(Circulation. 1995;92:107-112.)
© 1995 American Heart Association, Inc.
Articles |
Determining Surgical Indications for Acute Type B Dissection Based on Enlargement of Aortic Diameter During the Chronic Phase
From the Division of Cardiovascular Surgery (M. Kato, H.-z.B., M. Kaneko, T.U., D.K., K.O.), Division of Diagnostic Imaging (K.S., S.K.), Osaka Prefectural Hospital, Osaka, Japan.
Correspondence to Masaaki Kato, MD, Division of Cardiovascular Surgery, Osaka Prefectural Hospital, 3-1-56 Mandai-higashi, Sumiyoshiku, Osaka 558, Japan.
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Abstract |
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Background In patients with Stanford type B dissection who have been treated successfully with medical hypotensive therapy during the acute phase, a large number have incurred the risk of surgery during their chronic phases because of enlargement of the dissected aorta. The purpose of this study was to determine the indications for surgical treatment of acute type B dissection by studying chronic-phase enlargements of aortic dissections in patients treated successfully with medical hypotensive therapy during the acute phase.
Methods and Results In 41 patients with type B dissection who had
been treated medically during the acute phase, univariate
and multivariate factor analyses were made to
determine the predominant predictors for chronic-phase enlargement
(
60 mm) of the dissected aorta. Computed tomography was performed
every 4 to 14 months to observe whether there was enlargement of the
maximum aortic diameter. The predominant predictors for aortic
enlargement in the chronic phase were the existence of a maximum aortic
diameter of 40 mm during the acute phase (P<.001) and a
patent primary entry site in the thoracic aorta (P=.001).
The values of actuarial freedom from aortic enlargement for the
patients with a large aortic diameter (40 mm) during the acute phase
and a patent primary entry site in the thorax at 1, 3, and 5 years were
70%, 29%, and 22%, respectively. No aortic enlargement was observed
in the other patients throughout the entire follow-up period.
Conclusions These data suggest that patients with acute type B
dissection who have a large aortic diameter (40 mm) and a patent
primary entry site in the thorax should be treated surgically during
the acute phase on the condition that the surgical risk in this phase
is limited.
Key Words: surgery • aorta • follow-up studies • risk factors
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Despite the improvement of surgical results for acute type B dissection, medical hypotensive therapy has been preferred for the patient with acute type B dissection in many institutions.1 2 3 4 5 6 7 8 However, 20% to 40% of patients who have passed their acute phases with medical hypotensive therapy probably need surgery during the chronic phase because of enlargement of the aortic dissection.1 2 3 9 10 These patients who have to undergo chronic-phase surgery incur double the risk of medical hypotensive therapy during the acute phase and subsequent chronic-phase surgery. Prophylactic surgical treatment during the acute phase might reduce the total risk for the patients who are predicted to have chronic-phase enlargement of the dissected aorta. The purpose of this study was to determine the indications for surgical treatment of acute type B dissection by studying chronic-phase enlargements of dissections in patients treated successfully with medical hypotensive therapy during the acute phase.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Patient Population
Between January 1983 and September 1994, 61 patients were admitted to Osaka Prefectural Hospital within 14 days of the onset of acute type B dissection. Of the 61 patients, 41 patients were entered into this study as cases treated successfully with hypotensive therapy during the acute phase. The reasons for the 20 exceptions included 6 emergent surgeries during the acute phase, 11 elective surgeries during the subacute phase (within 2 months of onset), 1 aortic rupture, 1 retrograde dissection and subsequent rupture during the acute phase, and 1 suicide before the initial follow-up examination. The age range of the subject patients was 33 to 83 years (mean age, 63.2 years), and there were 12 women (29%). No patient with Marfan's syndrome was included. Two patients who had received axillofemoral bypass surgery for ischemia of both legs were included because surgical interventions were not performed for the dissection itself.
Diagnosis and Predictive Variables
In each patient, the
diagnosis of type B dissection was
confirmed by aortography and enhanced computed tomography (CT) scan
immediately after the emergent admission. By using the results from
these radiological examinations at emergent admission, we obtained the
data about the extent of the dissection (above the diaphragm or
thoracoabdominal), the location of the primary entry site (patent in
thorax or absent in thorax), the blood status in the false lumen
(flowing, stagnant, or thrombosed), the maximum diameter of the
dissected aorta, and the area ratio of the true lumen to the entire
lumen at the level of maximum diameter. The primary entry site was
defined radiographically by the existence of unobstructed
blood outflow into the false lumen, and the ulcer-like
projection on the aortic wall was distinguished from the primary
entry site.11 Left ventricular ejection
fraction (LVEF) and presence of aortic valve
regurgitation (AR) were measured by precordial
echocardiography and Doppler
echocardiography after introducing medical
hypotensive therapy. These data on the acute phase, along with baseline
medical characteristics (including concomitant hypertension, diabetes
mellitus, and hemodialysis), are shown in Table 1
as
predictive variables for aortic enlargement.
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Treatment
During the acute phase of dissection, nitrate,
calcium-channel antagonist, and ß-adrenergic
receptor blockade were administered intravenously to reduce
systolic BP and diminish the velocity of LV ejection (dV/dt).
To maintain the hypotension and the reduced dV/dt during the chronic
phase, several antihypertensive drugs such as nitrate,
calcium-channel antagonists,
angiotensin-converting enzyme inhibitors,
or ß-adrenergic receptor blockade were administered orally. After
discharge, patients were followed up at regular intervals, and BP was
measured every 3 months using a standard bulk sphygmomanometer. The
mean systolic BP, obtained from serial BP measurements during
the chronic phase, and the administration of ß-blockade were
entered into the predictive variables for aortic enlargement (Table
1
).
Follow-up Study and Definitions
CT scan (1983 to 1986 using
model TCT-70A, 1987 to 1994 using
model TCT-900S, Toshiba Co) was performed every 4 to 14 months (mean, 9
months) to examine the serial maximum diameters of the dissected aorta.
The criteria defining aortic enlargement during the chronic phase were
as follows: (1) maximum diameter of the dissected aorta 60 mm, (2)
rapid enlargement of the dissected aorta >10 mm/year, or (3) rupture
of the dissected aorta. These criteria were decided in conformity with
the surgical indications for chronic type B aortic dissection in our
institute as well as others.12 The expansion rate of each
dissected aorta was obtained by calculating the difference in diameter
between the initial measurement and the most recent follow-up and
dividing by the time interval between the two measurements.
Statistical Analysis
The Cox proportional-hazards model was
used to identify
predominant predictors for aortic enlargement throughout the entire
follow-up period using univariate and stepwise
multivariate analyses (entry and removal
thresholds, 0.05 and 0.1, respectively). For statistical
analyses, all the continuous variables were categorized as
shown in Table 1. The 
2 test and
Fisher's exact
test were used for univariate analyses with 14
predictive variables for aortic enlargement within 3 years of the
onset. Freedom from aortic enlargement was computed by the method of
Kaplan-Meier, and event-free curves were compared by the Mantel-Cox
tests. Unless stated otherwise, all results were expressed as mean±SD.
A value of P<.05 was considered statistically significant.
Data analysis was performed using SPSS for
Windows, Advance Statistics (SPSS Inc).
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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All 41 type B dissection patients who had passed the acute phase with medical hypotensive therapy were followed as outpatients. Follow-up data (BP every 3 months and CT scan every 4 to 14 months) were 100% complete, and the mean follow-up time was 38.4 months (range, 4 to 140 months). Two patients died during the follow-up period: 1 due to rupture of dissected aorta and 1 due to gastric cancer. The rupture of the dissected aorta was confirmed by autopsy. Five patients died after the follow-up period; 4 due to surgical interventions during the chronic phase and 1 due to lung cancer after the surgical treatment.
Of the 41 patients, 15 met the criteria for enlargement of the
dissected aorta during their chronic phase. In these 15 patients,
follow-up time from onset to enlargement was 4 to 79 months, with a
mean follow-up time of 31 months (Table 2). Eleven
of the 15 patients (73%) met the criterion of maximum aortic diameter
of 60 mm; 3 (20%) met the criterion of rapid aortic enlargement; and
1 (7%) met the criterion of rupture during the chronic phase. Precise
data on the 14 variables for 15 cases of enlargement and the
remaining 26 cases are provided in Table 2. The values for
actuarial
freedom from enlargement of the dissected aorta in all cases at 1, 3,
and 5 years after the onset were 88%, 68%, and 60%, respectively
(Fig 1).
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The 14 variables, which were enumerated in Table 1, were
correlated
with aortic enlargement throughout the entire follow-up period by
univariate analysis (Table 3).
Maximum aortic diameter of 40 mm (P<.001), a patent
primary entry site in the thorax (P=.001), the blood status
in the false lumen (P=.018), and hemodialysis
(P=.042) were found to be significantly correlated with
enlargement of the dissected aorta (Table 3). To determine the
independent predictors for aortic enlargement throughout the entire
follow-up period, forward stepwise Cox regression analysis
was performed. The only significant predictive variable for aortic
enlargement was maximum aortic diameter of 40 mm (P=.041)
(Table 3). Relative risk for the presence of aortic diameter of
40 mm
was nine times higher than that for <40 mm. The 41 subjects were
divided into two subgroups according to the independent
predictive variable selected by multivariate Cox
regression analysis. The values for freedom from aortic
enlargement for the group of maximum aortic diameter of 40 mm at 1,
3, and 5 years were 76%, 44%, and 35%, respectively (Fig 2). No
aortic enlargement was observed in the group of
<40 mm. The event-free curve for the group with maximum aortic
diameter of 40 mm was significantly lower than that of the group with
diameters <40 mm (P<.01).
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To obtain a more accurate estimate of chronic-phase aortic
enlargement, the 41 subjects were divided into two subgroups, again
according to the combination of maximum aortic diameter of 40 mm and
a patent primary entry site in the thorax, which were selected as
predominant predictive factors from the univariate
analysis. The values for freedom from aortic enlargement for
the group with maximum aortic diameter of 40 mm as well as patent
primary entry site in the thorax at 1, 3, and 5 years were 70%, 29%,
and 22%, respectively (Fig 3). No aortic enlargement
was observed among the others. The event-free curve for the group
with a maximum aortic diameter of 40 mm as well as a patent primary
entry site in the thorax was significantly lower than that for the
other group (P<.01).
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For the 41 patients receiving medical hypotensive therapy during the
acute phase, the mean expansion rate for type B dissected aorta during
the chronic phase was 0.4 mm/year (ranging from -0.3 to 20 mm/y) (Fig
4). The mean expansion rate for the group with maximum
aortic diameter of 40 mm, as well as a patent primary entry site in
the thorax (17 cases, shown as solid boxes), was 0.8 mm/y, whereas the
mean expansion rate for the others (24 cases, shown as open circles)
was 0.2 mm/y.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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It is quite important to predict chronic-phase aortic enlargement of type B dissection in order to discuss the indications for treating acute type B dissection surgically. Our results indicate that chronic-phase aortic enlargement of type B dissection can be predicted satisfactorily by using two independent factors—maximum diameter of dissected aorta and the location of the primary entry site—that were obtained at the onset of dissection.
Most acute type B dissections are treated with medical hypotensive
therapy because its mortality rate is reported to be equal to or
slightly better than that for surgical treatment during the acute
phase.1 2 3 4 5 6 7 8
However, more than a few patients with medically
treated dissection have subsequent aortic enlargement and have to
receive the surgical treatment during the chronic
phase.1 2 3 9 10
Surgical results for these cases of
enlarged aorta are definitely not better than the results for
acute-phase
surgery12 13 14 15 because
more extended
surgeries and concomitant reconstructions of visceral arteries and the
narrowed true lumen are necessary in most of these surgeries during the
chronic phase. Our surgical mortality during the chronic phase was
relatively high, 4 of 14 (28.5%), because 3 of 4 mortality cases
needed a complete thoracoabdominal reconstruction. On the other hand,
surgical mortality during the acute and the subacute phases was
lower than we expected, 2 of 17 (11.8%). For these reasons, our
results on the predictability of aortic enlargement in type B
dissection might help patients avoid the twofold life-threatening
risk of medical hypotensive therapy during the acute phase and surgery
during the chronic phase. Furthermore, our results on the predictive
value of acute-phase variables for chronic-phase aortic
enlargement should stimulate a reconsideration of surgical indications
during the acute phase. We consider that patients with acute type B
dissection who have a large aortic diameter (40 mm) during the acute
phase and a patent primary entry site in the thoracic aorta should be
treated surgically during the acute phase if the surgical risk is
limited.
Surgical results for acute type B dissection are fairly good, except for cases with vital organ ischemia.8 12 14 15 Glower et al8 reported a lower mortality for surgical treatment of uncomplicated acute type B dissection than for medical treatment: 1 of 11 (9.1%) versus 3 of 19 (15.7%), respectively. Miller et al15 also reported good surgical results, 13±12%, for acute type B dissection and a 2.2-fold to 3.9-fold lower risk in the absence of renal/visceral ischemia and aortic rupture. The surgical method has been improving because of technologies such as surgical glue16 and extracorporeal circulation.17 In addition, the entry site of acute type B dissection can now be closed with a stent-graft that can be inserted through a catheter sheath with minimal invasiveness.18 Given these developments, surgical treatment for acute type B dissection no longer has to be avoided; in fact, hesitancy about acute-phase surgery might put the patient at higher risk of a chronic-phase surgery and continuous fear of aortic rupture.
Most of the literature on aortic enlargement or rupture concerns abdominal aortic aneurysm.19 20 21 22 The majority of predictive factors for enlargement or rupture of an abdominal aortic aneurysm are constituent factors of wall stress on the aneurysm wall, such as BP,19 diameter of the aneurysm,20 21 and administration of ß-blockade.22 By analogy, the enlargement of type B dissection is closely correlated with wall stress on the dissected aorta. It is well known that wall stress on the vascular wall is proportional to internal pressure and diameter and is inversely proportional to wall thickness. In patients with type B dissection, because BP is controlled with various antihypertensive drugs during the follow-up period, the diameter and wall thickness of the dissected aorta are the main factors correlated with aortic wall stress. A large aortic diameter and a patent primary entry site will provide the adventitia of the false lumen with high wall stress. We suspect that the reason these two factors were selected statistically as the predominant predictors is that they are closely correlated with wall stress on the dissected aorta.
Masuda et al23 in their precise follow-up report about
aortic dissections referred to the maximum diameter of the dissected
aorta during the acute phase as a risk factor for survival during the
chronic phase. Their report supports our finding that the maximum
diameter of the dissected aorta during the acute phase was the best
independent predictor for aortic enlargement throughout the entire
follow-up period. However, this finding based on Cox
multivariate regression analysis was not strong
enough to offer a distinct prediction about chronic-phase aortic
enlargement, especially about the likelihood of its presence during the
early stage. To obtain a more accurate prediction for chronic-phase
aortic enlargement, we combined two factors: the presence of a patent
primary entry site in thorax, which was the predominant predictor from
univariate analysis, and the presence of a maximum
aortic diameter of 40 mm. Together, these two factors provided a more
satisfactory prediction for chronic-phase aortic enlargement.
Many analyses in the literature for patients with medically
controlled type B dissection concentrate their discussions on survival
during the chronic phase and have little to say about
dissection-related events or aortic enlargement during the chronic
phase. Our study is innovative in its exclusive concentration on
chronic-phase enlargement of the dissected aorta. We do not think
the indications for surgical treatment of acute type B dissection that
we referred to in this study should be applied to all cases of acute
type B dissection. It would be necessary to decide the surgical
indications during the acute phase, taking into consideration advanced
age and presence of cardiac disease because these factors, unrelated to
dissection, were selected as independent predictors for
chronic-phase mortality.8 23 The expansion rates for
type B dissection shown in Fig 4 may also be of assistance in
making
decisions about acute-phase surgery under these difficult
conditions.
In summary, aortic enlargement in chronic type B dissection can be predicted by using two factors obtained at the onset of dissection: maximum diameter of the dissected aorta and location of the primary entry site. These factors can accurately select patients who have the twofold risk of medical therapy during the acute phase and surgery during the chronic phase. Further, they suggest that the indications for surgical treatment of acute type B dissection must be extended to patients who are predicted to have enlargement during the chronic phase and are presumed to have limited surgical risk during the acute phase. Furthermore, this study might provide a new direction for the continued discussion of management of patients with acute type B dissection.
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Acknowledgments |
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The authors are grateful to Dr Hiroshi Takano and Dr Tatsuya Shoji for statistical analysis, Tomoko Okuda for secretarial assistance, and Al Averbach for editorial assistance in the preparation of this manuscript.
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