital
Canada.
Manuscript received June 19, 1997; revision accepted September
3, 1997.
result, our view of the natural history of aortic
stenosis is largely retrospective, introducing inherent
biases to patient selection into these studies. Over
time, the primary etiology of aortic stenosis has
changed from rheumatic to senile degeneration and
calcification and our patient population is older and
has more associated coronary artery disease.131718
Thus, the external validity (patient generalizability)
of earlier studies must be questioned.
The hemodynamic burden of aortic stenosis is
primarily a pressure load to the left ventricle. In
accordance to the law of Laplace (wall stress
[pressure X radius]/2X wallin thickness), as left ven¬
=
tricular pressure increases, order to maintain wall
stress, ventricular wall thickness must increase. If the
increase in wall thickness is unable to match the rise
left ventricular pressure, wall stress (afterload)
increases, which impairs ventricular performance.
This phenomenon is referred to as afterload mis¬
match. Systolic dysfunction in aortic stenosis is
largely a result of afterload mismatch.19-20 Transvalvular flow has two determinants: pressure gradient
and orifice area. Therefore, one must interpret with
caution literature that defines the severity of aortic
in
solely on the basis of a high pressure
gradient proportion of patients with poor left
ventricular systolic function, and thus low gradients
may be missed. The prognosis of these patients is
worse than those with preserved left ventricular
systolic function.21-23
some of its
stenosis
as a
limitations, what can one
Recognizing
discern from the literature?
Symptoms and Survival
Symptomatic Aortic Stenosis: The cardinal mani¬
festations of aortic stenosis include syncope, angina
pectoris, and dyspnea. Once these symptoms deCHEST/ 113/4 /APRIL, 1998
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.1109
velop, the prognosis is poor. The onset of angina,
syncope, and dyspnea has been shown to correlate
with an average time to death of 5, 3, and 2 years,
respectively.24 This clinical course has been derived
from postmortem studies on adults with
primarily aortic
stenosis57'910 (Fig 1). The average
acquired
age at death of these patients was 63 years.
Minimally Symptomatic or Asymptomatic Aortic
Stenosis: As technology advances so, too, do our
clinical tools of observation. The routine use of
cardiac catheterization and the availability of Dopp¬
ler echocardiography facilitates the diagnosis of aor¬
tic stenosis. Clinical findings suggestive of aortic
stenosis can be confirmed easily. As a result, many
patients with limited or no symptoms yet hemody¬
aortic stenosis are being identi¬
namically dilemma
significantis how
best to treat these
fied. The
patients.
concerning the treatment of asymp¬
tomatic patients with significant aortic stenosis has
The debate
been settled through the following lines of
largely
evidence: In
Contratto and Levine5 followed
1937,
patients with valvular aortic stenosis over a
25-year period. They reported that sudden death
occurred "rarely" in totally asymptomatic patients
and was often preceded by the development of
symptoms. In 1968, Ross and Braunwald,24 in their
up 180
classic review ofthe natural history of aortic stenosis,
reemphasized that sudden death occurred predom¬
inantly
in
symptomatic patients.
In
asymptomatic
patients with acquired aortic stenosis, the risk of
sudden death was reported to be between 3% and
5%. At this time, it was proposed that patients with
acquired valvular aortic stenosis have surgery de¬
ferred until the onset of symptoms.
Now, three decades later, despite technological
advancement allowing us to identify more occult
valvular heart disease, the evidence continues to
VALVULAR AORTIC STENOSIS M ADULTS
AVERAGE COURSE
(Pott Mortem Dolo)
60 63
ACE. YEARS
Figure 1. Average course of valvular aortic stenosis in adults.
Data assembled from postmortem studies. Reprinted with per¬
mission from Ross and Braunwald.24
support this proposed conservative treatment of
patients with asymptomatic acquired valvular aortic
stenosis.
Turina et al13 retrospectively reviewed 73 patients
with aortic stenosis in whom cardiac catheterization
had been performed between 1963 and 1983. The
severity of stenosis was primarily determined by the
Gorlin-derived aortic valve area (<0.9 cm2 severe;
0.95 to 1.4 cm2 moderate; >1.5 cm2 mild). In 15
patients, the aortic valve area was not calculated. In
these patients, mean pressure gradient was used to
define the hemodynamic severity ofthe disease (>50
mm Hg severe, <20 mm Hg mild). In a group of 17
asymptomatic or mildly symptomatic patients with
severe aortic stenosis or combined aortic stenosis
and aortic regurgitation, none of the patients died or
required75%valve surgery during the first 2 years. At 5
were event free (alive and not had
years,
and
surgery) 94% survived. In the group with mod¬
erate aortic disease, none of the asymptomatic or
mildly symptomatic patients died, but 27% under¬
went valve surgery within 5 years. The actuarial
survival in relation to New York Heart Association
classification was 99% and 76% at 2 and 5 years,
for patients with functional class I to II.
respectively,
In patients with functional class III to IV, the
actuarial survival was 31% and 22% at 2 and 5 years,
respectively. They concluded that asymptomatic or
minimally symptomatic patients with severe aortic
stenosis are at low risk of death and that surgical
treatment can be postponed until "marked symp¬
toms" appear.10
A cohort of 51
asymptomatic patients with severe
followed up by Kelly and coworkers25 for
of 17 months. A Dopplerderived peak systolic pressure gradient of ^50 mm
Hg was used to define severe aortic stenosis. The
aortic valve area was not calculated in this study.
Twenty-one (41%) ofthe patients became symptom¬
atic. Only two died of cardiac causes, but both had
become symptomatic for at least 3 months prior to
their deaths. The conclusion was, again, that patients
be followed up until symptoms develop.
The conclusion that asymptomatic patients with
acquired valvular aortic stenosis be followed up
closely until symptoms develop was echoed by Pellikka et al.26 They followed up 113 asymptomatic
patients with significant aortic stenosis as deter¬
mined by a Doppler-derived peak instantaneous
systolic pressure
gradient of ^64 mm Hg. The
mean
average
gradient was 47 mm Hg. The mean
duration of follow-up was 20 months. The death of
three patients was ascribed to aortic stenosis (two,
sudden death; one, congestive heart failure). In each
case, the development of symptoms preceded death
by at least 3 months. The actuarial probability of
aortic stenosis
were
a mean
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Reviews
survival
was
96%, 94%, and 90%
at
6, 12, and 24
months, respectively. The survival did
not
differ
from that predicted for age- and gender-matched
control subjects.
Another review of 66 patients with moderate
aortic stenosis again identified that symptoms predict
adverse outcomes.21 Mortality was significantly
greater (p<0.05) among symptomatic (New York
Heart Association functional class III to IV) vs
minimally symptomatic patients (23% vs 4%). Mod¬
erate aortic stenosis was defined as an aortic valve
area of 0.7 to 1.2 cm2 derived by the formula of
Hakki. The mean duration of follow-up was 35
months (maximum 7.2 years).
Despite the limitations of the studies, the consen¬
sus is that asymptomatic patients are at low risk for
complications or mortality. However, following the
onset of symptoms, the prognosis worsens dramati¬
cally. Surgical therapy should be considered as soon
as the patient develops symptoms ascribed to aortic
stenosis22 and if considered a viable option should be
performed without delay.
Stenosis Progression
A concern, identified in the studies cited
above,2526 is that a small proportion of asymptomatic
patients may progress very rapidly to develop symp¬
toms and then die suddenly. If, however, one could
reliable predictors to the rate of progression
identify
of aortic stenosis, then surgical consideration may be
given to these high-risk, yet asymptomatic patients.
In
a common
clinical scenario is that of a
addition,
with
documented
aortic stenosis, not of a
patient
that
would
severity
routinely result in a surgical
intervention, in whom cardiac surgery is planned for
other reasons. The question is whether the aortic
valve should be replaced at the time of this surgery?
Knowledge of reliable predictors to stenosis progres¬
sion would greatly aid in clinical decision making.
Table 1 summarizes a review of the literature on
the progression of aortic stenosis. Doppler echocar¬
diography records the maximal difference between
the instantaneous left ventricular and aortic pres¬
sures at any point during the systolic ejection period.
Catheter-derived peak-to-peak gradient is a nonsimultaneous measurement determined by the differ¬
ence between the peak left ventricular and aortic
systolic pressures. The Doppler-derived peak instan¬
taneous gradient is thus always higher than the
peak-to-peak gradient. The difference in these val¬
ues decreases as the absolute gradient increases.27
The mean gradient, which is the average gradient
throughout
systole, should theoretically be equiva¬
lent, and studies have shown this to be true.28
When cardiac catheterization is used as the tool of
observation to follow the rate of progression of aortic
stenosis, there will be inherent biases as to the
patients selected for follow-up. Only patients who
have progressed symptomatically would be subjected
to the risk of a second cardiac catheterization. Dopp¬
ler echocardiography is a noninvasive, reliable tool,
ideally suited to follow up asymptomatic patients
with aortic stenosis and thus allow a more accurate
reflection of the natural progression.
Otto et al29 prospectively followed up 42 adults
with valvular aortic stenosis for a mean duration of
20 months. The average Doppler-derived peak sys¬
tolic gradient was 54 mm Hg (range, 27 to 108 mm
Hg). The peak transaortic pressure gradient changed
by +12 mm Hg/yr (-10 to +34 mm Hg) and the
+8 mm Hg/yr ( 7 to
gradient changed
bycalculation
for
the
of aortic valve
Hg).
available in 25 of the 42
mean
+23 mm
Data
area were
a mean
patients, and
reduction in aortic valve area of
.0.1 cm2/yr (0.0 to .0.5 cm2). Those patients who
subsequently required valve replacement as a result
of progressive symptoms had a more rapid rate of
hemodynamically determined deterioration. Howrevealed
Table 1.Rate of Progression of Aortic Stenosis: A Review*
Source
Wagner and Selzer43
Year
No.
Method
Follow-up,
Initial AP,
mm Hg
yr
3.5 38
5.4f
| AP
per Year
1982
50 Catheter
Nittaetal44
1987
11 Catheter
3 23
7.7f
Turinaetal13
1987
29 Catheter
7 50
3.4*
Schuler et al45
1991
11
Catheter
3.4 56
8.4f
Davies et al46
1991
65 Catheter
7
10
6.5f
Ottoetal29 1989
42
1.7
5412§
Doppler
1990
112
2.1 35
4.8§
Roger etal30
Doppler
1992
45 Doppler
1.5 64
15*
Faggiano et al31
Peter etal32
1993
49
2.6 38
7.2*
Doppler
*
from
al.c
Peter et
Adapted
AP=pressure gradient; LV=left ventricle; AVA=aortic valve area.
JAVA
Faster Rate of Increase
per Year
Older age, calcific valve
Older age
None
None
Calcific valve
0.1
Progressive symptoms
Progressive symptoms
Lower LV systolic function
Older age, coronary artery disease
0.1
fPeak to peak AP.
*Mean AP.
^Peak instantaneous AP.
CHEST/113/4/APRIL, 1998
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1111
ever, they were unable to identify variables to predict
who these "fast progressors" would be.
Roger and colleagues30 reviewed 112 adult pa¬
tients with aortic stenosis who underwent at least
three echocardiographic evaluations during a mean
25-month period. At entry, the peak instantaneous
was 35± 18 mm Hg (6 to 100 mm Hg). After
gradient
a mean interval of 25 months, the peak instantaneous
gradient increased to 44 ±16 mm Hg, corresponding
to an average increase of 4.8 mm Hg/yr. It was also
that those who progressed symptomatirecognized
had
a
cally
significantly more rapid rate of hemody¬
namic progression. Again, no variables were identi¬
fied that could predict the "fast progressors."
A cohort of 45 adults with aortic stenosis was
followed up by Faggiano and coworkers31 for a mean
duration of 18 months. At entry, the peak instanta¬
neous gradient varied from 25 to 174 mm Hg and
valve area ranged between 0.35 and 1.6 cm2. The
transaortic pressure gradient changed on aver¬
peak15±10
mm Hg/yr (range, .8 to +38 mm Hg/yr).
age
The change in calculated aortic valve area was, on
average, -0.1±0.13 cm2/yr (range, -0.72 to +0.14
Once again it should be noted that the rate
cm2/yr).
of progression was variable among patients and that
in general, no parameters could be identified to help
differentiate "rapid" from "slow progressors." One
caveat to this was that those with a reduction in left
ventricular systolic function had a faster rate of
progression than did those with normal systolic
function. This finding has not been consistently
in other series.
duplicated
Peter et al32 prospectively followed up 49 adults
with aortic stenosis. At entry, the average peak
gradient was 38±15 mm Hg (range,
Hg). Patients were followed up for a
mean duration of 32 months. The peak transaortic
pressure gradient changed by +16 to +93 mm Hg,
to a mean increase of 10.6±11 mm
corresponding
49 patients, 21 were identified as
Of
the
Hg/yr.
"rapid progressors" as defined by a >10 mm Hg/yr
increase in the peak gradient. These patients were
older (64 vs 53 years, p<0.01) and coronary artery
disease was more prevalent (38% vs 7%, p=0.01).
The rate of
was not found to correlate
instantaneous
16 to 78
mm
progression
with either age or the extent of coronary artery
disease when evaluated in other studies.252629
When 123 adults were followed up prospectively
for a mean duration of 2.5±1.4 years, once again,
marked individual variability in the rate of hemody¬
namic progression was seen.33 The Doppler-derived
mean gradient increased by 7±7 mm Hg/yr (.5 to
31 mm Hg) and the valve area decreased by
0.12±0.19 cm2/yr (-0.35 to 1.16). Clinical factors to
the rate of hemodynamic progression were
predict
not found. However, the echocardiographic severity
of aortic stenosis
the rate of
along with
of
clinical
out¬
change
predictors
come.death or need for valve
over
at
time
baseline
were
surgery.
Overall, with respect to the rate of progression of
acquired
valvular aortic stenosis, on average, the
area decreases by approximately 0.1
and
the
cm2/yr
peak instantaneous
gradient increases
mm
10
in
individual
However,
by
Hg/yr.
any
patient,
at best we can say that that it is highly variable. There
can be identified two distinct types of patients: those
whose conditions progress slowly and others whose
conditions progress rapidly. Unfortunately, unless
privy to knowledge of prior hemodynamic data, there
are no reliable clinical predictors to help us identify
into which subgroup an individual patient will fall.
Although it is generally accepted that patients
presenting for coronary artery bypass grafting with
moderate or severe aortic stenosis (regardless of
symptom status) undergo concomitant aortic valve
replacement, the treatment of patients presenting
for myocardial revascularization with coexisting
asymptomatic mild aortic stenosis remains challeng¬
ing. Given the bimodal rate of progression, it is no
wonder that there is no consensus on how to deal
with such patients.
Proponents of prophylactic aortic valve replace¬
ment at the time of myocardial revascularization
argue that repeated surgery is technically more
challenging and carries a higher operative mortali¬
ty.34 Fiore and colleagues35 reviewed 28 patients
who had aortic valve replacement surgery subse¬
quent to coronary bypass surgery and found an
operative mortality rate of 18%, compared with 9.1%
in those undergoing combined valve and coronary
surgery. This is very similar to the 18.2% perioper¬
ative mortality in a review of 44 patients requiring
aortic valve replacement who had previously under¬
gone coronary bypass surgery.36
If one elects to be conservative and initially per¬
form coronary bypass surgery alone, retrospective
studies suggest that the average time to subsequent
aortic valve replacement is between 5 and 7.6
years.34'3637 Otto and her colleagues33 suggest that
when patients are prospectively followed up, those
patients with a baseline Doppler jet velocity of <3.0
aortic valve
(peak instantaneous gradient of <36 mm Hg)
to develop symptoms due to aortic
"unlikely
stenosis over the next 5 years." Assuming an annual
risk of serious prosthetic valve-related complication
to be 2%,4 then the 5-year risk would be approxi¬
mately 10%. Others have estimated the 5-year risk
for serious valve-related complications to be higher
at approximately 15 to 20%.3839
In the review of 28
mentioned
m/s
are
patients
above,35
the actuarial survival at 1 and 5 years was no different
in patients who had combined coronary and valve
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surgery vs those who had valve surgery subsequent to
coronary bypass. At 10 years, there was a trend
toward a greater survival advantage in those patients
in whom valve surgery had been delayed. These data
risk of combined
along withandthetheincreased operative
risk
of valve-related
surgery
subsequent
make
it
hard
to
complications
justify routine prophy¬
lactic aortic valve replacement surgery.
of hemodynamic severity and clinical symptoms. In
addition, it may prove to be a more sensitive marker
of disease progression and one could speculate that a
deterioration in the dynamic change in orifice area
be a marker of impending "classically" determined
hemodynamic deterioration.
Conclusion
Thoughts
for the
Future
Torricelli's law, the first hydraulic formula that the
Gorlin's used to develop their formula for the calcu¬
lation of valve area, states that flow is directly
to orifice area and flow velocity. Mea¬
proportional
surements of aortic valve area are made at a single
point in time, and thus are based on the assumption
that orifice area remains constant throughout ejec¬
tion. During each ejection, transvalvular flow and
pressure gradient increase from zero, reach a peak,
and then decrease back to zero. Effective orifice area
should thus be constantly changing throughout ven¬
tricular systole. Doppler echocardiography will allow
one to measure instantaneous aortic valve area at
different times during ejection.40
When 26 patients with valvular aortic stenosis
were evaluated, significant changes in effective aortic
orifice area were identified during ejection 41 The
and mean transvalvular gradients were 82 ±24
peak
mm Hg and 50 ±19 mm Hg, respectively, and the
valve area calculated was 0.7±0.3 cm2. When valve
area was calculated at the mid-acceleration point of
the flow velocity, it was 84 ±15% ofthe valve area at
velocity (p<0.0001) and 113±17% (p<0.01) of
peak
the valve area at peak velocity when calculated at
mid-deceleration. In normal subjects, the valve area
remained constant during ejection. This indicates
that the stenotic valve opens slowly and continues to
open during ejection where the normal valve opens
orifice size. As well, the
rapidly to itsof full effective
in
effective
orifice area did not
magnitude change
correlate with the usual indexes of hemodynamic
severity such as valve area at peak velocity and
pressure gradient.
When Doppler echocardiography was used to
assess the physiologic response to exercise in 28
asymptomatic patients with aortic stenosis, a sub¬
group of patients showed an increase in aortic flow
velocitytheir
during exercise that was less than expected
should
orifice area be fixed.42
The concept of a dynamic aortic valve orifice area
needs validation. If veritable, an assessment of valve
derived by Doppler-determined changes in
pliability
the instantaneous orifice area may provide important
clinical information with respect to the relationship
It has been well established that in patients with
acquired valvular aortic stenosis, the development of
symptoms portends a poor prognosis. Therefore, it is
will be another true natural
unlikely that asthere
history study once a patient develops symptoms,
surgical treatment will interrupt the natural course of
the disease.
The decision of when to operate
patients with
hemodynamically significant yet asymptomatic ac¬
on
quired valvular aortic stenosis is based on less than
valve is
perfect data. Untilwillthe ideal beprosthetic
some
debate
on
there
developed,
always
when to intervene surgically. The risks and benefits
of conservative vs surgical therapy must be weighed
in each individual patient. Unfortunately, our ability
to predict the rate of progression in an individual
patient is insufficient. The clinician, therefore, is
faced with making a decision under some uncer¬
tainty, which is often very difficult. What evidence
we do have tends to support a conservative approach
to the asymptomatic patient. The greatest risk to the
patient with asymptomatic or minimally symptomatic
acquired valvular aortic stenosis may well be aortic
valve surgery. Only with further experimentation will
we be able to develop new conceptual models to
enhance our clinical decision making.
References
C,
A, Solis E, et al. Calcific aortic stenosis:
risk.
Heart J 1988; 9(suppl E): 105-07
Eur
operative
Janatuinen MJ, Vanttinen EA, Rantakokko V, et al. Early and
1 Cabrol
2
Pavie
late results of aortic valve
replacement:
a
series of 510
patients. Scand J Thorac Cardiovasc Surg 1991; 25:119-25
3 Stahle E, Bergstrom R, Nystrom SO, et al. Early results of
aortic valve replacement with or without concomitant coro¬
nary- artery bypass grafting. Scand J Thorac Cardiovasc Surg
1991; 25:29-35
4 Carabello BA. Indications for valve surgery in asymptomatic
patients with aortic and mitral stenosis. Chest 1995; 108:
1678-82
5 Contratto AW, Levine SA. Aortic stenosis with special refer¬
ence to angina pectoris and syncope. Ann Intern Med 1937;
10:1636-53
6 Dry TJ, Willius FA. Calcareous disease of the aortic valve: a
study of 228 cases. Am Heart J 1939; 17:138-57
7 Takeda J, Warren R, Holzman D. Prognosis of aortic stenosis.
Arch Surg 1963; 87:931-36
8 Kiloh GA. Pure aortic stenosis. Br Heart J 1950; 12:33-44
CHEST/113/4/APRIL, 1998
Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21763/ on 05/02/2017
1113
9 Mitchell AM, Sackett CH, Hunzicker WJ, et al. The clinical
features of aortic stenosis. Am Heart J 1954; 48:684-720
10 Bergon J, Abelmann WH, Vazquez-Milan H, et al. Aortic
11
12
13
14
15
16
17
18
stenosis: clinical manifestations and course of the disease.
Arch Intern Med 1954; 94:911-24
Frank S, Johnson A, Ross J Jr. Natural history of valvular
aortic stenosis. Br Heart J 1973; 35:41-46
Rapaport E. Natural history of aortic and mitral valve disease.
Am J Cardiol 1975; 35:2211-17
Turina J, Hess O, Sepulcri F, et al. Spontaneous course of
aortic valve disease. Eur Heart J 1987; 8:471-83
Chizner MA, Pearle DL, DeLeon AC Jr. The natural history
of aortic stenosis in adults. Am Heart J 1980; 99:419-24
Nestico PF, DePace NL, Kimbiris D. et al. Progression of
isolated aortic stenosis: analysis of 29 patients having more
than one cardiac catheterization. Am J Cardiol 1983; 52:
1054-58
Jonasson R, Jonsson B, Nordlander R, et al. Rate of progres¬
sion of severity of valvular aortic stenosis. Acta Med Scand
1983; 213:51-54
Passik CS, Ackermann DM, Pluth JR, et al. Temporal
changes in the cases of aortic stenosis: a surgical pathologic
study of 646 cases. Mayo Clin Proc 1987; 62:119-23
Horskotte D, Loogen F. The natural history of aortic valve
stenosis. Eur Heart J 1988; 9(suppl):E57-E64
19 Gunther S, Grossman W. Determinants of ventricular func¬
tion in pressure-overload hypertrophy in man. Circulation
1979; 59:679-88
20 Ross J Jr. Afterload mismatch and preload reserve: a concep¬
tual framework for the analysis of ventricular function. Prog
Cardiovasc Dis 1976; 18:255-64
21 Kennedy K, Nishimura R, Holmes D, et al. Natural history of
moderate aortic stenosis. J Am Coll Cardiol 1991; 17:313-19
22 Braunwald E. On the natural history of severe aortic stenosis
[editorial]. J Am Coll Cardiol 1990; 15:1018-20
23 Lund O. Preoperative risk evaluation and stratification of
long-term survival after valve replacement for aortic stenosis:
reasons for earlier operative intervention. Circulation 1990;
82:124-39
24 Ross J, Braunwald E. Aortic stenosis. Circulation 1968;
25
38(suppl 5):V61-67
of
Kelly TA, Rothbart RM, Copper CM, et al. Comparison
older than
outcome
of asymtomatic to
symptomatic patients
20 years of age with valvular aortic stenosis. Am
1988; 61:123-30
26 Pellikka P, Nishimura R,
28
et
al. The natural history
asymptomatic, hemodynamically significant
1990; 15:1012-17
Weyman AE. Principles and practice of echocardiography.
Philadelphia: Lea & Febiger, 1994; 520
Currie PJ, Seward JB, Reeder GS, et al. Continuous wave
Doppler echocardiographic assessment of severity of calcific
aortic stenosis: a simultaneous Doppler-catheter correlative
study in 100 adult patients. Circulation 1985; 71:1162-69
of adults with
27
Bailey K,
J Cardiol
aortic stenosis. J Am Coll Cardiol
29 Otto C, Pearlman A, Gardner C. Hemodynamic progression
of aortic stenosis in adults assessed by Doppler echocardiog¬
raphy. J Am Coll Cardiol 1989; 13:545-50
30 Roger V, Tajik J, Bailey K, et al. Progression of aortic stenosis
in adults: new appraisal using Doppler echocardiography. Am
Heart J 1990; 2:331-38
31 Faggiano P, Ghizzoni G, Sorgato A, et al. Rate of progression
of valvular aortic stenosis in adults. Am J Cardiol 1992;
70:229-33
32 Peter M, Hoffmann A, Parker C, et al. Progression of aortic
stenosis: role of age and concomitant coronary arteiy disease.
Chest 1993; 103:1715-19
33 Otto CM, Burwash IG, Malcollm EL, et al. Prospective study
of
asymptomatic valvular
aortic stenosis. Circulation
1997;
95:2262-70
Wong PS, Davies SW, Youhana A, et al. Coronary artery
and minor aortic stenosis.to replace or not to
bypass surgery
replace? J Heart Valve Dis 1993; 2:649-52
35 Fiore AC, Swartz MT, Naunheim KS, et al. Management of
asymptomatic mild aortic stenosis during coronary artery
operations. Ann Thorac Surg 1996; 61:1693-98
36 Collins JJ Jr, Aranki SF. Management of mild aortic stenosis
during coronary artery bypass graft surgery. J Cardiac Surg
1994; 9(suppl 2):145-47
37 Hoff SJ, Merill WH, Stewart JR, et al. Safety of remote aortic
valve replacement after prior coronary artery bypass grafting.
Ann Thorac Surg 1996; 61:1689-92
38 Akins CW. Long-term results with the Medtronic-Hall valvu¬
lar prosthesis. Ann Thorac Surg 1996; 61:806-13
39 Jones EL, Weintraub WS, Craver JM, et al. Ten-year expe¬
rience with the porcine bioprosthetic valve: interrelationship
of valve survival and patient survival in 1,050 valve replace¬
ments. Ann Thorac Surg 1990; 49:370-84
40 Lloyd TR. Variation in Doppler-derived stenotic aortic valve
area during ejection. Am Heart J 1992; 124:529-32
41 Badano L, Cassottana P, Bertoli D, et al. Changes in effective
aortic valve area during ejection in adults with aortic stenosis.
Am J Cardiol 1996; 78:1023-28
34
42 Otto CM, Pearlman AS, Kraft CD, et al. Physiologic changes
with maximal exercise in asymptomatic valvular aortic stenosis
assessed by Doppler echocardiography. J Am Coll Cardiol
1992; 20:1160-67
43 Wagner S, Selzer P. Patterns of progression of aortic stenosis:
a longitudinal hemodynamic study. Circulation 1982; 65:
709-12
44 Nitta M, Nakamura T, Hultgren HN, et al. Progression of
aortic stenosis in adult men: detection by noninvasive meth¬
ods. Chest 1987; 92:40-43
45 Schuler G, Hambercht R, Farahmandi R, et al. Unter-
schiedleihe progressionsraten bei Herzklappenfehlern. Z
Kardiol 1991; 80:44-50
46 Davies SW, Gershnick AH, Balcon R. Progression of valvular
aortic stenosis:
1991; 12:10-14
a
long-term retrospective study. Eur Heart J
1114
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