Different remodeling of descending thoracic aorta after acute
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Jae-Kwan Song MDa, ,
, Duk-Hyun Kang MDa, Tae-Hwan Lim MDb, Meong-Gun Song MDc, Jae-Joong Kim MDa, Seong-Wook Park MDa, Seung-Jung Park MDa
a | Division of Cardiology, Asan medical Center, University of Ulsan, College of Medicine, Seoul, North Korea |
b | Division of Diagnostic Radiology, Asan Medical Center, University of Ulsan, College of Medicine, Seoul, North Korea |
c | Division of Cardiac Surgery, Asan Medical Center, University of Ulsan, College of Medicine, Seoul, North Korea |
Received 22 June 1998; revised 23 October 1998; Accepted 23 October 1998. Available online 15 March 1999.
Abstract
The natural healing process of medically treated aortic dissection (AD) and aortic intramural hemorrhage (AIH) developed in the descending
thoracic
aorta
was compared to test the hypothesis that absence of intimal tear and flow communication in AIH may have
different
impact on the
remodeling
of the affected
aorta
after
the
acute
event. In 25 patients with AD and 20 with AIH involving distal
descending
thoracic
aorta
stabilized with medical treatment, follow-up (mean 9 months) transesophageal echocardiography was performed to measure the maximal dimensions of
aorta
, true lumen, false lumen in AD, and abnormal wall thickening in AIH. The sex ratio, prevalence of hypertension, baseline maximal dimension, and longitudinal extent of the affected
aorta
did not show any significant difference in both groups. Patients with AIH were older than those with AD (63 ±10 vs 50 ± 9, p <0.01). Disappearance of abnormal wall thickening with complete restoration of the
aorta
occurred in 70% (14 of 20) patients with AIH, which was significantly more frequent than in AD (8%, p <0.01). In AD, progressive dilatation of the
aorta
with continuous flow communication in the false lumen resulted in larger dimension of the
aorta
than in AIH (44 ±13 vs 35 ± 7 mm, p <0.01). Absence of persistent flow communication resulted in a favorable
remodeling
process in AIH affecting distal
descending
aorta
. This finding, along with
different
mean age in AIH and AD, may suggest that AIH is not just a precursor of overt AD but a distinct disease entity with
different
pathophysiology.
Article Outline
Along with recent advances in various noninvasive imaging modalities for the aorta
,1 physicians can successfully identify aortic intramural hemorrhage (AIH), a variant form of aortic dissection (AD), which is characterized by absence of characteristic intimal tear and typical double-channel
aorta
. [2] , [3] , [4] , [5] , [6] and [7] AIH has been considered as a precursor or very early stage of AD, having a high rate of progression to overt dissection with direct flow communication between true and false lumens [3] and [5] based on limited clinical studies using transesophageal echocardiography (TEE), contrast-enhanced x-ray computed tomography, and magnetic resonance imaging. The same treatment strategy has been applied for AIH according to the site of the affected
aorta
as classic AD. [3] , [5] and [8]
In previous clinical studies on patients with classic AD, persistent flow communication in the false lumen has been reported as one of the important variables determining long-term morbidity and mortality [9] , [10] and [11] ; in an early clinical study using invasive angiography, radiologically demonstrable flow into the false lumen associated with continued chronic patency of the false lumen was a poorer prognostic factor than no flow or only sluggish flow in the false lumen.12 Late aorta
-related complications including expansion or rupture of the
descending
aorta
and distal false lumen-related vascular complications were encountered more frequently in patients with a persistent distal false lumen than those with closed false lumen
after
repair of
acute
type A AD.13 Some investigators suggested early surgical treatment in the
acute
phase for selected patients with type B distal AD to minimize late complications associated with persistent flow in the false lumen. [14] , [15] and [16] All these findings support the idea that persistence of flow communication or intimal tear may have tremendous detrimental impact on aortic
remodeling
after
the
acute
event and long-term prognosis.
AIH was first described as “dissection without intimal tear” at necropsy.17 Although absence of intimal tear may have different
impact on the natural healing process of the
aorta
after
an
acute
event, there have been no systematic investigations including long-term TEE follow-up to compare the
remodeling
pattern in AD versus AIH. We hypothesized that patients with AIH may have a favorable
remodeling
process
after
acute
injury, since there is no direct flow communication. To overcome the heterogeneity of the patient population, which was a significant confounding variable of previous studies, [3] , [4] , [5] , [6] and [7] we selected patients with distal AIH and AD in whom the same medical treatment was administered. This study compares the natural healing process of medically treated AD and AIH developing in the
descending
thoracic
aorta
using follow-up imaging study.
Methods
Patients
Between January 1994 and September 1997, routine clinical and diagnostic evaluation consisting of random combinations of contrast-enhanced x-ray computed tomography, magnetic resonance imaging, and TEE diagnosed 37 patients as having distal AD and 26 as having distal AIH in the acute
phase. Typical double-channel
aorta
with dissecting membrane or intimal tear was an imaging criterion for AD. [3] and [5] Exclusion of dissecting flap or intimal disruption was a prerequisite for diagnosis of AIH by any imaging modality. Regional thickening of the aortic wall >7 mm in a circular or crescent shape and/or evidence of intramural accumulation of blood in TEE3 and a crescentic or circular high attenuation area along the aortic wall without enhancement
after
contrast injection in contrast-enhanced x-ray computed tomography and magnetic resonance imaging5 were considered diagnostic of AIH. During TEE the position of the probe was recorded in a super-VHS videotape simultaneously as depth from the incisor of the patient. An aortic segment showing maximal dimension of the false lumen or abnormal wall thickening was selected for future follow-up TEE and measurement.
The following inclusion criteria were used for selection of the subjects for this study: (1) patients in whom initial TEE was performed within 2 days after
the onset of chest pain; (2) uneventful recovery without operation or mortality; (3) excellent compliance with antihypertensive medications and well-controlled blood pressure during follow-up (systolic pressure ≤120 mm Hg); and (4) follow-up TEE performed at least 6 months
after
the initial event. Among 37 patients with AD, operation was performed in 2 within 2 weeks; 2 died of aortic rupture during the first 2 weeks; TEE was not performed during
acute
stage in 3, and inadequate control of hypertension and loss of follow-up were main causes of exclusion in 5. Among 26 patients with AIH, TEE was not performed in 1 within 2 days; operation was performed in 2 within 2 weeks; 1 patient died of aortic rupture during the first 2 weeks; and 2 patients were excluded due to inadequate control of hypertension. With these criteria, 25 patients with AD and 20 with AIH were selected for analysis of this study.
Measurement
TEE was performed by 2 experienced echocardiographers (JKS and DHK) as described previously.18 On initial TEE, the image frame showing aortic segment with maximal diameter of the false lumen in AD and abnormal wall thickening in AIH was selected. Measurements were obtained in a diastolic frame, with maximal dimension of the false lumen in AD or maximal thickness of abnormal walls in AIH. The maximal dimensions of the affected aorta
, true lumen, false lumen, and abnormal thickening were measured (Figure 1) using on-line measurement software of the echocardiography machine (Hewlett-Packard SONOS 2500, Andover, Massachusetts). On follow-up TEE study of each patient, the same aortic segment that showed maximal diameter of false lumen or aortic thickening in the initial study was selected based on the depth from the incisor. Measurements were repeated using the same methods as in the initial study. Three separate measurements were done in each study and their average was used as a representative value. “Complete resolution”
after
medical treatment was defined as disappeared false lumen in AD or abnormal wall thickening with <3 mm in AIH.
Figure 1.
Diagram showing the measurement method. The maximal dimension (a) of the false lumen in aortic dissection or abnormal wall thickening in intramural hemorrhage was measured. With use of the arbitrary extension of this line, maximal dimension of true lumen (b) could be measured. The sum of 2 measurements (a+b) represented the maximal dimension of the affected aorta
.
Statistical analysis
Data are expressed as the mean ± SD. Maximal dimensions of the aorta
, true lumen, false lumen, and abnormal wall thickening were compared using unpaired (between groups) and paired Student’s t test (within group). Frequency ratio was compared using the chi-square test. A p value <0.05 was considered statistically significant.
Results
Table Isummarizes baseline characteristics of the subjects. In AD, progressive enlargement of the false lumen without any significant change in the true lumen was a common finding (Figure 2). However, in AIH, progressive decrease of abnormal wall thickening of the affected aorta
with nearly complete normalization of true luminal flow occurred frequently (Figure 3).
Figure 3.
Representative transesophageal echocardiograms (A, B) and computed tomograms (C, D) of a section of the descending
aorta
in intramural hemorrhage. Crescentic thickening of the aortic wall without any evidence of flow communication or intimal tear (A, C) normalized completely at the follow-up study (B, D).
The maximal aortic dimension did not change significantly during follow-up in AIH, whereas it increased significantly from 38 ± 8 to 44 ± 13 mm during follow-up in AD (p <0.01). There was no correlation between follow-up duration and change in aortic dimension. In AIH, the diameter of the true lumen increased progressively as abnormal thickening of the aortic wall decreased (Figure 4). In 1 patient with AIH, follow-up TEE revealed overt progression to AD, with a big intimal tear and flow communication in the false lumen (Figure 5). In AIH complete resolution was observed in 70% (14 of 20), but only 8% (2 of 25) of those with AD had complete resolution (p <0.01). During the follow-up period, there was no delayed operation, mortality, or hospital admission in both groups.
Figure 4.
Follow-up changes in maximal dimensions of the affected aorta
, true lumen, false lumen in aortic dissection, and abnormal wall thickening in intramural hemorrhage. A, maximal dimension of the affected
aorta
; B, maximal dimension of the false lumen in aortic dissection and abnormal wall thickening in intramural hemorrhage. C, maximal dimension of the true lumen.
Figure 5.
Transesophageal echocardiograms of a section of the descending
aorta
in a patient with intramural hemorrhage. At the initial study (A), there was no evidence of flow communication or intimal flap. Follow-up study performed 6 months later showed big intimal tear (B) and color Doppler flow mapping (C) with CW tracing (D) revealing definite flow communication, which was compatible with development of aortic dissection.
Discussion
The main finding of our study is that although the clinical outcomes of medically treated AD and AIH affecting descending
thoracic
aorta
are both favorable, AIH has a significantly higher frequency of complete resolution of aortic pathology. In AD, progressive dilatation of the false lumen was a common finding, which represents detrimental impact of persistent flow communication in the false lumen on aortic
remodeling
after
the
acute
event. These findings, along with
different
mean age between the 2 groups, may suggest that AIH is not just a precursor of overt AD but a distinct disease entity with
different
pathophysiology and prognosis.
One limitation of this study is the diagnostic criteria of AIH. Because we selected patients with distal AIH or AD in whom medical therapy was applied, surgical confirmation could not be made in any case. The issue of “microtear,” which could not be demonstrated by conventional noninvasive diagnostic imaging modalities, needs some comment. This is related with some uncertainty as to how to distinguish AIH from limited AD with a thrombosed false lumen or noncommunicating AD.5 Because we believe it would take some time for complete thrombosis to occur in the false lumen, we selected cases in which diagnostic imaging studies were performed in the relatively early phase (within 2 days). It may not be an ideal way for differential diagnosis, but it can be a rational practical method. Moreover, we believe that pathologic demonstration of microtear is not enough to negate our results, because our point is that the hemodynamic information of the false lumen has a major impact on the remodeling
process
after
acute
distal aortic syndromes. Even though one may have microtear or noncommunicating AD, if the initial imaging study reveals no evidence of flow communication, favorable healing of the distal
descending
aortic pathology with medical treatment can be expected.
The high rate of complete resolution of distal AIH with appropriate medical treatment, the main finding of this study, supports the previous observation in patients with classic AD; the hemodynamic status of the false lumen determines the fate and prognosis of the affected aorta
after
an
acute
event. The wide use of noninvasive imaging modalities for differential diagnosis of
acute
aortic syndromes will enable in vivo identification of AIH more frequently. Because the hemodynamic data of the false lumen can be obtained easily by noninvasive imaging modalities, including contrast-enhanced x-ray computed tomography and TEE, in patients with an uneventful clinical course during the
acute
phase, we can predict whether patients will have a favorable healing process
after
acute
aortic syndrome of the distal
descending
thoracic
aorta
.
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