(Circulation. 1999;100:II-275.)
© 1999 American Heart Association, Inc.
Aortic and Peripheral Vascular Surgery |
From the Departments of Cardiovascular Surgery (A.M., T.M., N.M., T.K.), Radiology (F.K.), and Anesthesiology (M.H.), Akane-Foundation Tsuchiya General Hospital, Hiroshima, Japan.
Correspondence to Akira Marui, MD, Department of Cardiovascular Surgery, Akane-Foundation Tsuchiya General Hospital, 3-30 Nakajima, Naka, Hiroshima 730-8655, Japan. E-mail malmaru{at}tb3.so-net.ne.jp
| Abstract |
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Methods and ResultsIn 101 patients with type B acute dissection
who had no complications, univariate and
multivariate factor analyses were performed to
determine the predictors for chronic-phase enlargement (
60 mm)
of the dissected aorta. The independent predominant predictors for
aortic enlargement in the chronic phase were a maximum aortic diameter
of
40 mm and a patent false lumen during the acute phase. The
values of actuarial freedom from aortic enlargement for the patients
with a maximum aortic diameter of 40 mm and a patent false lumen
at 1, 5, and 10 years were 43%, 33%, and 22%, respectively, whereas
in patients with a maximum aortic diameter of <40 mm and a closed
false lumen, the values were 97%, 94%, and 84%, respectively.
ConclusionsThese results suggest that patients with type B acute
aortic dissection who show a maximum aortic diameter of
40 mm
and a patent false lumen should undergo surgery earlier during the
chronic phase before enlargement of aorta, whereas patients with a
maximum aortic diameter of <40 mm and a closed false lumen should
continue to receive hypotensive therapy.
Key Words: aorta aneurysm follow-up studies risk factors surgery
| Introduction |
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However, some patients show good long-term results because the dissected aorta shows a natural course of recovery (ie, thromboembolization of the false lumen and a reduction in diameter). Patients who are expected to have a lower probability of chronic-phase aortic enlargement and a high likelihood of natural recovery should not undergo surgery during the acute phase because they are at a higher risk than are patients in the subacute or chronic phase in terms of fragility of the aortic wall.
We hypothesized that the following 2 therapeutic options for type B acute aortic dissection might provide better long-term results. The first option is surgery during the subacute or earlier chronic phase before aortic enlargement in patients who are expected to have a high likelihood of aortic enlargement. The second option is drug-based treatment for patients who are expected to show a natural course of recovery of the aortic dissection. In the present study, we examined which factors during the acute phase affect the chronic-phase enlargement of type B aortic dissection by studying chronic-phase enlargement of dissections in patients who had received successful drug-based hypotensive therapy during the acute phase.
| Methods |
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Diagnosis and Predictive Variables
In each patient, the diagnosis of type B dissection was
confirmed with the use of digital subtraction aortography and enhanced
CT scanning immediately after the emergent admission. By using the
results from these radiological examinations at emergent admission, we
obtained data regarding the extent of the dissection (above the
diaphragm or thoracoabdominal), the patency in the false lumen (patent
or closed), and the maximum diameter of the dissected aorta. We
measured the maximum aortic diameter anywhere in the descending
thoracic aorta. We defined a patent false lumen as a false lumen that
was enhanced at either an early or a delayed phase. A closed false
lumen is not enhanced at either the early or delayed phase. The
findings were reviewed by a radiologist (F.K.). These data on the acute
phase, along with basic characteristics (including concomitant
hypertension, diabetes mellitus, ischemic heart disease,
cerebrovascular disease, hemodialysis, and left ventricular
ejection fraction
70%), are shown in Table 1
as predictive variables for
aortic enlargement during the chronic phase.
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Medical Treatment
Patients were admitted to a critical care unit, where ECG and
blood pressure were closely monitored. During the acute phase of
dissection, nitrate, calcium channel antagonist, and
ß-adrenergic receptor blocker medications were administered
intravenously to regulate systolic blood pressure
and to reduce the velocity of left ventricular ejection
(dP/dt). To maintain systolic blood pressure at <140
mm Hg during the chronic phase, several antihypertensive drugs,
including nitrates, calcium channel antagonists, ACE
inhibitors, or ß-adrenergic receptor blockers, were
administered orally. After discharge, patients were followed up at
regular intervals, and blood pressure was measured every 1 month with
the use of a standard bulk sphygmomanometer. The mean systolic
blood pressure, which was obtained from serial blood pressure
measurements during the chronic phase, was entered into the predictive
variables for aortic enlargement (Table 1
).
Follow-Up Study and Definitions
CT scanning (from 1988 to 1993 with model TCT-300, Toshiba Co;
from 1994 to 1998 with ProSeed, Yokogawa Medical Systems) was performed
every 2 to 26 months (mean, 17.4 months), depending on the aortic
diameter and progression of aortic disease, to examine the serial
maximum diameter of the dissected aorta. Aortic enlargement is a
predictor of subsequent aortic rupture without surgical
intervention.9 10 11 The criteria defining aortic
enlargement during the chronic phase were (1) maximum diameter of the
dissected aorta
60 mm, (2) rapid enlargement of the dissected
aorta >10 mm/y, (3) rupture of the dissected aorta, and (4) rapid
enlargement of ulcer-like projection (ULP) by >5 mm/y. These
criteria conformed with the surgical indications for chronic type B
aortic dissection at our hospital. We obtained the expansion rate of
each dissected aorta or ULP by calculating the difference in diameter
between the initial measurement and the most recent follow-up and
dividing that value by the time interval between the 2
measurements.
Statistical Analysis
The Cox proportional hazards model was used to identify
predominant predictors for aortic enlargement throughout the entire
follow-up period with the use of univariate and stepwise
multivariate analyses (entry and removal
thresholds 0.05 and 0.1, respectively). For statistical
analysis, all of the continuous variables were categorized
as shown in Table 1
. Freedom from aortic enlargement was
computed according to the Kaplan-Meier technique, and event-free curves
were compared with the use of the log-rank test. Unless stated
otherwise, all results are expressed as mean±SD. A value of
P<0.05 was considered statistically significant. Data
analysis was performed with the use of StatView J-4.5 for
Macintosh.
| Results |
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Of the 101 patients, 43 met the criteria for enlargement of the
dissected aorta during the chronic phase. In these 43 patients, the
follow-up period from onset to enlargement was 2 to 120 months, with a
mean follow-up time of 59 months. Of the 43 patients, 29 (67%) met the
criterion of maximum aortic diameter of >60 mm, 7 (16%) met the
criterion of rapid aortic enlargement, 4 (9%) met the criterion of
rupture during the chronic phase, and 3 (7%) met the criterion of
rapid enlargement of ULP. Precise data on the 12 variables for 43
cases are provided in Table 2
. The values
for actuarial freedom from aortic enlargement of the dissected aorta in
all cases at 1, 5, and 10 years after the onset were 76%, 60%, and
47%, respectively.
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The 12 variables, which are listed in Table 1
, were
correlated with aortic enlargement throughout the entire follow-up
period with the use of univariate analysis (Table 3
); a past history of cerebrovascular
disease (P=0.37), hemodialysis (P=0.31), a
patency in the false lumen (P=0.001), and a maximum aortic
diameter of 40 mm (P<0.001) were found to be
significantly correlated with enlargement of the dissected aorta. To
determine the independent predictors for aortic enlargement throughout
the entire follow-up period, forward stepwise Cox regression
analysis was performed. Both a maximum aortic diameter of
40 mm (P<0.001) and blood status in the false lumen
(P=0.024) were shown to be significantly predictive of
enlargement with the use of multivariate Cox regression
analysis. The hazard ratio for the presence of aortic diameter
of
40 mm was 3.97 times higher than that for <40 mm, and
the hazard ratio for the presence of patent false lumen was 2.09 times
higher than that for closed false lumen.
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To obtain a more accurate estimate of chronic-phase aortic enlargement,
the 101 patients were divided into 4 subgroups according to 4
combinations of the 2 independent predictive variables selected
with the use of multivariate Cox regression
analysis: maximum aortic diameter of <40 mm and a closed
false lumen (group A), maximum aortic diameter of <40 mm and a
patent false lumen (group B), maximum aortic diameter of
40 mm
and a closed false lumen (group C), and maximum aortic diameter of
40 mm and a patent false lumen (group D). The values for freedom
from aortic enlargement for group A at 6 months and 1, 5, and 10 years
were 100%, 97%, 94%, and 84%, respectively; values were 93%, 87%,
66%, and 58% for group B; 90%, 79%, 52%, and 28% for group C; and
53%, 43%, 33%, and 22% for group D (Figure 1
).
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| Discussion |
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Recently, however, it was advocated that patients who had type B acute aortic dissection without complications, such as rupture or organ ischemia, be treated with hypotensive drugs during the acute phase, because the mortality rate with this treatment is reported to be equal to or slightly better than that for surgical treatment during the acute phase.4 5 12 13 14 15 16 17 Surgical treatment should be selected if the aortic diameter becomes enlarged during the chronic phase; careful observation of aortic enlargement in all patients treated during the chronic phase is very important but very difficult. Unfortunately, some patients who have successfully gone through the acute phase with medical hypotensive therapy suddenly die during the chronic phase of aortic rupture; ideally, enlargement of the aorta should be predicted and surgery should be performed early, before the aorta becomes enlarged.6 7 8
The recommendations at several institutions are that surgical treatment be offered for all patients during the acute phase because the prevention of aortic rupture and organ ischemia through acute-phase surgery contributes to a better mortality or morbidity rate and because a number of patients with medically treated dissection have subsequent aortic enlargement and must undergo surgical treatment during the chronic phase.4 8 10 12 13 18 In addition, the surgical results for these chronic-phase cases of enlarged aorta are definitely not better than the results for acute-phase surgery because more extended surgery and concomitant reconstruction of visceral arteries and the narrowed true lumen are necessary, and because respiratory complications due to severe adhesion of the lung occur during most of these operations in patients in the chronic phase.9 16 17
However, surgical intervention must not be performed too prematurely in patients who have a low probability of aortic enlargement, because early surgery could be a cause of in-hospital death. In this study, we found that a number of patients without surgical interventions have good long-term results because the dissected aorta shows a natural course of recovery (ie, a reduction in diameter). Patients who have a lower probability of chronic-phase aortic enlargement and a high likelihood of natural recovery should not undergo surgery during the acute phase, because in terms of fragility of the aortic wall, surgery in the acute phase carries a higher risk than subacute or chronic-phase surgery. A natural course of recovery remains the optimal treatment for aortic dissections and should be the goal whenever possible. Therefore, we considered the 2 therapeutic options for type B acute aortic dissection that might provide better long-term results: surgery during the subacute or earlier chronic phase before enlargement of the aorta in patients who are expected to have a high likelihood of aortic enlargement and drug-based treatment for patients who are expected to show a natural course of recovery from aortic dissection.
Our results indicate that chronic-phase aortic enlargement of type B
dissection can be predicted with 2 independent factors: maximum
diameter of the dissected aorta and the patency of the false lumen,
which may be obtained at the onset of dissection. What kind of
acute-phase factors do patients have who will show a high incidence of
aortic enlargement during the chronic phase? The value for freedom from
aortic enlargement in patients with a maximum aortic diameter of
40 mm and a patent false lumen (group D) at 6 months was 53%,
indicating that about half of the group D patients required surgical
intervention within 6 months from onset (Figure 2
). The event-free rates of group D at 5
and 10 years were low (33% and 22%, respectively). These results
suggest that group D patients undergo surgery during the subacute
or early chronic phase before enlargement of the aorta. We compared
group D patients with patients who had a maximum aortic diameter of
40 mm and a closed false lumen (group C). The event-free rates
of group D at 6 months and 1 year fell abruptly to 53% and 43%,
respectively, whereas those of group C remained relatively good (90%
and 79%, respectively). However, by 10 years, the event-free rate of
group C at 10 years (28%) was approaching that of group D (22%).
Moreover, the event-free curves of groups C and D were not
significantly different from each other (P=0.14). These
results indicate that the number of patients who showed aortic
enlargement during the chronic phase was equivalent in groups C and D
in the long term, although the rate of expansion of the aortic diameter
of group C was slower than that of group D; therefore, earlier surgery
should be considered for group C patients.
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We suggest that patients with a maximum aortic diameter of
40 mm
and a patent false lumen undergo surgery during the subacute or
early chronic phase, because the mortality rate for surgical treatment
for patients with acute type B aortic dissection without complications
has recently decreased to
10%3 5 ; the surgical results
for late chronic-phase cases of enlarged aorta are clearly no better
than the results for acute-phase surgery, and the strength of the
dissected aorta during the early chronic phase is satisfactory. We
would consider earlier surgery for patients with a maximum aortic
diameter of
40 mm but a closed false lumen.
Not all patients should undergo surgery earlier during the chronic
phase. In this study, we found that a number of patients without
surgical interventions showed good long-term results because the
dissected aorta showed a natural course of recovery. Event-free rates
of patients with a maximum aortic diameter of <40 mm and a closed
false lumen (group A) at 1, 5, and 10 years were satisfactory (97%,
94%, and 84%, respectively) (Figure 3
).
No patients died of aortic events, and 14 patients (35%) showed a
reduction in aortic diameter; patients with a maximum aortic diameter
of <40 mm and a closed false lumen are expected to have a high
likelihood of natural course of recovery. However, there is 1 important
result: although only 4 patients (10%) of group A showed an aortic
enlargement, 3 of 4 causes of enlargement were due to rapid
growth of the ULP. Thus, with the exception of patients with ULP,
patients with a maximum aortic diameter of <40 mm and a closed
false lumen are expected to have satisfactory long-term results.
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The 55% incidence of closed false lumen in the acute phase is much higher than that reported in previous series.8 19 Although the reasons for this are not clear, we propose the following explanation. We believe that at most of the other institutions, CT scanning is not always performed on patients with chest or back pain who do not have specific findings on ECG, chest radiography, or blood analysis. However, we routinely perform enhanced CT scanning on all patients with chest or back pain. We believe that closed false lumen and small aortic diameter were often accidentally detected on routine CT scanning in patients with chest or back pain who did not have specific findings on chest radiography, such as wide mediastinum or large aortic diameter. We believe that these patients may be often overlooked at other institutions; this is a possible reason for the high incidence of closed false lumen in patients in the acute phase at our institution.
Because the event-free curve for patients with a maximum aortic diameter of <40 mm and a patent false lumen (group B) was significantly lower than that of group A patients (P=0.021), group B patients were expected to have a higher incidence of aortic enlargement than group A patients during the chronic phase. However, we believe that group B patients can be treated medically, because 60% of group B patients did not show aortic enlargement, and none died of aortic events. With more careful observation of aortic diameter, patients with a maximum aortic diameter of <40 mm and a patent false lumen should be treated medically as long as the aortic diameter does not become enlarged.
In conclusion, if patients with type B acute aortic dissection show a
maximum aortic diameter of
40 mm and a patent false lumen at
onset, they are predicted to have a high incidence of aortic
enlargement during the chronic phase. We suggest that they undergo
surgery during the subacute or early chronic phase due to the
difficulties associated with surgery during the late chronic phase. We
recommend the consideration of early surgery for patients with a
maximum aortic diameter of
40 mm but a closed false lumen;
however, patients with a maximum aortic diameter of <40 mm and a
closed false lumen should continue to receive hypotensive therapy
because they are predicted to have a low probability of aortic
enlargement and to have a high likelihood of a satisfactory course of
recovery of the dissected aorta. Patients with a maximum aortic
diameter of <40 and a patent false lumen can also be treated medically
with more careful observation of the aortic dissection.
| Acknowledgments |
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| References |
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