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Department of Radiology, Nagasaki University School of Medicine, Nagasaki, Japan
Accepted for publication June 9, 2009.
* Address correspondence to Dr Sueyoshi, Department of Radiology, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki, 852-8501, Japan (Email: eijunsueyoshi{at}aol.com).
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Abstract |
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Methods: Seventy-one patients (mean age, 64.4 years) who had experienced AD were enrolled in this study. Regular follow-up computed tomography studies (mean, 48.9 months) were performed. During the follow-up period, aortic diameter was measured with computed tomography. The fastest GR was calculated.
Results: Based on final computed tomography findings, the patients were divided into three groups: those with completely closed false lumens (n = 8), those with partially closed false lumens (n = 20), and those with patent false lumens (n = 43). Among the patients with partially closed false lumens, 3 of 20 (15%) had a sac formation type and 17 (85%) had a non–sac formation type. The mean fastest GRs for groups with a completely closed false lumen, partially closed false lumen, and patent false lumen were –0.2 ± 0.6, 4.0 ± 4.3, and 4.9 ± 4.5 mm/year, respectively. The differences among the three groups were statistically significant (p = 0.0149). In the partially closed false lumen group, the mean fastest GRs of the sac and non–sac formation types were 12.7 ± 1.1 and 2.6 ± 2.7 mm/year, respectively; this difference is statistically significant (p = 0.007).
Conclusions: Affected aortas with partially closed false lumens do not exhibit the highest GR. The status of a partially closed false lumen is not a significant risk factor for enlargement; however, careful follow-up study is needed whenever the sac formation type of partially closed false lumen is identified.
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Introduction |
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Many reports about aneurysmal dilation group patients according to whether their false lumens have closed completely, owing to the presence of a thrombus, or remain patent. Several studies have suggested that patients with complete thrombosis of the false lumen have improved outcomes, whereas those with patent false lumens have an increased risk of aortic enlargement and death [5, 8, 9].
A more recent study introduced a third category, that of patients with partial thrombosis of the false lumen, and showed that these patients have an increased risk of death; this report, however, did not describe the natural history of the affected aorta or the cause of death in patients with partial thrombosis of the false lumen [10].
The natural history of the affected aorta and the cause of death in patients with partially closed false lumens have not yet been elucidated. The purpose of this study was, therefore, to clarify the natural history of the affected aorta in cases of partially closed false lumen and to determine whether a partially closed false lumen affects aortic enlargement in patients with type B double-barrelled AD. We evaluated the evolution of the affected aorta and the growth rate of type B double-barrelled AD using computed tomography (CT) examination, grouping patients into three false lumen conditions: completely closed false lumen, partially closed false lumen, and patent false lumen.
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Material and Methods |
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The patients consisted of 49 men and 22 women between the ages of 40 and 83 years, with a mean age of 64.4 ± 11.9 years. All patients experienced sudden back or chest pain at onset. Fifty-three of the 71 patients (74.6%) had a history of hypertension. Patients with Marfan's syndrome or traumatic AD were excluded from this study.
The diagnosis of type B (ascending aorta not affected) double-barrelled (classic) AD was established with initial CT within 12 hours from onset. In all cases, an intimal flap and contrast enhancement within the false lumen were seen on post–contrast CT. The mean CT follow-up period was 48.9 ± 49.4 months (range, 6 to 120). Regular follow-up studies were performed every week during the first month, and from one to three times a year after the second month. If patients experienced additional episodes, suggesting complications during the follow-up period, additional studies were performed. The CT follow-up period after surgery was excluded from this study.
Computed Tomography Examination
A total of 513 examinations with spiral CT scanners were performed on our 71 patients (n = 511). Follow-up CT studies were performed with nonenhanced and enhanced CT in all patients; enhanced CT was done with a bolus injection of 100 mL of nonionic contrast material applied through a power injector; the two phases of imaging began 20 s to 30 s and 120 s to 150 s after the start of contrast material injection. The CT scans were performed with either a high-speed advantage, Light Speed Qx/i scanner (GE Medical Systems, Milwaukee, WI), a Somatom Plus 4 scanner (Siemens Medical Systems, Erlagen, Germany), or an Aquilion 16 scanner (Toshiba Medical Systems, Tokyo, Japan). All of these scanners generated axial images with contiguous sections from the top of the aortic arch to the abdominal aorta as volume data.
Image Analysis
The CT images from each patient were evaluated by two experienced cardiovascular radiologists (Eijun Sueyoshi and Ichiro Sakamoto, who have over 15 years' experience each). Final decisions regarding the findings were reached by consensus. The absence of blood flow in the entire false lumen was indicated by the absence of contrast enhancement in the false lumen on post–contrast CT.
Based on the status of the false lumen according to final CT findings, we divided patents into three groups: completely closed false lumen, partially closed false lumen, and patent false lumen. It should be noted that, at the first CT after AD onset, all patients had patent false lumens.
Patients assigned to the completely closed false lumen group had completely thrombosed false lumens and an absence of blood flow in the entire false lumen (Fig 1A). Patients assigned to the patent false lumen group had continuous blood flow in their false lumens from entry to reentry; this assignment was made regardless of whether a thrombus was present in the false lumen (Fig 1B). Patients assigned to the partially closed false lumen group had false lumens that were partially closed owing to the presence of a thrombus in any part of the false lumen (Fig 1C). In addition, we divided the partially closed false lumen group into two subgroups: patients with the sac formation type of false lumen and patients with the non–sac formation type. The non–sac formation type was defined as a partially closed false lumen at the entry site of false lumen. In this type, blood flow enters the false lumen from small orifices of arterial branches (such as the intercostal, lumbar, brachial, superior mesenteric, celiac trunk, or renal arteries) or only at the reentry site in cases where the entry is closed by a thrombus. The sac formation type was defined as a partially closed false lumen at the reentry site of the false lumen (a blind pouch with a persistent entry tear; Fig 1D; Figs 2 and 3).
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The affected aortas were divided into five segments (aortic arch, 55; descending thoracic aorta, 70; suprarenal abdominal aorta, 47; infrarenal abdominal aorta, 26; and iliac artery, 12). In this study, the aortic arch is defined as beginning after the brachiocephalic artery and ending at the level of the ligament arteriosus. The descending aorta is defined as extending from the level of the ligament arteriosus to the aortic hiatus of the diaphragm. A total of 210 segments was evaluated.
The initial and final CT measurements were compared to calculate changes in aortic size in a single region in each segment on work station [6]. The largest short-axial diameter of the outer contour of the affected aorta (a 1 mm-thick image) was measured [11,12]. In the aortic arch, the largest diameter perpendicular to the curvature was measured (Fig 4) [11, 12]. The growth rate of each segment was calculated at the region of the largest diameter on the final CT. The growth rate was calculated in the following manner [11–13]: the difference in the diameter between initial (D1) and final (D2) measurements was divided by the time interval (T) between the two measurements, and expressed as an equation: growth rate = (D2 – D1)/T.
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Statistical Analysis
All values are expressed as means. Statistical analysis was performed using clinical and morphological variables, with the 
2 or Fisher's exact test used for categorical variables, and the paired t test and Mann-Whitney's U test for continuous variables. If the expected number of cells was less than five, Fisher's exact test was used for categorical variables. Variables with statistical significance set at p less than 0.05 (two-sided) were included in a multivariate logistic regression model. Estimates of risk (odd ratios) were calculated based on coefficients from logistic models. In all tests, p less than 0.05 was considered significant. Data analysis was performed using Stat-View J-5.0 for Windows (Abacus Concepts, Berkeley, CA).
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Results |
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During the period between 6 and 112 months after the onset of AD, 22 of the 71 patients (31.0%) underwent surgery (for aneurysmal dilatation in 19 cases, aortic rupture in 2, retrograde ascending dissection in 1, and organ ischemia including renal infarction and lower limb ischemia in 3). In 17 of the 19 patients with aneurysmal dilatation, the size threshold of 6 cm was used to determine need for surgery. In 2 patients, surgery was performed because of rapid aneurysm formation (more than 5 mm in 6 months). Figure 5 shows the Kaplan-Meier freedom from aortic repair; event-free curves are compared among patients with completely closed false lumens (n = 8), partially closed false lumens (n = 20), and patent double-barrelled false lumens (n = 43). The freedom from aortic repair values at 1, 2, 5, and 10 years are 100%, 100%, 75%, and 75%, respectively, for the completely closed false lumen group; 84.7%, 79.4%, 67.6%, and 59.1% for the partially closed false lumen group; and 88%, 78%, 61.2%, and 61.2% for the patent double-barrelled false lumen group.
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Of the 210 segments measured in our 71 patients, 152 (74.6%) increased in size during the follow-up period. Fifty-eight segments (25.4%) showed no change or decreased in size. In 67 segments (28.8%), the false lumens became completely thrombosed (no blood flow) at some point between 1 day and 72 months after onset. Of the 51 segments without blood flow in the false lumen, 19 (37.3%) increased in size during the follow-up period. In contrast, of the 126 segments with blood flow in the false lumen, 113 (89.7%) increased in size. The difference between the rates of diameter increase in segments with blood flow in the false lumen and those without was statistically significant (p < 0.0001).
Table 1 shows the mean initial diameters, final diameters, and growth rates of the segments in the three groups. In the completely closed false lumen group, 18 segments were evaluated, and the mean growth rate was –4.5 ± 8.1 mm/year. In the partially closed false lumen group, 54 segments were evaluated, and the mean growth rate was 0.4 ± 10.4 mm/year. In the patent false lumen group, 138 segments were evaluated, and the mean growth rate was 2.8 ± 4.1 mm/year. The difference in growth rates among the completely closed false lumen, partially closed false lumen, and patent double-barrelled false lumen groups was statistically significant (p < 0.0001).
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The mean growth rate of the fastest growing segment in each patient was 4.1 ± 4.5 mm/year. Table 2 shows the mean growth rate of the fastest growing segment in each patient according to group. In the completely closed false lumen group, the mean fastest growth rate was –0.2 ± 0.6 mm/year. In the partially closed false lumen group, the mean fastest growth rate was 4.0 ± 4.3 mm/year. In the patent false lumen group, the mean fastest growth rate was 4.9 ± 4.5 mm/year. The difference among the three groups was statistically significant (p = 0.0149), as was the difference between the partially closed false lumen group and the patent false lumen group (p = 0.0426). The patent false lumen group had the highest mean fastest growth rate.
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Tables 3 and 4
show that, according to our univariate analysis, patient characteristics such as sex, age 70 years or older, atherosclerotic disease (including atherosclerotic aneurysm, ischemic heart disease, and cerebrovascular disease), chronic renal failure, diabetes mellitus, blood pressure 140 mm Hg or higher, initial diameter less than 40 mm, and a partially closed false lumen were not significant risk factors for increased diameter of the false lumen (fastest growth rate more than 0 mm/year). A patent false lumen, on the other hand, was a significant risk factor for increased diameter according to univariate analysis. The location of the entry site in the arch was a significant risk factor for increased diameter according to univariate and multivariate analyses. A completely closed false lumen was associated with a significantly reduced risk for increased diameter according to univariate and multivariate analyses.
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Comment |
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A recent study showed that the risk of death is increased in patients with partial thrombosis of the false lumen compared with patients who have completely patent false lumens [10]; however, this report did not describe the natural history of the affected aorta or the cause of death in patients with partial thrombosis of the false lumen. The authors simply speculate that several possible contributing factors deserve mention. One potential explanation relates the presence of partial thrombosis to the pressure within the false lumen: whereas a patent false lumen may be perfused by a proximal entry tear and decompressed through distal reentry tears, the formation of a partial thrombus may occlude these distal tears, impeding outflow and, in the most extreme situation, resulting in a blind sac [10].
Several studies have shown that pulsatile inflow into a lumen with impaired outflow may lead to a significant increase in mean arterial and diastolic pressure over the pressure levels seen in a lumen with adequate outflow, despite similar systolic pressure [15–17]. The discovery of the "sac formation" subgroup and the rapid aortic growth associated with this condition may help to explain the previous reports of adverse outcomes in patients with partial thrombosed false lumens [10]. Similarly, our study shows that, within the partially closed false lumen group, the mean fastest growth rate in the sac formation type was significantly higher than that in the non–sac formation type. This result appears at first to support the theory that partial thrombosis increases pressure, but it should be noted that the sac formation type had a low incidence (15%) even within the partially closed false lumen group. According to our results, moreover, the partially closed false lumen condition (including the sac formation and non–sac formation types) did not have the highest growth rate and was not a significant risk factor for increased diameter of the false lumen (fastest growth rate greater than 0 mm/year). Therefore, our results do not appear to support the hypothesis that the formation of a partial thrombus per se leads to an increased risk of death. Significantly, neither does the fact that the intimal tears (entry or reentry) are not the only connections between the true and false lumens: there are also the orifices of arterial branches (intercostal, lumbar, brachial arteries, superior mesenteric, celiac trunk, renal, and so forth). These small communications may reduce the pressure in the false lumen, counteracting the presence of partial thrombosis. Therefore, our evidence does not indicate that the partially closed false lumen condition in general is associated with a particularly high growth rate or with poorer outcomes.
This study shows that the patent false lumen group had the highest growth rate. The completely closed false lumen group had the lowest growth rate and was associated with a significantly lower risk of increased diameter of the false lumen. According to previous studies that compared the two conditions of completely closed and patent false lumen, patent false lumens tend to progress to enlargement [15–17]. For this reason, a reduction in blood flow can decrease the diameter of the false lumen. In the patent false lumen, blood flow causes progressive aneurysmal dilatation of a segment through both the structural weakness of the aortic wall and the direct mechanical stress from blood flow. According to our study, the location of the entry site in the arch was a significant risk factor for increased diameter in univariate and multivariate analyses. Generally, the amount of blood flow and the pressure of the aortic arch are highest in patients with type B AD; therefore, our results support the above theory.
Previous studies have also suggested that patients with complete thrombosis of the false lumen have improved outcomes, whereas patients with patent false lumens have an increased risk of aortic expansion and death [6–9]. A recent study showed that the risk of death is increased by a factor of 2.7 among patients with partial thrombosis of the false lumen compared with patients who have completely patent false lumens (no thrombus) [10]. Our study shows that the partially closed false lumen condition was not associated with the highest growth rate and was not a significant risk factor for increased diameter of the false lumen. These results suggest that aneurysmal dilation may not be a common cause of death in patients with partial thrombosis of the false lumen. It is not clear why the risk of death is increased by a factor in patients who have partial thrombosis of the false lumen compared with patients who have completely patent false lumens. One possibility is that a thrombus in the false lumen may itself be a risk for poor prognosis. Generally, AD activates the coagulation system; therefore, plasma D-dimer measurement has been used to diagnose AD [18, 19]. A previous study showed that D-dimer measurement not only correlated with mortality but also with the development of multiple systemic organ failure, sepsis, and vascular thrombosis. False lumen patency may enhance the coagulation cascade [20, 21]. We speculate that a partially closed false lumen or a patent false lumen with thrombus may enhance the coagulation cascade more than a patent false lumen without thrombus does. Patients with a thrombus may therefore be at greater risk of having multisystem organ failure, sepsis, and vascular thrombosis; further studies are needed to clarify this issue, however.
A previous study has indicated that partial thrombosis may also have a role in the rupture of the false lumen, similar to its role in the rupture of abdominal aortic aneurysms [10]. Other previous studies have suggested a direct relationship between intraluminal thrombosis and the risk of rupture of an abdominal aortic aneurysm as a result of hypoxia of the arterial wall adjacent to the intraluminal thrombus, which leads to increased local inflammation, neovascularization, and localized wall weakening [10, 22, 23]. This mechanism may be even more pertinent to the false lumen of a dissected aorta, because in this setting the residual outer layers of the aortic wall already have diminished strength. In this study, the fastest growth rate of the affected aorta was higher in completely patent false lumens than in partially patent false lumens. With regard to aneurysmal dilatation, our results did not support the theory that partial thrombosis can cause rupture of the false lumen; further studies are needed to clarify the true causes of abrupt rupture of the affected aorta.
This study had several limitations. First was the difficulty of obtaining accurate measurements of aortic diameter on CT images. We measured the largest short-axial diameter of the outer contour of the aorta to avoid any errors due to the tortuosity or curvature of some aortas, so that the measurement would be accurate on axial CT images. Previous studies have used a measurement method similar to ours. It can be very difficult, however, to measure the distal arch in a superior to inferior path, as this gives the aorta a sort of camel's hump look in that region. Multiplanar reconstructed images and three-dimensional images, including the use of volume measurements, may be needed to obtain more accurate sizing of the aorta. Even when such techniques are used, however, it may be very difficult to objectively measure distances between the same points of the aorta on three-dimensional images.
Second, the sample size was small, and the follow-up periods of patients varied. The sample size of the sac formation type group was particularly small (n = 3). Further studies involving a larger number of patients and a longer follow-up period are needed to confirm our findings.
Third, the false-lumen status was determined at final CT, and our definitions of the three false lumen statuses were not the same as those used in previous reports; therefore, our results are not directly comparable with those of previous studies under the same conditions. In one previous study, for example, the false-lumen status was determined once during hospitalization and was not changed, regardless of any changes in status observed during the follow-up period. This method does not consider the fact that false-lumen status can change during the follow-up period, and that a thrombus in the false lumen can increase or decrease in size over time [24]. We believe that a false-lumen status determined at final CT may be more reliable in terms of predicting outcome than a false-lumen status determined early in treatment.
In conclusion, in type B chronic aortic dissection, affected aortas with partially closed false lumens do not exhibit the highest growth rate, and a partially closed false lumen is not a significant risk factor for enlargement; however, careful follow-up study is needed whenever the sac formation type of partially closed false lumen is identified. The highest growth rate observed in this study was exhibited by affected aortas with patent false lumens; therefore, careful follow-up study is also needed in this situation.
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