Acute Type B Aortic Dissection With Communicating vs. Non-Communicating False Lumen

– Analysis of 502 Patients From the Tokyo CCU-Network Database –

Abstract

Background: In practice, patients with acute aortic dissection (AAD) are generally divided into 2 groups according to the status of the false lumen: non-communicating or communicating. The similarities and differences between the 2 groups, however, have not been fully determined in a large population.

Methods and Results: We studied 502 patients with Stanford type B AAD. Clinical background at symptom onset was compared, and similarities and differences characterized, for patients with non-communicating (NC group, n=288) vs. communicating (C group, n=214) false lumens. Time of day (00.00–06.00 hours, 06.00–12.00 hours, 12.00–18.00 hours, and 18.00–24.00 hours) and extent of physical activity (extreme exertion, slight exertion, at rest, and sleeping) at symptom onset were similar between groups. Patients in the NC group were older (mean age, 71±11 years vs. 64±14 years, P<0.01) and had lower prevalence of distally extended aortic dissection (26% vs. 8%, P<0.01) and deaths in hospital (2% vs. 7%, P=0.011) than those in the C group.

Conclusions: At symptom onset, clinical circumstances and physical activity were similar between the groups, and old age and a background of DeBakey IIIa aortic dissection may be associated with determination of false lumen status. The outcome in the NC group was better than in the C group.

Acute aortic dissection (AAD) is a potentially fatal cardiovascular disease, but the prevalence of AAD is lower than that of acute myocardial infarction, so data collected from a single center in order to characterize the disease are unlikely to be representative of the entire population. The Tokyo CCU Network consisted of 62 hospitals in Tokyo in 2009 and encompassed the entire Tokyo metropolitan area. The large number of patients presenting to hospitals in the network affords a unique opportunity to collect data that are likely to be highly representative of cardiovascular diseases – including AAD – in the real world.^1–4

In practice, we generally divided patients with AAD into 2 groups: those with a communicating false lumen and those in whom the false lumen is non-communicating.^5–7 The mechanism of the development of each type of aortic dissection, however, remains unclear.

The purpose of this study was to compare Stanford type B AAD patients with communicating false lumens with those with non-communicating false lumens in order to elucidate the differences between the 2 groups. To accomplish this, we retrospectively analyzed the Tokyo CCU-Network database.

Methods

Patients

In 2009, the Tokyo CCU Network encompassed 62 hospitals that fulfilled certain clinical criteria and received patients from ambulance units coordinated by the Tokyo Fire Department. We retrospectively analyzed the Tokyo CCU Network database, which contained the records of patients with AAD treated between 2007 and 2009. Of 1,534 registered patients with AAD and/or aortic aneurysm with rupture or impending rupture, 502 patients were definitively diagnosed with type B AAD and were included in the present study. They were divided into 2 groups based on the status of the false lumen: communicating (C group) and non-communicating (NC group). A flow diagram of patient selection is shown in Figure 1. Between-group comparisons of demographic and clinical characteristics; symptoms experienced; time of day, season, and physical activity at the time of symptom onset; clinical status after symptom onset; and clinical course of AAD, including outcome, were performed. The study was performed according to the ethics provisions established at each member institution of the Tokyo CCU Network.

Figure 1.

Flow chart of patient selection. Of 1,534 patients with aortic aneurysm or dissection, 502 patients with type B aortic dissection were analyzed.

Definitions

AAD was diagnosed according to the Japanese Circulation Society Guidelines for Diagnosis and Treatment of Aortic Aneurysm and Aortic Dissection (2006)⁸ at each hospital participating in the present study. A non-communicating-type AAD was defined as complete thrombosis of the false lumen without communication of true-lumen blood flow with the false lumen (Figure 2A), and thrombosis of the false lumen with ulcer-like projections (ULP; Figure 2B). AAD with ULP now belongs to a new category, ULP-type, in the 2011 guidelines.^9,10 In the present study, however, because the data were collected from a database comprising patients admitted to the hospital from 2007 to 2009, AAD with ULP was included in the NC group in accordance with the 2006 guidelines. In those guidelines, ULP were defined as focal, well-defined pouches of contrast medium measuring ≤10 mm in length and projecting into the non-communicating false lumen along the long axis of the aorta. If a pouch of contrast medium along the long axis of the aorta measured >10 mm in length on contrast-enhanced computed tomography (CT) and true-lumen blood flow communicated with the false lumen (Figure 2C), it was defined as a communicating-type AAD. Partial thrombosis of the false lumen (Figure 2D) and absence of thrombosis (Figure 2E) were regarded as a communicating-type AAD.

Figure 2.

Non-communicating-type false lumen includes (A) complete thrombosis of the false lumen, and (B) thrombosis of the false lumen with ulcer-like projection (ULP), which was defined as focal, well-defined pouches of contrast medium measuring ≤10 mm in length and projecting into the thrombosed false lumen along the long axis of the aorta. (C) If the length of the pouches of contrast medium measured >10 mm, it was defined as communicating-type false lumen. (D) Partial thrombosis of the false lumen and (E) absence of thrombosis of the false lumen are also categorized as communicating-type false lumen.

Physical activity at onset was categorized as 1 of 4 intensities: extreme exertion (vigorous exercise, more intense exercise than usual, or physical therapy), slight exertion (regular daily activity, bathing, defecating or urinating, eating, drinking alcohol, driving, changing clothes, quarrelling, singing, or standing in a train), at rest, and sleeping. Time of day at onset was categorized as follows: 00.00–06.00 hours, 06.00–12.00 hours, 12.00–18.00 hours, and 18.00–24.00 hours. Season at onset was categorized as spring, summer, autumn, and winter.

Statistical Analysis

Continuous variables are expressed as mean±SD, and differences in continuous variables between the 2 groups were examined using Student’s t-test. Categorical variables are expressed as number (%) and were compared using Fisher’s exact test. SPSS for Windows, version 16.0 (SPSS, Chicago, IL, USA), was used for all statistical analysis. P<0.05 was considered statistically significant.

Results

The NC group consisted of 288 patients and the C group, 214 patients. Clinical characteristics and the time of day, season, and physical activity at symptom onset are listed in Table 1. Patients in the NC group were older than patients in the C group (P<0.01). The time of day, season, and physical activity at symptom onset were similar between the groups, although in the NC group the onset of aortic dissection was slightly less common in spring (P=0.04).

Table 1. Subject Characteristics

	C group (n=214)	NC group (n=288)	P-value
Age (years)	64±14	71±11	<0.01
Men	167 (78)	210 (73)	0.211
Onset season
Spring	67/213 (31)	66/288 (23)	0.040
Summer	33/213 (15)	59/288 (20)	0.163
Autumn	49/213 (23)	76/288 (26)	0.405
Winter	65/213 (31)	87/288 (30)	1
Time of day of symptom onset (hours)
00.00–06.00	26/150 (17)	36/226 (16)	0.777
06.00–12.00	43/150 (29)	69/226 (31)	0.731
12.00–18.00	45/150 (30)	59/226 (26)	0.413
18.00–24.00	36/150 (24)	62/226 (27)	0.474
Physical activity at onset
Sleeping	20/193 (10)	33/265 (12)	0.555
At rest	75/193 (39)	101/265 (38)	0.922
Slight exertion	91/193 (47)	124/265 (47)	1
Extreme exertion	7/193 (4)	7/265 (3)	0.590

Data given as mean±SD or n (%). C, communicating false lumen; NC, non-communicating false lumen.

Clinical status after symptom onset is shown in Table 2. Except for gastrointestinal symptoms, which were significantly less frequent in the NC group than in the C group (P=0.036), symptoms at onset were also similar between the groups. There were significantly older (P<0.01) and more patients with DeBakey type IIIa aortic dissection (P<0.01) in the NC group than in the C group.

Table 2. Clinical Status After Symptom Onset

	C group (n=214)	NC group (n=288)	P-value
Symptom
Chest pain	108/208 (52)	143/281 (51)	0.855
Back pain	57/208 (27)	92/281 (33)	0.233
Chest and back pain	24/208 (12)	29/281 (10)	0.663
Gastrointestinal symptom	16/208 (8)	9/281 (3)	0.036
Impaired consciousness	3/208 (1)	3/281 (1)	0.703
Dyspnea	4/208 (2)	11/281 (4)	0.290
Hemiplegia	4/208 (2)	0/281 (0)	0.033
Paraplegia	1/208 (0.5)	1/281 (0.3)	1
None	2/208 (1)	0/281 (0)	0.180
Other	1/208 (0.5)	4/281 (1)	0.400
SBP on admission (mmHg)	161±36	166±38	0.191
DeBakey classification
IIIa	16/208 (8)	72/277 (26)	<0.01
IIIb	192/208 (92)	205/277 (74)	–

Data given as mean±SD or n (%). SBP, systolic blood pressure. Other abbreviations as in Table 1.

Clinical outcome is listed in Table 3. The prevalence of hemothorax and lower limb ischemia was significantly lower in the NC group than in the C group (P<0.01). More patients had medical treatment in the NC group (P<0.01), and the prevalence of surgery and in-hospital death was also significantly lower in the NC group than in the C group (P<0.01 and P=0.011, respectively). The prevalence of in-hospital death after medical treatment was higher in C group (P=0.025), as was that for in-hospital death after surgical repair (10% vs. 0%), although this did not reach significance. In-hospital death after surgery in all patients was 7.3% (3/41).

Table 3. Clinical Outcome

	C group (n=214)	NC group (n=288)	P-value
Complication of aortic dissection
Rupture	10 (5)	5 (2)	0.066
Hemothorax	5 (2)	0 (0)	<0.01
Lower limb ischemia	14 (7)	2 (0.7)	<0.01
Mesenteric ischemia	2 (0.9)	3 (1)	1
Cerebral ischemia	1 (0.5)	0	1
Myocardial ischemia	0	0	1
Renal failure or infarction	10 (5)	12 (4)	0.828
Spinal cord infarction	0	2 (0.7)	0.510
Therapy
Surgery	30 (14)	11 (4)	<0.01
Stent or graft	1 (0.4)	1 (0.3)	1
Medical treatment	183 (86)	276 (96)	<0.01
Outcome
In-hospital death	15 (7)	6 (2)	0.011
After surgery	3 (10)	0	0.551
After medical therapy	12 (0.7)	6 (0.2)	0.025

Data given as n (%). Abbreviations as in Table 1.

Discussion

Comparison of NC and C group type B AAD patients showed that the clinical circumstances and physical activity at symptom onset were very similar. In contrast, patients in the NC group were older, and fewer of them had distally extended aortic dissections. The outcome in the NC group was better than that in the C group

Similarities Between C and NC Groups

The essential characteristic of aortic dissection is the existence of a false lumen separated by an intimal flap. The mechanism of development of a false lumen, however, remains a question, and the intimal tear is a key factor in its answer.

Whether an intimal tear is present in all patients with non-communicating-type AAD is a difficult question, which ULP may be able to resolve. Clinically, ULP has been regarded as the remnant intimal tear of a non-communicating-type AAD.^11–14 Intimal tear or ULP, however, is not always observed on CT in non-communicating-type AAD. In such cases, there are 2 possible explanations for the development of hematoma in the false lumen. First, the hematoma might have resulted from rupture of the vasa vasorum without an intimal tear, which is the original definition of intramural hematoma (IMH),^15,16 although the term “IMH” is often misused in cases of ULP, which is a remnant intimal tear. The true prevalence of rupture of the vasa vasorum is extremely difficult to estimate. Second, an intimal tear may exist but be too small to be detected even on high-resolution CT, although such tears are often identified by sagittal multiplanar reconstraction images (Figure 3) or during emergency surgical treatment.¹⁷ Recently, Uchida et al studied a series of patients with type A aortic dissection with non-communicating false lumen who underwent surgical repair.¹⁸ The authors reported that intimal tears were detected on preoperative CT in 52% of patients, and under direct visualization during surgical repair in 78% of patients. This means that intimal tears failed to be detected even on high-resolution CT in 26% of all cases and that 22% of patients might have no intimal tears even on direct visualization, which may actually mean IMH. The prevalence of IMH reported from the International Registry of Aortic Dissection (IRAD) study was estimated to be 12% of 790 patients with type B AAD.¹⁹ Thus, approximately 80–90% of non-communicating-type aortic dissection cases may have an intimal tear. The present study, in which the clinical circumstances and physical activity at symptom onset were found to be extremely similar in the NC and C groups, may provide a clue in the consideration of these issues.

Figure 3.

Sagittal multiplanar reconstruction showing ulcer-like projection (ULP) at the aortic arch. (A) Axial image with 5-mm-thick sections showing contrast media pooling at the aortic arch (arrow). (B) Axial image with 0.625-mm-thick sections clearly showing ULP (arrow). (C) Sagittal image showing a ULP located at the lesser curvature side of the aortic arch (arrow).

Differences Between C and NC Groups

Substantial differences between these groups have previously been reported, and the differences between the 2 types of AAD are associated with some of the differences in characteristics between the 2 groups as follows. AAD patients with a non-communicating false lumen have been reported to be older,^6,19,20 to have a greater intima-media thickness,²¹ to experience dissection with limited extension to the supraceliac aorta more frequently, and to exhibit lower incidences of leg ischemia and renal failure^19,22 but an increased risk of true aneurysm.²³ In the present study, we found older age and DeBakey type IIIa AAD (ie, limited extension of aortic dissection), to be more prevalent but lower-limb ischemia less prevalent, in the NC group than in the C group. Because atherosclerosis is known to be associated with older age, hypertension, diabetes mellitus, dyslipidemia,²⁴ smoking, and true aneurysm,²⁵ we consider that AAD with a non-communicating false lumen may be associated with atherosclerosis, and atherosclerosis causes stiffness of the aortic wall, which may make extension of the dissection and reentry difficult. Laboratory data on diabetes mellitus and dyslipidemia, however, were not available in the present study, and our hypothesis is not sufficiently supported by the present data. At a minimum, old age and a background of DeBakey IIIa aortic dissection may be associated with determination of false-lumen status.

Clinical outcome was better in the NC group than in the C group in this large cohort, that is, death in hospital was less prevalent in the NC group. The better outcome in the NC group was in accordance with previous reports.^22,26,27 Poor outcome after surgical repair in type B AAD has been demonstrated,^28,29 and in the present study mortality after surgical repair of all type B patients was 7.3% and that of C group was 10%, similar to that in a recent study.³⁰

Prevalence of Non-Communicating False Lumen and IMH in AAD

The appropriateness of the terminology “hematoma of the false lumen” is debatable. Because an intimal tear accompanying a false lumen is extremely difficult to confirm in clinical practice, we did not use the term “IMH” in the present study. Instead, we used the term “non-communicating false lumen”, which allows for the inclusion of ULP. Therefore, the prevalence of IMH and non-communicating false lumen depends on whether their definitions include ULP. The prevalence of IMH ranges between 9% and 45% in patients with type B aortic dissection.^19,31–34

We found that a substantially greater proportion of patients had a non-communicating false lumen than the proportion in the IRAD registry considered to have IMH¹⁹ (57% vs. 12%). This difference can be explained as follows: first, the present study included patients with ULP in the NC group. The IMH group in the IRAD study would not have included patients with ULP if IMH was defined as hematoma in the media without an intimal tear. ULP have been reported in 33–36% of patients with type B AAD.^35,36 Data collected for the present study, however, did not include whether patients with non-communicating false lumens had ULP. We were therefore unable to determine how many patients with non-communicating false lumens had ULP on CT. Second, large (>10 mm) long-axis-direction pouches of contrast medium in the non-communicating false lumen (Figure 2C), which should be classified as belonging to the C group, may mistakenly have been classified as ULP with a non-communicating false lumen (Figure 2B) in the NC group.

Study Limitations

Our study had some limitations. First, this study analyzed data collected at 62 hospitals. Despite the high standards required for membership in the Tokyo CCU Network, because each hospital has its own protocol for record-keeping or patient evaluation or imaging interpretation, standard of evaluation and interpretation of data were not always uniform. Although the CT findings were assessed by staff at each hospital according to the Japanese Circulation Society Guidelines for Diagnosis and Treatment of Aortic Aneurysm and Aortic Dissection (2006),⁸ CT images should have been reviewed by designated staff at the core laboratory. Second, we did not record the timing of the preoperative CT on which AAD was diagnosed, and it is possible in some cases for a non-communicating false lumen to change to a communicating false lumen over time. Third, it is difficult to distinguish false-lumen rupture in AAD from rupture of a dilated aneurysm resulting from chronic aortic dissection. Although patients with chronic aortic dissection should have been excluded from the analysis, this diagnostic difficulty might have led to some being included inadvertently. Fourth, we could not include clinical outcome at remote period because this is not included in the Tokyo CCU Network database. Finally, the time of onset of symptoms may not always have been recorded accurately or remembered with sufficient precision by patients or their caregivers; indeed, one-quarter of these data were missing.

Conclusions

We retrospectively studied the data of 502 patients with type B AAD from the Tokyo CCU Network database. At symptom onset, clinical circumstances and physical activity in the NC and C groups were similar; and old age and a background of DeBakey IIIa aortic dissection may be associated with determination of false lumen status.

Acknowledgments

The authors thank participating hospitals and leading members of the Tokyo CCU Network (Appendix). Furthermore, the authors deeply thank Mitsuhiro Hayashi (Nippon Medical School) and Takahiko Mine (Nippon Medical School), who advised us on ULP images and selected appropriate images of ULP in patients with AAD, which are used in Figure 3. We also thank Ms. Nobuko Yoshida for her assistance with the manuscript.

Disclosures

None of the authors has financial conflicts of interest to disclose.

Appendix

Participating Hospitals and Leading Members of the Tokyo CCU Network

Mitsui Memorial Hospital, Kazuhiro Hara; Nihon University Itabashi Hospital, Tadateru Takayama; Juntendo University Hospital, Hiroyuki Daita; Toho University, Ohashi Medical Center, Masato Nakamura; Saiseikai Central Hospital, Hideo Mitamura; Showa University Hospital, Youichi Kobayashi; Sakakibara Heart Institute, Tetsuya Sumiyoshi; Kosei General Hospital, Masao Kawaguchi; St. Luke’s International Hospital, Yutaro Nishi; Tokyo Women’s Medical University Hospital, Nobuhisa Hagiwara; Nishiarai Hospital, Katsumi Saito; Teikyo University Hospital, Takaaki Isshiki; The Cardiovascular Institute, Akira Koike; Toranomon Hospital, Sugao Ishiwata; Toho University Omori Medical Center, Nobuya Koyama; Surugadai Nihon University Hospital, Ken Nagao; Tokyo Medical University Hachioji Medical Center, Hiroshi Kobayashi; Kyorin University Hospital, Hideaki Yoshino; Tokyo Metropolitan Geriatric Hospital, Kazumasa Harada; Tokyo Metropolitan Hiroo Hospital, Harumizu Sakurada; Nippon Medical School Hospital, Keiji Tanaka; Tokyo Women’s Medical University Medical Center East, Kuniaki Otsuka; Bokutoh Metropolitan General Hospital, Ichiro Kubo; Tobu Chiiki Hospital, Takashi Tamura; Musashino Red Cross Hospital, Tohru Obayashi; Showa General Hospital, Yuji Kira; Tokyo Metropolitan Fuchu Hospital, Tetsuro Ueda; Disaster Medical Center, Yasuhiro Satoh; Ome Municipal General Hospital, Shigeo Shimizu; Edogawa Hospital, Yoji Oohira; Tokyo Rinkai Hospital, Toru Kono; Jikei University Katsushika Medical Center, Shingo Seki; IMS Katsushika Heart Center, Sakakibara Masayoshi; Ayase Heart Hospital, Imun Tei; Hakujikai Memorial Hospital, Kunio Tanaka; Jikei University Hospital, Michihiro Yoshimura; Senpo Tokyo Takanawa Hospital, Masato Yamamoto; Kanto Medical Center NTT EC, Ohnishi Satoshi; Ikegami General Hospital, Takao Machimura; University of Tokyo Hospital, Ryozo Nagai; Tokyo Metropolitan Police Hospital, Tetsuro Shirai; Kohseichuo General Hospital, Akio Hirai; Mishuku Hospital, Akimi Uehata; Keio University Hospital, Tsutomu Yoshikawa; Tokyo Medical University Hospital, Akira Yamashina; Toyama Hospital, International Medical Center of Japan, Michiaki Hiroe; Kawakita General Hospital, Yoichi Sugimura; Itabashi Chuo Medical Center, Hiroshi Ota; Tokyo Metropolitan Health and Medical Treatment Corporation Toshima Hospital, Takashi Shibui; Nishitokyo Central General Hospital, Suesada Hiroyuki; Yamatokai, Inc. Med. Inst. Higashiyamato Hospital, Masao Kuwada; Tokai University Hachioji-hospital, Yoshinori Kobayashi; Nippon Medical School Tama-Nagayama Hospital, Hirotsugu Atarashi; Tama Nambu Chiiki Hospital, Takata Hiroyuki; Tokyo Medical and Dental University, Mitsuaki Isobe; Japanese Red Cross Medical Center, Akihiko Aoyagi; Kanto Central Hospital, Hiroshi Ikenouchi; National Hospital Organization Tokyo Medical Center, Yukihiko Momiyama; Social Insurance Central General Hospital, Makoto Noda; Tokyo Kosei Nenkin Hospital, Seiji Ayabe; Nihon University Nerima Hikarigaoka Hospital, Seiji Fukushima; Jikei University Daisan Hospital, Takahiro Shibata.

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