- Email: [email protected]
Outcomes of thoracic endovascular repair for type B aortic dissection with multichanneled morphology
Outcomes of thoracic endovascular repair for type B aortic dissection with multichanneled morphology Baolei Guo, MD, PhD,a Kai Hou, MD,b Daqiao Guo, MD,a Xin Xu, MD,a Zhenyu Shi, MD,a Yan Shan, MD,b Peng Lv, MD,b and Weiguo Fu, MD,a Shanghai, China
ABSTRACT Objective: Clinical outcomes after thoracic endovascular aortic repair (TEVAR) for patients with multichanneled aortic dissection (MCAD) are poorly understood but seem substantially different from those for patients with double-channeled aortic dissection (AD). This study compared the anatomic and clinical factors for patients with MCAD who underwent TEVAR with or without full true lumen (TL) collapse. Methods: From January 2012 to March 2016, 54 of 644 consecutive type B AD patients (8.4%) who presented with MCAD were reviewed. Patients were classified as MCAD with full TL collapse and without full TL collapse according to computed tomography angiography findings. We analyzed potential variables including clinical characteristics, anatomic morphologic features, and procedural details. Multivariable analysis was performed to determine independent predictors of AD-related deaths. Results: A total of four patients (7.4%) died preoperatively of aortic rupture, all of whom experienced full TL collapse. MCAD patients with full TL collapse showed significantly higher 30-day major adverse events than those without full TL collapse (36.8% vs 9.7%; P ¼ .030). The mean follow-up duration was 25.6 6 13.2 months (range, 3-53 months). The overall mortality for all MCAD patients was 16.7%, whereas the follow-up major adverse events rate was 40.0% after TEVAR. Significant differences were present between patients with full TL collapse and patients without full TL collapse in survival at 3 years (55.4% vs 94.7%; P ¼ .002). Maximum diameter of affected aorta (hazard ratio, 1.176; 95% confidence interval, 1.015-1.362; P ¼ .031) was identified as the only predictor of AD-related deaths. Conclusions: MCAD was identified in a small but not insignificant number of our patients presenting with type B AD. Urgent or elective TEVAR was indicated in all our patients with MCAD. In patients with MCAD, full TL collapse was associated with worse outcomes, and this finding may indicate the need for more urgent or emergent repair. (J Vasc Surg 2017;-:1-11.)
Thoracic endovascular aortic repair (TEVAR) is a promising treatment for patients with type B aortic dissection (AD) with chest pain, malperfusion, rupture, and acute aortic enlargement.1-4 The therapeutic strategy and risk factors for AD-related events and deaths are well established for patients with classic double-channeled AD (DCAD). However, multichanneled AD (MCAD) is considered a relatively rare condition and was first reported in 1978 by McReynolds et al.5 Previous studies suggested that the presence of MCAD is a powerful predictor of AD-related deaths after open surgery or TEVAR.6,7 The elevated pressure in different false lumens (FLs) for patients with MCAD results in complex communications to the true lumen (TL), which may cause these patients to
From the Department of Vascular Surgery, Institute of Vascular Surgery,a and Department of Radiology,b Zhongshan Hospital, Fudan University.
be at a higher risk for TL collapse, aneurysm, and rupture. Treatment for TL collapse involves decreasing the flow of blood into the FL and increasing the flow from it.8,9 On the basis of this mechanism, MCAD detected on computed tomography angiography (CTA) might help predict which patients will suffer from adverse events. However, the clinical characteristics, natural history, and follow-up outcomes of MCAD after TEVAR have not been widely recognized or evaluated. To the best of our knowledge, the morphologic classifications of MCAD and perioperative and midterm clinical outcomes after TEVAR have not been previously evaluated. The purpose of the study was to analyze a cohort of patients who underwent TEVAR for all MCADs in our center. We reported the clinical features, morphologic findings, perioperative outcomes, and follow-up results of 54 patients with MCAD to explore its progression and to evaluate the role of TEVAR.
Author conflict of interest: none. Additional material for this article may be found online at www.jvascsurg.org. Correspondence: Weiguo Fu, MD, Department of Vascular Surgery, Zhongshan Hospital Fudan University, Institute of Vascular Surgery, Fudan University, 180 Fenglin Rd, Shanghai 200032, PR China (e-mail: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a conflict of interest. 0741-5214 Copyright Ó 2017 by the Society for Vascular Surgery. Published by Elsevier Inc. http://dx.doi.org/10.1016/j.jvs.2016.12.145
METHODS Study design and population of patients. Data collection and analysis for this study were approved by the Institutional Review Board from the Ethics Committee of Zhongshan Hospital Fudan University. Informed consent was obtained from all patients. This was a retrospective review of 644 consecutive patients with type B AD in our vascular center between January 2012 and March 1
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Fig 1. Summary flow diagram by presentation and treatment of the patient. AD, Aortic dissection; TEVAR, thoracic endovascular aortic repair.
2016. A total of 54 patients with MCAD were analyzed in this study. Clinical data regarding patients’ baseline characteristics, presentation, inpatient management, and follow-ups were collected. The data were analyzed to determine the perioperative complications and followup outcomes of MCAD patients with or without full TL collapse according to the CTA findings. Twenty-three patients who experienced full TL collapse were included in the MCAD with full TL collapse group, and the remaining 31 patients were included in the MCAD without full TL collapse group. In general, patients with complicated acute type B AD underwent TEVAR in a subacute phase.10 Notably, a specific indication for TEVAR was MCAD in patients with severely recurrent chest or back pain. All patients who presented with signs of rupture and with suspected or known aortic propagation underwent TEVAR urgently (Fig 1). TEVAR procedure. TEVAR was performed on patients under general anesthesia using commercially available endografts (Valiant and Valiant Captivia [Medtronic, Minneapolis, Minn]; Zenith TX2 [Cook, Bjaeverskov, Denmark]; Ankura [Lifetech, Shenzhen, China]; or TAG [W. L. Gore & Associates, Flagstaff, Ariz]) through the unilateral common femoral artery with either traditional exposure or a percutaneous puncture secured by two ProGlide stitches (Abbott Vascular, Abbott Park, Ill). Oversizing (3%-5%) was calculated according to the distance from the adventitia to the adventitia of the proximal landing zone on CTA. A basic goal of TEVAR was to completely cover the primary entry tear with a single 15- to 20-cm-long endograft unless there were endoleaks after the initial endograft repair. We avoided performing angioplasty after deployment. If the proximal landing zone (the distance from the origin of the left
subclavian artery [LSA] to the primary entry) measured <15 mm, one of two strategies would be applied to create an extra anchoring area: (1) intentional coverage of LSA, if the right vertebral artery was patent and the left one was not dominant; or (2) revascularization of LSA with bypass or chimney technique. If necessary, intravascular ultrasound catheters were introduced to intraoperatively confirm the location of the TL or FLs and the origin of the visceral arteries. We primarily used the Vision PV 8.2F, 10 MHz catheter (Volcano Therapeutics, Rancho Cordova, Calif) for aortic procedures. Definitions and image analysis. AD was classified as type B, according to the Stanford classification, if the dissection did not involve the ascending aorta. Acute AD was defined as <14 days from the onset of symptoms; chronic AD was defined by an elapsed time $14 days from symptom onset.1,4 MCAD was defined as AD with more than two FLs on contrast-enhanced computed tomography (CT) images. We excluded the images with just a single FL that wraps around the TL in a U or O shape according to the CTA reconstruction. The length of each FL was >2 cm to distinguish it from the aortic cobweb,7,11 ulcerated mural thrombus, intimal tears, and penetrating ulcers. The diagnoses of MCAD were made on the initial or follow-up CT findings. Malperfusion syndrome was defined as end-organ ischemia caused by branch vessel involvement and resulting in clinical symptoms and functional impairment in a wide range of arterial beds.12 We included free rupture (in which disruption of all the layers of the aortic wall leads to massive hematoma) and impending rupture in the analysis. Signs of active contrast material extravasation from the aorta, large pleural effusion, periaortic hematoma, mediastinal hematoma, areas of compromised
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Fig 2. Computed tomography (CT) images of multichanneled aortic dissection (MCAD) with full true lumen (TL) collapse. In the proximal descending thoracic aorta, the TL, which had a small channel, was severely compressed by two isolated false lumens (FLs; A and B). There was a “false-true-false” lumen configuration (coexisting dissections on either side of the TL). However, the capacity of the TL (<3 mm in diameter) was fully collapsed from the distal thoracic aorta to the abdominal aorta, which indicated pronounced distal collapse of a flakelike lumen (C-H). Dynamic obstruction of the superior mesenteric artery was also observed (D and E).
perfusion, and symptoms related to the enlarging dissected aorta (hoarseness, new-onset chest pain) indicated rupture. We categorized patients with the TL that completely collapsed because of compression of FLs, resulting in pronounced distal collapse of a flakelike lumen (TL <5%) at least 5 cm in length, as those with full TL collapse (Fig 2). Patients with the TL that incompletely collapsed, resulting in a less pronounced distal collapse with an apparently normal distal TL, were categorized as patients without full TL collapse (Fig 3). Clinical success was defined as an outcome in which the preoperative pathologic conditions and symptoms were resolved by TEVAR. Event rates were defined as the total number of vascular events that led to separate clinical presentations during the study period. Preoperative and follow-up evaluations were performed using spiral CTA. CTA images were independently analyzed by two experienced cardiovascular radiologists (Y.S. and P.L.), who paid particular attention to the morphologic features of dissected aorta. The radiologists were blinded to the clinical data when reviewing the images. The aortic changes regarding the morphology and diameter of the TL and FL were assessed and compared with the preoperative CTA findings. End points. The primary end point was AD-related death. Secondary end points were major adverse events and secondary interventions that occurred perioperatively and during the follow-up period. Major adverse events included acute renal failure, major stroke,
organ ischemia, aneurysmal dilation, retrograde dissection, endoleak, and stent graft-induced new entry. Follow-up. Postoperative medical management included beta blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and calcium antagonists administered alone or in combination to maintain patients’ systolic blood pressure at <140 mm Hg. Antiplatelet therapy was recommended for patients who had undergone bypass surgery, such as that targeting the carotid-carotid artery, aorta-carotid artery, or carotid-subclavian artery. After treatment, patients were evaluated at 3 months, 6 months, and 12 months and yearly thereafter. At every follow-up visit, the patients received a thorough clinical evaluation and CT scan to assess aortic remodeling. In case of anomalous findings, digital subtraction angiography was performed. Statistical analysis. The results were analyzed with SPSS version 20.0 (IBM Corp, Armonk, NY). Data were assessed for normality and expressed as number (%) for category and as mean 6 standard deviation or median (range) for continuous variables. Categorical variables were analyzed using the c2 or Fisher exact test, and continuous variables were analyzed using the twotailed Student t-test or Mann-Whitney U test. The baseline characteristics and procedural factors associated with the primary and secondary end points were explored using a logistic regression model. Factors for which P < .10 in the univariate analysis were included in the multivariate analysis. The results were represented as
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Fig 3. Computed tomography (CT) images of multichanneled aortic dissection (MCAD) without full true lumen (TL) collapse. The morphology of the multiple channels indicated a second dissection in the outer wall of the original false lumen (FL), which had a “true-false-false” lumen configuration (A-D). The incompletely collapsed TL showed less pronounced distal collapse with an apparently normal distal capacity. The additional FL at the outer curvature was perfused with partial thrombosis (C-F). Malperfusion syndrome was caused by the static obstruction of the left renal artery (G).
hazard ratios and 95% confidence intervals. Survival rates were derived using Kaplan-Meier analysis. A P value of < .05 was considered significant.
RESULTS A total of 54 consecutive patients with MCAD (8.4%; age, 49.9 6 11.8 years) were reviewed of 644 patients who were diagnosed with type B AD. Fifty of 54 (92.6%) were male, which was more frequently associated with MCAD. Thirty-seven patients had acute type B AD, whereas 17 patients (31.5%) had chronic type B AD and presented with recurrent chest or back pain. A total of 36 patients (66.7%), including 17 with chronic AD and 19 with acute AD, had previous dissection history. The patients’ characteristics are summarized in Table I. CTA findings indicated that six patients (11.1%) showed signs of aortic rupture when admitted to the center, all of whom were in the MCAD with full TL collapse group (26.1%; P ¼ .004). The preoperative mortality rate was 7.4% (4 of 54), and there was a significant difference in the mortality rates of the MCAD with full TL collapse (17.4%) and without full TL collapse (0%; P ¼ .028) groups. In the MCAD with full TL collapse group, 17.4% of patients presented with quadruple-channeled ADs. The percentage of large entry tears ($10 mm) in the MCAD with full TL collapse group (78.3%) was higher than in
the MCAD without full TL collapse group (48.4%; P ¼ .026). MCAD patients with full TL collapse were more frequently diagnosed with malperfusion syndrome, and there was a statistical difference between the two groups (P ¼ .047). The mean maximum diameter of the affected aorta in patients with full TL collapse (54.1 6 15.1 mm) was much larger than that in patients without full TL collapse (42.6 6 9.2 mm; P ¼ .002). The mean diameter of the primary entry tear tended to be larger in the MCAD with full TL collapse group, but the difference between the groups was not significant (P ¼ .067). The aortic morphologic features and characteristics of the two groups are presented in Table II. Procedural details. In the MCAD with full TL collapse group, 42.1% of patients underwent TEVAR urgently, which was a significantly higher rate than in the MCAD without full TL collapse group (9.7%; P ¼ .013). Intraoperative intravascular ultrasound-assisted TEVAR was more frequently performed in the MCAD with full TL collapse group (P ¼ .030). In addition, the percentage of coverage of the LSA in TEVAR was higher in patients with fully collapsed TLs (P ¼ .004). The procedural details are described in Table III. The clinical success rates of MCAD with and without full TL collapse were 94.7% and 100%, respectively. One
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Table I. Baseline characteristics of patients with multichanneled aortic dissection (MCAD) Variable Age, years Male sex
MCAD with full TL collapse (n ¼ 23) 48.9 6 8.1
MCAD without full TL collapse (n ¼ 31) 50.5 6 14.1
.630
22 (95.7)
28 (90.3)
.628
17 (73.9)
20 (64.5)
Dissection phase Acute dissection Chronic dissection Time interval of onset, days
.462 6 (26.1)
11 (35.5)
7.2 (1-60)
18.6 (1-180)
No. of chest pain Once Twice (recurrent pain)
P value
.180 .436
9 (39.1) 14 (60.9)
9 (29.0) 22 (71.0)
Femoral pulses Normal (þþ)
8 (34.9)
14 (45.2)
.443
Reduced (þ)
13 (56.5)
16 (51.6)
.721
Disappeared in at least one leg () Previous dissection history Signs of aortic rupture
2 (8.7)
1 (3.2)
.569
14 (60.9)
22 (71.0)
.436
6 (26.1)
0
.004
Comorbidity Hypertension Diabetes mellitus
22 (95.7)
25 (80.6)
.218
2 (8.7)
3 (9.7)
1.000
Marfan syndrome
1 (4.3)
5 (16.1)
.224
Current smoking
11 (47.8)
9 (29.0)
.254
Aortic surgery history
1 (4.3)
7 (22.6)
.119
Bicuspid aortic valve
3 (13.0)
5 (16.1)
1.000 1.000
Family history
2 (8.7)
4 (12.9)
Preprocedural death
4 (17.4)
0
.028
Preoperative laboratory data BUN, mmol/L Creatinine, mmol/L INR Hemoglobin, g/L
6.7 6 2.8
8.0 6 5.9
123.3 6 76.3
87.3 6 35.3
.025
1.1 6 0.3
.643
1.1 6 0.1 117.9 6 20.7
124.6 6 21.8
.318
.253
BUN, Blood urea nitrogen; INR, international normalized ratio; TL, true lumen. Continuous variables are presented as mean 6 standard deviation or median (range), and categorical variables are presented as number (%).
intraoperative death occurred in a patient with full TL collapse. This patient with an isolated ascending aortic aneurysm (5.5 cm in maximum diameter) underwent TEVAR and chimney stent technique in LSA urgently for progressive renal artery malperfusion; unfortunately, he died of aortic sinus rupture when the endograft systems coupled with stiff wires were being delivered to the ascending aorta. Outcomes. The overall 30-day mortality rate was 4.0% (2 of 50). Besides an intraoperative death, one MCAD patient with full TL collapse developed retrograde type A dissection at 29 days after TEVAR that caused death. The major adverse events rate associated with full TL collapse was 36.8% (7 of 19) compared with a significantly lower percentage rate in patients without full TL collapse (9.7% [3 of 31]; P ¼ .030). The most common major adverse
event was acute renal failure (8.0%), followed by retrograde dissection (4.0%), organ ischemia (4.0%), major stroke (2.0%), and paraplegia (2.0%). No differences were noted in these major adverse events between groups (Table IV). The mean duration of follow-up was 25.6 6 13.2 months (range, 3-53 months). Overall mortality during follow-up was 6.0%, and the AD-related mortality was 2.0%. In the MCAD with full TL collapse group, one patient died of aortic rupture at 3 months after TEVAR; the other one died of multiple organ dysfunction 3 days after a secondary intervention (debranching and endovascular repair; Fig 4). One death in the MCAD without full TL collapse group was related to gastric cancer. There were no significant differences regarding all-cause and AD-related mortality between groups during follow-up of endograft implantation. A high incidence of major
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Table II. Aortic morphology and characteristics Variable
MCAD with full TL collapse (n ¼ 23)
MCAD without full TL collapse (n ¼ 31)
19 (82.6)
31 (100)
Dissection morphology
P value .028
Triple channeled Quadruple channeled
4 (17.4)
Arch branches affected
0
21 (91.3)
26 (83.9)
At the inner curvature
18 (78.3)
22 (70.9)
At the outer curvature
5 (21.7)
9 (29.0)
5 (21.7)
6 (19.4)
.830 .846
Location of the PET
.685 .545
No. of side branches involved LSA SMA
8 (34.8)
10 (32.3)
CA
12 (52.2)
15 (48.4)
.783
RRA
11 (47.8)
9 (29.0)
.157
LRA
12 (52.2)
12 (38.7)
.325 .010
19 (82.6)
15 (48.4)
Mean diameter of the PET, mm
IA
14.6 6 8.3
10.9 6 6.1
.069
Large entry tear ($10 mm)
18 (78.3)
15 (48.4)
.026
Thoracoabdominal extension
23 (100)
31 (100)
Malperfusion syndrome
12 (52.2)
8 (25.8)
Pleural fluid
13 (56.5)
10 (32.3)
.075
32.7 (0-80.5)
34.1 (0-95.5)
.738
Maximum diameter of affected aorta, mm
54.1 6 15.1
42.6 6 9.2
.002
No. of entry tears
3.6 (1-5)
3.7 (1-7)
.720
Distance between LSA and PET, mm
.047
CA, Celiac artery; IA, iliac artery; LRA, left renal artery; LSA, left subclavian artery; MCAD, multichanneled aortic dissection; PET, primary entry tear; RRA, right renal artery; SMA, superior mesenteric artery; TL, true lumen. Continuous variables are presented as mean 6 standard deviation or median (range), and categorical variables are presented as number (%).
Table III. Procedural details of patients with multichanneled aortic dissection (MCAD) Variable Urgent TEVAR
MCAD with full TL collapse (n ¼ 19)
MCAD without full TL collapse (n ¼ 31)
P value
8 (42.1)
3 (9.7)
Hospital stay, days
13.5 6 8.1
12.6 6 4.1
.585
Duration of procedure, minutes
92.1 6 37.8
102.7 6 20.3
.202
109.1 6 18.7
114.0 6 19.6
Contrast agent dose, mL Intraprocedural death Clinical success
1 (5.3) 18 (94.7)
0 31 (100)
.013
.385 .380 .380
Stent graft types Valiant
5 (26.3)
4 (12.9)
.273
Valiant Captivia
7 (36.8)
13 (41.9)
.721
Ankura
3 (15.6)
3 (9.7)
.661
Zenith TX2
3 (15.6)
9 (29.0)
.332
1 (5.3)
2 (6.4)
1.000
7 (36.8)
3 (9.7)
.030
TAG IVUS-assisted TEVAR TEVAR þ chimney or debranching
5 (26.3)
6 (19.4)
.727
15 (78.9)
18 (58.1)
.218
Type Ia
7 (36.8)
12 (38.7)
.895
Type Ib
2 (10.5)
1 (3.2)
.549
Coverage of LSA Endoleaks
IVUS, Intravascular ultrasound; LSA, left subclavian artery; TEVAR, thoracic endovascular aortic repair; TL, true lumen. Continuous variables are presented as mean 6 standard deviation, and categorical variables are presented as number (%).
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Table IV. Perioperative events after thoracic endovascular aortic repair (TEVAR) and follow-up results Variable
Total cohort (N ¼ 50)
MCAD with full TL collapse (n ¼ 19)
MCAD without full TL collapse (n ¼ 31)
P value
Perioperative outcomes (30 days) AD-related deaths
2 (4.0)
2 (10.5)
0
.140
10 (20.0)
7 (36.8)
3 (9.7)
.030
ARF
4 (8.0)
3 (15.8)
1 (3.2)
Retrograde dissection
2 (4.0)
2 (10.5)
0
Organ ischemia
2 (4.0)
1 (5.3)
1 (3.2)
Major stroke
1 (2.0)
0
1 (3.2)
Paraplegia
1 (2.0)
1 (5.3)
0
All deaths
3 (6.0)
2 (10.5)
1 (3.2)
AD-related deaths
1 (2.0)
1 (5.3)
0
.380
20 (40.0)
9 (47.4)
11 (35.5)
.405
Aneurysmal dilation
8 (16.0)
5 (26.3)
3 (9.7)
Endoleaks
8 (16.0)
3 (15.8)
5 (16.1)
SINE
3 (6.0)
1 (5.3)
2 (6.5)
1 (2.0)
Major adverse events
Follow-up events
Major adverse events
Organ ischemia
.549
0
1 (3.2)
13 (26.0)
7 (36.8)
6 (19.4)
.199
Incomplete
20 (40.0)
10 (52.6)
10 (32.3)
.153
Complete
28 (56.0)
7 (36.8)
21 (67.7)
.033
25.6 6 13.2
22.8 6 17.1
27.2 6 10.2
.264
Secondary intervention FL thrombosis
Follow-up period, months
AD, Aortic dissection; ARF, acute renal failure; FL, false lumen; MCAD, multichanneled aortic dissection; SINE, stent graft-induced new entry; TL, true lumen. Continuous variables are presented as mean 6 standard deviation, and categorical variables are presented as number (%).
adverse events (40%) had been noted during follow-up, which did not result in a significant difference between the two groups (Table IV). We observed no statistical difference in secondary interventions (36.8% vs 19.4%; P ¼ .199). The overall rate of complete thrombosis in FLs was 56.0%, and it presented with a higher rate in patients without full TL collapse (67.7%) than in patients with full TL collapse (36.8%; P ¼ .033). The overall mortality rate for all MCADs was 16.7% (9 of 54) perioperatively and during follow-up. There was a significant difference in the overall survival rate of the patients with and without full TL collapse at 3 years after TEVAR (55.4% vs 94.7%; P ¼ .002; Fig 5). There was no independent predictor for the 30-day major adverse events in the multivariate analysis (Table V). The univariate analysis revealed that signs of aortic rupture, quadruple-channeled AD, maximum diameter of the affected aorta, and malperfusion syndrome were significant predictors of AD-related deaths. In multivariate analysis, however, the maximum diameter of the affected aorta (hazard ratio, 1.176; 95% confidence interval, 1.015-1.362; P ¼ .031) is the only independent predictor of AD-related deaths (Table VI).
DISCUSSION So far, most descriptions of MCAD have been limited to isolated case reports5,13-15 or studies evaluating poor outcomes and complications by open surgery and endovascular treatment.6,7 According to previous studies, the incidence of MCAD varied from 4.9% to 9%.5-7,13-15 We observed dissections with more than two adjacent FLs in 54 (8.4%) of 644 patients treated with TEVAR. This incidence was similar to that in previous reports, suggesting that the condition may occur frequently and is of great concern. Ando et al6 noted three-channeled AD in 31 (7.3%) of 426 patients with AD who underwent surgical treatment, and the incidence was higher in patients with Marfan syndrome (58% [18 of 31]). However, Sueyoshi et al7 found no significant differences between MCAD and DCAD in terms of clinical characteristics, including the presence of Marfan syndrome. In our study, the percentage of patients who had both Marfan syndrome and MCAD was 11.1% (6 of 54). Because the morbidity of type B AD in patients diagnosed with Marfan syndrome was not high (9%), it is unclear whether multichanneled morphologic features are associated with vasculitis diseases.16,17
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Fig 4. Aneurysmal dilation of multichanneled aortic dissection (MCAD) with full true lumen (TL) collapse after thoracic endovascular aortic repair (TEVAR) and chimney stent in left subclavian artery (LSA). Computed tomography (CT) images at 26 months showed that the false lumens (FLs) near the proximal entry tear were completely thrombosed and the chimney stent was patent (A and B). The “true-false-false” lumen configuration still appeared in the distal endograft (C and D). The FLs, with an increased blood flow from TL through the distal re-entry tears, were expanding into dissecting aneurysms.
Fig 5. Overall survival of multichanneled aortic dissection (MCAD) patients with and without full true lumen (TL) collapse.
In all the previous reports, however, the most important question remains unanswered: Why does MCAD have a significantly poorer survival rate than DCAD? The results of this study suggest that the morphologic features of the TL and FLs contributed to the mixed causes,
including fragility of the aortic wall and multiple-lumen configuration as the pathologic background and complicated AD hemodynamics as the most important provocative aspect. Fragility of the aortic wall and multiple-lumen configuration may be deemed the most basic factors contributing to the high mortality rate found in our study. A secondary FL may develop on the lateral wall of the first TL, which has a “true-false-false” or “false-false-true” lumen configuration. In our study, this multichanneled morphology was more common in patients without full TL collapse (Fig 3). A secondary FL may also exist on the other side of the TL, which has a “false-true-false” lumen configuration. This morphology may often cause full TL collapse (Fig 2). DCAD was complicated by additional new FLs that usually had no re-entry formation. Then, an increase in inflow and low or no outflow increased the pressure in the FLs and caused the TL to collapse.18 In addition, because the lateral wall of the FLs and dissection flaps were fragile and pliable as a result of the two layers of dissection, the patients’ risk of rupture
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Table V. Univariate and multivariate analysis for 30-day major adverse events Univariate analysis Parameter Malperfusion syndrome
Multivariate analysis
HR
95% CI
P value
HR
95% CI
P value
3.867
1.049-14.248
.042
1.933
0.422-8.856
.396
12.000
1.125-127.969
.040
2.717
0.196-37.650
.456
Maximum diameter of the affected aorta
1.081
1.019-1.147
.009
1.038
0.967-1.114
.300
Full TL collapse
7.179
1.687-30.552
.008
3.994
0.821-19.431
.086
Quadruple channeled
CI, Confidence interval; HR, hazard ratio; TL, true lumen.
Table VI. Univariate and multivariate analysis for aortic dissection (AD)-related deaths Univariate analysis
Multivariate analysis
HR
95% CI
P value
Signs of aortic rupture
46.000
5.048-419.440
.001
Quadruple channeled
22.000
1.959-247.056
.012
1.188
1.075-1.313
.001
22.000
2.484-194.876
.005
Parameter
Maximum diameter of the affected aorta Malperfusion syndrome
HR
95% CI
P value
1.176
1.015-1.362
.031
CI, Confidence interval; HR, hazard ratio.
was increased.6 Sueyoshi et al7 demonstrated that the presence of MCAD was the most powerful predictor of AD-related deaths. The literature also indicates that the aortic wall may suffer from medial degeneration and cystic medial necrosis.6,15 These factors may be the pathologic background for propagation of MCAD. As is well known, hemodynamics plays a major role in the initiation, acute propagation, and chronic development of dissections.19 A transmural pressure gradient between the TL and FLs is generated across the dissection flap and moves it. If the dissection flap does not balance the pressures of different channels, acute propagation causes signs of aortic rupture or hemodynamic instability. The primary strategy of intervention is closure of the primary entry tear to decompress the TL, to restore distal perfusion by expanding the TL, and finally to stabilize segments with impending rupture (Video, online only).20,21 Full TL collapse causes a series of detrimental effects and increases the risk of aortic rupture. In our study, there was a significant difference in the perioperative mortality rate between patients with full TL collapse (17.4%) and patients without full TL collapse (0%; P ¼ .028). In clinical practice, however, there were no tools available to identify hemodynamic instability in a timely and effective manner unless there were signs of instability. Thus, we suppose the morphology of full TL collapse may be an indicator of hemodynamic instability because we could not conclusively determine the reason for the observed disparity. To date, few studies have examined the role of natural history and factors affecting the effectiveness of TEVAR for treating MCAD. Sueyoshi et al7 reported that of 20 MCAD patients, 9 patients suffered from AD-related
death (45%), including aortic rupture (8 of 20) and redissection (1 of 20), whereas the mortality rate in patients with DCAD was much lower (17.4%; P ¼ .0002). Ando et al6 found that recurring pain in patients with chronic AD was a strong indicator of three-channeled dissection. Similarly, in this study, the overall mortality rate for patients with MCAD was 16.7% perioperatively and during the follow-up period. Therefore, clinical observation of MCAD was of importance during either interpretation of the initial CTA findings or the follow-up period. MCAD patients with full TL collapse should alert their physicians of the possibility of hemodynamic instability and the necessity of urgent intervention. In our cohort, the morbidity of 30-day major adverse events was 20.0% (10 of 50), and a significant difference was found between the two groups (36.8% vs 9.7%; P ¼ .030). Apart from acute malperfusion and hemodynamic redistribution after TEVAR, endograft-related aortic wall injury may be another important risk factor for the adverse events, especially retrograde dissection.22 Cheng et al15 reported that a patient with triple-channeled AD developed retrograde type A AD during endograft repair. Identifying the possible risk factors for AD-related deaths and future adverse events would improve the management of patients with multichanneled morphologic features. Several studies have suggested that saccular formation of FLs, number of intimal tears, large entry tears ($10 mm), location of the primary entry tear, and configuration of the FL may influence the aortic growth rate during the follow-up period.23-25 In this study, however, the maximum diameter of the affected aorta was the only independent predictor of AD-related deaths. These findings suggested that increased inflow due to a large entry tear and damaged FL media may
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result in hemodynamic redistribution and acute dissection propagation. Study limitations. First, this study was performed as an observational study in our study population. The number of cases of MCAD was relatively small; thus, the results should be limited to hypothesis deriving. Second, nongated CT technology was used, and not all patients were examined with CT in the follow-up, which might have biased our results. Third, we did not compare the DCAD with the study cohort; therefore, it has unfortunately not been investigated whether TL collapse in general (MCAD and DCAD) yields worse outcome. However, we attempted to highlight this kind of type B AD with multichanneled morphology as a high mortality was observed in clinical practice.
CONCLUSIONS Of patients with type B AD, 8.4% presented with multichanneled morphology. Urgent or elective TEVAR was indicated in all our patients with MCAD. In patients with MCAD, full TL collapse was associated with worse outcomes, and this finding may represent an adjunct for physicians to stratify patients at high risk of complications and indicate the need for more urgent or emergent repair. Further studies are necessary to determine the optimal therapeutic strategy for this type of dissection. We thank Professor Xiao Yun Xu (Department of Chemical Engineering, Imperial College London, South Kensington Campus, London, UK) for her support in the hemodynamic discussion of aortic dissection.
AUTHOR CONTRIBUTIONS Conception and design: BG, DG, WF Analysis and interpretation: BG, KH, XX, PL, WF Data collection: KH, ZS, YS, PL Writing the article: BG, DG Critical revision of the article: BG, DG, XX, ZS, WF Final approval of the article: BG, KH, DG, XX, ZS, YS, PL, WF Statistical analysis: BG, YS Obtained funding: Not applicable Overall responsibility: WF
REFERENCES 1. Erbel R, Aboyans V, Boileau C, Bossone E, Bartolomeo RD, Eggebrecht H, et al. 2014 ESC guidelines on the diagnosis and treatment of aortic diseases: document covering acute and chronic aortic diseases of the thoracic and abdominal aorta of the adult. The Task Force for the Diagnosis and Treatment of Aortic Diseases of the European Society of Cardiology (ESC). Eur Heart J 2014;35: 2873-926. 2. Andacheh ID, Donayre C, Othman F, Walot I, Kopchok G, White R. Patient outcomes and thoracic aortic volume and morphologic changes following thoracic endovascular aortic repair in patients with complicated chronic type B aortic dissection. J Vasc Surg 2012;56:644-50.
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3. White RA, Miller DC, Criado FJ, Dake MD, Diethrich EB, Greenberg RK, et al. Report on the results of thoracic endovascular aortic repair for acute, complicated, type B aortic dissection at 30 days and 1 year from a multidisciplinary subcommittee of the Society for Vascular Surgery Outcomes Committee. J Vasc Surg 2011;53:1082-90. 4. Nienaber CA, Kische S, Rousseau H, Eggebrecht H, Rehders TC, Kundt G, et al. Endovascular repair of type B aortic dissection: long-term results of the randomized investigation of stent grafts in aortic dissection trial. Circ Cardiovasc Interv 2013;6:407-16. 5. McReynolds RA, Shin MS, Sims RD. Three-channeled aortic dissection. AJR Am J Roentgenol 1978;130:549-52. 6. Ando M, Okita Y, Tagusari O, Kitamura S, Matsuo H. Surgery in three-channeled aortic dissection. A 31-patient review. Jpn J Thorac Cardiovasc Surg 2000;48:339-43. 7. Sueyoshi E, Nagayama H, Hayashida T, Sakamoto I, Uetani M. Comparison of outcome in aortic dissection with single false lumen versus multiple false lumens: CT assessment. Radiology 2013;267:368-75. 8. Williams DM, Lee DY, Hamilton BH, Marx MV, Narasimham DL, Kazanjian SN, et al. The dissected aorta: part III. Anatomy and radiologic diagnosis of branch-vessel compromise. Radiology 1997;203:37-44. 9. Chung JW, Elkins C, Sakai T, Kato N, Vestring T, Semba CP, et al. True-lumen collapse in aortic dissection: part I. Evaluation of causative factors in phantoms with pulsatile flow. Radiology 2000;214:87-98. 10. Fanelli F, Cannavale A, O’Sullivan GJ, Gazzetti M, Cirelli C, Lucatelli P, et al. Endovascular repair of acute and chronic aortic type B dissections: main factors affecting aortic remodeling and clinical outcome. JACC Cardiovasc Interv 2016;9:183-91. 11. Williams DM, Joshi A, Dake MD, Deeb GM, Miller DC, Abrams GD. Aortic cobwebs: an anatomic marker identifying the false lumen in aortic dissectiondimaging and pathologic correlation. Radiology 1994;190:167-74. 12. Midulla M, Fattori R, Beregi JP, Dake M, Rousseau H. Aortic dissection and malperfusion syndrome: a when, what and how-to guide. Radiol Med 2013;118:74-88. 13. Einstein AJ, Dellegrottaglie S, Rajagopalan S. Triple-barrelled aortic dissection in Ehlers-Danlos syndrome. Heart 2006;92: 1166. 14. Sueyoshi E, Nagayama H, Sakamoto I, Ariyoshi T, Hashizume K, Eishi K, et al. Triple-barreled aortic dissection developing into quadruple-barreled dissection. Ann Thorac Surg 2012;93:1320. 15. Cheng Z, Zhao S, Wang X. Acute retrograde ascending aortic dissection during thoracic endovascular aortic repair in a rare triple-barreled aortic dissection. Circ J 2014;78:2328-9. 16. den Hartog AW, Franken R, Zwinderman AH, Timmermans J, Scholte AJ, van den Berg MP, et al. The risk for type B aortic dissection in Marfan syndrome. J Am Coll Cardiol 2015;65: 246-54. 17. Schoenhoff FS, Jungi S, Czerny M, Roost E, Reineke D, Matyas G, et al. Acute aortic dissection determines the fate of initially untreated aortic segments in Marfan syndrome. Circulation 2013;127:1569-75. 18. Chung JW, Elkins C, Sakai T, Kato N, Vestring T, Semba CP, et al. True-lumen collapse in aortic dissection: part II. Evaluation of treatment methods in phantoms with pulsatile flow. Radiology 2000;214:99-106. 19. Williams DM, Lee DY, Hamilton BH, Marx MV, Narasimham DL, Kazanjian SN, et al. The dissected aorta: percutaneous treatment of ischemic complicationsd principles and results. J Vasc Interv Radiol 1997;8:605-25. 20. Weiss G, Wolner I, Folkmann S, Sodeck G, Schmidli J, Grabenwoger M, et al. The location of the primary entry tear
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in acute type B aortic dissection affects early outcome. Eur J Cardiothorac Surg 2012;42:571-6. 21. Cheng Z, Wood NB, Gibbs RG, Xu XY. Geometric and flow features of type B aortic dissection: initial findings and comparison of medically treated and stented cases. Ann Biomed Eng 2015;43:177-89. 22. Dong ZH, Fu WG, Wang YQ, Guo DQ, Xu X, Ji Y, et al. Retrograde type A aortic dissection after endovascular stent graft placement for treatment of type B dissection. Circulation 2009;119:735-41. 23. van Bogerijen GH, Tolenaar JL, Rampoldi V, Moll FL, van Herwaarden JA, Jonker FH, et al. Predictors of aortic growth in uncomplicated type B aortic dissection. J Vasc Surg 2014;59:1134-43.
24. Tolenaar JL, van Keulen JW, Jonker FH, van Herwaarden JA, Verhagen HJ, Moll FL, et al. Morphologic predictors of aortic dilatation in type B aortic dissection. J Vasc Surg 2013;58: 1220-5. 25. Kim TH, Ko YG, Kwon SW, Choi D, Lee DY, Shim WH, et al. Large false lumen area is a predictor of failed false lumen volume reduction after stent-graft repair in type B aortic dissection. J Endovasc Ther 2014;21:697-706. Submitted Oct 7, 2016; accepted Dec 27, 2016.
Additional material for this article may be found online at www.jvascsurg.org.
ABSTRACT Objective: Clinical outcomes after thoracic endovascular aortic repair (TEVAR) for patients with multichanneled aortic dissection (MCAD) are poorly understood but seem substantially different from those for patients with double-channeled aortic dissection (AD). This study compared the anatomic and clinical factors for patients with MCAD who underwent TEVAR with or without full true lumen (TL) collapse. Methods: From January 2012 to March 2016, 54 of 644 consecutive type B AD patients (8.4%) who presented with MCAD were reviewed. Patients were classified as MCAD with full TL collapse and without full TL collapse according to computed tomography angiography findings. We analyzed potential variables including clinical characteristics, anatomic morphologic features, and procedural details. Multivariable analysis was performed to determine independent predictors of AD-related deaths. Results: A total of four patients (7.4%) died preoperatively of aortic rupture, all of whom experienced full TL collapse. MCAD patients with full TL collapse showed significantly higher 30-day major adverse events than those without full TL collapse (36.8% vs 9.7%; P ¼ .030). The mean follow-up duration was 25.6 6 13.2 months (range, 3-53 months). The overall mortality for all MCAD patients was 16.7%, whereas the follow-up major adverse events rate was 40.0% after TEVAR. Significant differences were present between patients with full TL collapse and patients without full TL collapse in survival at 3 years (55.4% vs 94.7%; P ¼ .002). Maximum diameter of affected aorta (hazard ratio, 1.176; 95% confidence interval, 1.015-1.362; P ¼ .031) was identified as the only predictor of AD-related deaths. Conclusions: MCAD was identified in a small but not insignificant number of our patients presenting with type B AD. Urgent or elective TEVAR was indicated in all our patients with MCAD. In patients with MCAD, full TL collapse was associated with worse outcomes, and this finding may indicate the need for more urgent or emergent repair. (J Vasc Surg 2017;-:1-11.)
Thoracic endovascular aortic repair (TEVAR) is a promising treatment for patients with type B aortic dissection (AD) with chest pain, malperfusion, rupture, and acute aortic enlargement.1-4 The therapeutic strategy and risk factors for AD-related events and deaths are well established for patients with classic double-channeled AD (DCAD). However, multichanneled AD (MCAD) is considered a relatively rare condition and was first reported in 1978 by McReynolds et al.5 Previous studies suggested that the presence of MCAD is a powerful predictor of AD-related deaths after open surgery or TEVAR.6,7 The elevated pressure in different false lumens (FLs) for patients with MCAD results in complex communications to the true lumen (TL), which may cause these patients to
From the Department of Vascular Surgery, Institute of Vascular Surgery,a and Department of Radiology,b Zhongshan Hospital, Fudan University.
be at a higher risk for TL collapse, aneurysm, and rupture. Treatment for TL collapse involves decreasing the flow of blood into the FL and increasing the flow from it.8,9 On the basis of this mechanism, MCAD detected on computed tomography angiography (CTA) might help predict which patients will suffer from adverse events. However, the clinical characteristics, natural history, and follow-up outcomes of MCAD after TEVAR have not been widely recognized or evaluated. To the best of our knowledge, the morphologic classifications of MCAD and perioperative and midterm clinical outcomes after TEVAR have not been previously evaluated. The purpose of the study was to analyze a cohort of patients who underwent TEVAR for all MCADs in our center. We reported the clinical features, morphologic findings, perioperative outcomes, and follow-up results of 54 patients with MCAD to explore its progression and to evaluate the role of TEVAR.
Author conflict of interest: none. Additional material for this article may be found online at www.jvascsurg.org. Correspondence: Weiguo Fu, MD, Department of Vascular Surgery, Zhongshan Hospital Fudan University, Institute of Vascular Surgery, Fudan University, 180 Fenglin Rd, Shanghai 200032, PR China (e-mail: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a conflict of interest. 0741-5214 Copyright Ó 2017 by the Society for Vascular Surgery. Published by Elsevier Inc. http://dx.doi.org/10.1016/j.jvs.2016.12.145
METHODS Study design and population of patients. Data collection and analysis for this study were approved by the Institutional Review Board from the Ethics Committee of Zhongshan Hospital Fudan University. Informed consent was obtained from all patients. This was a retrospective review of 644 consecutive patients with type B AD in our vascular center between January 2012 and March 1
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Fig 1. Summary flow diagram by presentation and treatment of the patient. AD, Aortic dissection; TEVAR, thoracic endovascular aortic repair.
2016. A total of 54 patients with MCAD were analyzed in this study. Clinical data regarding patients’ baseline characteristics, presentation, inpatient management, and follow-ups were collected. The data were analyzed to determine the perioperative complications and followup outcomes of MCAD patients with or without full TL collapse according to the CTA findings. Twenty-three patients who experienced full TL collapse were included in the MCAD with full TL collapse group, and the remaining 31 patients were included in the MCAD without full TL collapse group. In general, patients with complicated acute type B AD underwent TEVAR in a subacute phase.10 Notably, a specific indication for TEVAR was MCAD in patients with severely recurrent chest or back pain. All patients who presented with signs of rupture and with suspected or known aortic propagation underwent TEVAR urgently (Fig 1). TEVAR procedure. TEVAR was performed on patients under general anesthesia using commercially available endografts (Valiant and Valiant Captivia [Medtronic, Minneapolis, Minn]; Zenith TX2 [Cook, Bjaeverskov, Denmark]; Ankura [Lifetech, Shenzhen, China]; or TAG [W. L. Gore & Associates, Flagstaff, Ariz]) through the unilateral common femoral artery with either traditional exposure or a percutaneous puncture secured by two ProGlide stitches (Abbott Vascular, Abbott Park, Ill). Oversizing (3%-5%) was calculated according to the distance from the adventitia to the adventitia of the proximal landing zone on CTA. A basic goal of TEVAR was to completely cover the primary entry tear with a single 15- to 20-cm-long endograft unless there were endoleaks after the initial endograft repair. We avoided performing angioplasty after deployment. If the proximal landing zone (the distance from the origin of the left
subclavian artery [LSA] to the primary entry) measured <15 mm, one of two strategies would be applied to create an extra anchoring area: (1) intentional coverage of LSA, if the right vertebral artery was patent and the left one was not dominant; or (2) revascularization of LSA with bypass or chimney technique. If necessary, intravascular ultrasound catheters were introduced to intraoperatively confirm the location of the TL or FLs and the origin of the visceral arteries. We primarily used the Vision PV 8.2F, 10 MHz catheter (Volcano Therapeutics, Rancho Cordova, Calif) for aortic procedures. Definitions and image analysis. AD was classified as type B, according to the Stanford classification, if the dissection did not involve the ascending aorta. Acute AD was defined as <14 days from the onset of symptoms; chronic AD was defined by an elapsed time $14 days from symptom onset.1,4 MCAD was defined as AD with more than two FLs on contrast-enhanced computed tomography (CT) images. We excluded the images with just a single FL that wraps around the TL in a U or O shape according to the CTA reconstruction. The length of each FL was >2 cm to distinguish it from the aortic cobweb,7,11 ulcerated mural thrombus, intimal tears, and penetrating ulcers. The diagnoses of MCAD were made on the initial or follow-up CT findings. Malperfusion syndrome was defined as end-organ ischemia caused by branch vessel involvement and resulting in clinical symptoms and functional impairment in a wide range of arterial beds.12 We included free rupture (in which disruption of all the layers of the aortic wall leads to massive hematoma) and impending rupture in the analysis. Signs of active contrast material extravasation from the aorta, large pleural effusion, periaortic hematoma, mediastinal hematoma, areas of compromised
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Fig 2. Computed tomography (CT) images of multichanneled aortic dissection (MCAD) with full true lumen (TL) collapse. In the proximal descending thoracic aorta, the TL, which had a small channel, was severely compressed by two isolated false lumens (FLs; A and B). There was a “false-true-false” lumen configuration (coexisting dissections on either side of the TL). However, the capacity of the TL (<3 mm in diameter) was fully collapsed from the distal thoracic aorta to the abdominal aorta, which indicated pronounced distal collapse of a flakelike lumen (C-H). Dynamic obstruction of the superior mesenteric artery was also observed (D and E).
perfusion, and symptoms related to the enlarging dissected aorta (hoarseness, new-onset chest pain) indicated rupture. We categorized patients with the TL that completely collapsed because of compression of FLs, resulting in pronounced distal collapse of a flakelike lumen (TL <5%) at least 5 cm in length, as those with full TL collapse (Fig 2). Patients with the TL that incompletely collapsed, resulting in a less pronounced distal collapse with an apparently normal distal TL, were categorized as patients without full TL collapse (Fig 3). Clinical success was defined as an outcome in which the preoperative pathologic conditions and symptoms were resolved by TEVAR. Event rates were defined as the total number of vascular events that led to separate clinical presentations during the study period. Preoperative and follow-up evaluations were performed using spiral CTA. CTA images were independently analyzed by two experienced cardiovascular radiologists (Y.S. and P.L.), who paid particular attention to the morphologic features of dissected aorta. The radiologists were blinded to the clinical data when reviewing the images. The aortic changes regarding the morphology and diameter of the TL and FL were assessed and compared with the preoperative CTA findings. End points. The primary end point was AD-related death. Secondary end points were major adverse events and secondary interventions that occurred perioperatively and during the follow-up period. Major adverse events included acute renal failure, major stroke,
organ ischemia, aneurysmal dilation, retrograde dissection, endoleak, and stent graft-induced new entry. Follow-up. Postoperative medical management included beta blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and calcium antagonists administered alone or in combination to maintain patients’ systolic blood pressure at <140 mm Hg. Antiplatelet therapy was recommended for patients who had undergone bypass surgery, such as that targeting the carotid-carotid artery, aorta-carotid artery, or carotid-subclavian artery. After treatment, patients were evaluated at 3 months, 6 months, and 12 months and yearly thereafter. At every follow-up visit, the patients received a thorough clinical evaluation and CT scan to assess aortic remodeling. In case of anomalous findings, digital subtraction angiography was performed. Statistical analysis. The results were analyzed with SPSS version 20.0 (IBM Corp, Armonk, NY). Data were assessed for normality and expressed as number (%) for category and as mean 6 standard deviation or median (range) for continuous variables. Categorical variables were analyzed using the c2 or Fisher exact test, and continuous variables were analyzed using the twotailed Student t-test or Mann-Whitney U test. The baseline characteristics and procedural factors associated with the primary and secondary end points were explored using a logistic regression model. Factors for which P < .10 in the univariate analysis were included in the multivariate analysis. The results were represented as
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Fig 3. Computed tomography (CT) images of multichanneled aortic dissection (MCAD) without full true lumen (TL) collapse. The morphology of the multiple channels indicated a second dissection in the outer wall of the original false lumen (FL), which had a “true-false-false” lumen configuration (A-D). The incompletely collapsed TL showed less pronounced distal collapse with an apparently normal distal capacity. The additional FL at the outer curvature was perfused with partial thrombosis (C-F). Malperfusion syndrome was caused by the static obstruction of the left renal artery (G).
hazard ratios and 95% confidence intervals. Survival rates were derived using Kaplan-Meier analysis. A P value of < .05 was considered significant.
RESULTS A total of 54 consecutive patients with MCAD (8.4%; age, 49.9 6 11.8 years) were reviewed of 644 patients who were diagnosed with type B AD. Fifty of 54 (92.6%) were male, which was more frequently associated with MCAD. Thirty-seven patients had acute type B AD, whereas 17 patients (31.5%) had chronic type B AD and presented with recurrent chest or back pain. A total of 36 patients (66.7%), including 17 with chronic AD and 19 with acute AD, had previous dissection history. The patients’ characteristics are summarized in Table I. CTA findings indicated that six patients (11.1%) showed signs of aortic rupture when admitted to the center, all of whom were in the MCAD with full TL collapse group (26.1%; P ¼ .004). The preoperative mortality rate was 7.4% (4 of 54), and there was a significant difference in the mortality rates of the MCAD with full TL collapse (17.4%) and without full TL collapse (0%; P ¼ .028) groups. In the MCAD with full TL collapse group, 17.4% of patients presented with quadruple-channeled ADs. The percentage of large entry tears ($10 mm) in the MCAD with full TL collapse group (78.3%) was higher than in
the MCAD without full TL collapse group (48.4%; P ¼ .026). MCAD patients with full TL collapse were more frequently diagnosed with malperfusion syndrome, and there was a statistical difference between the two groups (P ¼ .047). The mean maximum diameter of the affected aorta in patients with full TL collapse (54.1 6 15.1 mm) was much larger than that in patients without full TL collapse (42.6 6 9.2 mm; P ¼ .002). The mean diameter of the primary entry tear tended to be larger in the MCAD with full TL collapse group, but the difference between the groups was not significant (P ¼ .067). The aortic morphologic features and characteristics of the two groups are presented in Table II. Procedural details. In the MCAD with full TL collapse group, 42.1% of patients underwent TEVAR urgently, which was a significantly higher rate than in the MCAD without full TL collapse group (9.7%; P ¼ .013). Intraoperative intravascular ultrasound-assisted TEVAR was more frequently performed in the MCAD with full TL collapse group (P ¼ .030). In addition, the percentage of coverage of the LSA in TEVAR was higher in patients with fully collapsed TLs (P ¼ .004). The procedural details are described in Table III. The clinical success rates of MCAD with and without full TL collapse were 94.7% and 100%, respectively. One
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Table I. Baseline characteristics of patients with multichanneled aortic dissection (MCAD) Variable Age, years Male sex
MCAD with full TL collapse (n ¼ 23) 48.9 6 8.1
MCAD without full TL collapse (n ¼ 31) 50.5 6 14.1
.630
22 (95.7)
28 (90.3)
.628
17 (73.9)
20 (64.5)
Dissection phase Acute dissection Chronic dissection Time interval of onset, days
.462 6 (26.1)
11 (35.5)
7.2 (1-60)
18.6 (1-180)
No. of chest pain Once Twice (recurrent pain)
P value
.180 .436
9 (39.1) 14 (60.9)
9 (29.0) 22 (71.0)
Femoral pulses Normal (þþ)
8 (34.9)
14 (45.2)
.443
Reduced (þ)
13 (56.5)
16 (51.6)
.721
Disappeared in at least one leg () Previous dissection history Signs of aortic rupture
2 (8.7)
1 (3.2)
.569
14 (60.9)
22 (71.0)
.436
6 (26.1)
0
.004
Comorbidity Hypertension Diabetes mellitus
22 (95.7)
25 (80.6)
.218
2 (8.7)
3 (9.7)
1.000
Marfan syndrome
1 (4.3)
5 (16.1)
.224
Current smoking
11 (47.8)
9 (29.0)
.254
Aortic surgery history
1 (4.3)
7 (22.6)
.119
Bicuspid aortic valve
3 (13.0)
5 (16.1)
1.000 1.000
Family history
2 (8.7)
4 (12.9)
Preprocedural death
4 (17.4)
0
.028
Preoperative laboratory data BUN, mmol/L Creatinine, mmol/L INR Hemoglobin, g/L
6.7 6 2.8
8.0 6 5.9
123.3 6 76.3
87.3 6 35.3
.025
1.1 6 0.3
.643
1.1 6 0.1 117.9 6 20.7
124.6 6 21.8
.318
.253
BUN, Blood urea nitrogen; INR, international normalized ratio; TL, true lumen. Continuous variables are presented as mean 6 standard deviation or median (range), and categorical variables are presented as number (%).
intraoperative death occurred in a patient with full TL collapse. This patient with an isolated ascending aortic aneurysm (5.5 cm in maximum diameter) underwent TEVAR and chimney stent technique in LSA urgently for progressive renal artery malperfusion; unfortunately, he died of aortic sinus rupture when the endograft systems coupled with stiff wires were being delivered to the ascending aorta. Outcomes. The overall 30-day mortality rate was 4.0% (2 of 50). Besides an intraoperative death, one MCAD patient with full TL collapse developed retrograde type A dissection at 29 days after TEVAR that caused death. The major adverse events rate associated with full TL collapse was 36.8% (7 of 19) compared with a significantly lower percentage rate in patients without full TL collapse (9.7% [3 of 31]; P ¼ .030). The most common major adverse
event was acute renal failure (8.0%), followed by retrograde dissection (4.0%), organ ischemia (4.0%), major stroke (2.0%), and paraplegia (2.0%). No differences were noted in these major adverse events between groups (Table IV). The mean duration of follow-up was 25.6 6 13.2 months (range, 3-53 months). Overall mortality during follow-up was 6.0%, and the AD-related mortality was 2.0%. In the MCAD with full TL collapse group, one patient died of aortic rupture at 3 months after TEVAR; the other one died of multiple organ dysfunction 3 days after a secondary intervention (debranching and endovascular repair; Fig 4). One death in the MCAD without full TL collapse group was related to gastric cancer. There were no significant differences regarding all-cause and AD-related mortality between groups during follow-up of endograft implantation. A high incidence of major
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Table II. Aortic morphology and characteristics Variable
MCAD with full TL collapse (n ¼ 23)
MCAD without full TL collapse (n ¼ 31)
19 (82.6)
31 (100)
Dissection morphology
P value .028
Triple channeled Quadruple channeled
4 (17.4)
Arch branches affected
0
21 (91.3)
26 (83.9)
At the inner curvature
18 (78.3)
22 (70.9)
At the outer curvature
5 (21.7)
9 (29.0)
5 (21.7)
6 (19.4)
.830 .846
Location of the PET
.685 .545
No. of side branches involved LSA SMA
8 (34.8)
10 (32.3)
CA
12 (52.2)
15 (48.4)
.783
RRA
11 (47.8)
9 (29.0)
.157
LRA
12 (52.2)
12 (38.7)
.325 .010
19 (82.6)
15 (48.4)
Mean diameter of the PET, mm
IA
14.6 6 8.3
10.9 6 6.1
.069
Large entry tear ($10 mm)
18 (78.3)
15 (48.4)
.026
Thoracoabdominal extension
23 (100)
31 (100)
Malperfusion syndrome
12 (52.2)
8 (25.8)
Pleural fluid
13 (56.5)
10 (32.3)
.075
32.7 (0-80.5)
34.1 (0-95.5)
.738
Maximum diameter of affected aorta, mm
54.1 6 15.1
42.6 6 9.2
.002
No. of entry tears
3.6 (1-5)
3.7 (1-7)
.720
Distance between LSA and PET, mm
.047
CA, Celiac artery; IA, iliac artery; LRA, left renal artery; LSA, left subclavian artery; MCAD, multichanneled aortic dissection; PET, primary entry tear; RRA, right renal artery; SMA, superior mesenteric artery; TL, true lumen. Continuous variables are presented as mean 6 standard deviation or median (range), and categorical variables are presented as number (%).
Table III. Procedural details of patients with multichanneled aortic dissection (MCAD) Variable Urgent TEVAR
MCAD with full TL collapse (n ¼ 19)
MCAD without full TL collapse (n ¼ 31)
P value
8 (42.1)
3 (9.7)
Hospital stay, days
13.5 6 8.1
12.6 6 4.1
.585
Duration of procedure, minutes
92.1 6 37.8
102.7 6 20.3
.202
109.1 6 18.7
114.0 6 19.6
Contrast agent dose, mL Intraprocedural death Clinical success
1 (5.3) 18 (94.7)
0 31 (100)
.013
.385 .380 .380
Stent graft types Valiant
5 (26.3)
4 (12.9)
.273
Valiant Captivia
7 (36.8)
13 (41.9)
.721
Ankura
3 (15.6)
3 (9.7)
.661
Zenith TX2
3 (15.6)
9 (29.0)
.332
1 (5.3)
2 (6.4)
1.000
7 (36.8)
3 (9.7)
.030
TAG IVUS-assisted TEVAR TEVAR þ chimney or debranching
5 (26.3)
6 (19.4)
.727
15 (78.9)
18 (58.1)
.218
Type Ia
7 (36.8)
12 (38.7)
.895
Type Ib
2 (10.5)
1 (3.2)
.549
Coverage of LSA Endoleaks
IVUS, Intravascular ultrasound; LSA, left subclavian artery; TEVAR, thoracic endovascular aortic repair; TL, true lumen. Continuous variables are presented as mean 6 standard deviation, and categorical variables are presented as number (%).
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Table IV. Perioperative events after thoracic endovascular aortic repair (TEVAR) and follow-up results Variable
Total cohort (N ¼ 50)
MCAD with full TL collapse (n ¼ 19)
MCAD without full TL collapse (n ¼ 31)
P value
Perioperative outcomes (30 days) AD-related deaths
2 (4.0)
2 (10.5)
0
.140
10 (20.0)
7 (36.8)
3 (9.7)
.030
ARF
4 (8.0)
3 (15.8)
1 (3.2)
Retrograde dissection
2 (4.0)
2 (10.5)
0
Organ ischemia
2 (4.0)
1 (5.3)
1 (3.2)
Major stroke
1 (2.0)
0
1 (3.2)
Paraplegia
1 (2.0)
1 (5.3)
0
All deaths
3 (6.0)
2 (10.5)
1 (3.2)
AD-related deaths
1 (2.0)
1 (5.3)
0
.380
20 (40.0)
9 (47.4)
11 (35.5)
.405
Aneurysmal dilation
8 (16.0)
5 (26.3)
3 (9.7)
Endoleaks
8 (16.0)
3 (15.8)
5 (16.1)
SINE
3 (6.0)
1 (5.3)
2 (6.5)
1 (2.0)
Major adverse events
Follow-up events
Major adverse events
Organ ischemia
.549
0
1 (3.2)
13 (26.0)
7 (36.8)
6 (19.4)
.199
Incomplete
20 (40.0)
10 (52.6)
10 (32.3)
.153
Complete
28 (56.0)
7 (36.8)
21 (67.7)
.033
25.6 6 13.2
22.8 6 17.1
27.2 6 10.2
.264
Secondary intervention FL thrombosis
Follow-up period, months
AD, Aortic dissection; ARF, acute renal failure; FL, false lumen; MCAD, multichanneled aortic dissection; SINE, stent graft-induced new entry; TL, true lumen. Continuous variables are presented as mean 6 standard deviation, and categorical variables are presented as number (%).
adverse events (40%) had been noted during follow-up, which did not result in a significant difference between the two groups (Table IV). We observed no statistical difference in secondary interventions (36.8% vs 19.4%; P ¼ .199). The overall rate of complete thrombosis in FLs was 56.0%, and it presented with a higher rate in patients without full TL collapse (67.7%) than in patients with full TL collapse (36.8%; P ¼ .033). The overall mortality rate for all MCADs was 16.7% (9 of 54) perioperatively and during follow-up. There was a significant difference in the overall survival rate of the patients with and without full TL collapse at 3 years after TEVAR (55.4% vs 94.7%; P ¼ .002; Fig 5). There was no independent predictor for the 30-day major adverse events in the multivariate analysis (Table V). The univariate analysis revealed that signs of aortic rupture, quadruple-channeled AD, maximum diameter of the affected aorta, and malperfusion syndrome were significant predictors of AD-related deaths. In multivariate analysis, however, the maximum diameter of the affected aorta (hazard ratio, 1.176; 95% confidence interval, 1.015-1.362; P ¼ .031) is the only independent predictor of AD-related deaths (Table VI).
DISCUSSION So far, most descriptions of MCAD have been limited to isolated case reports5,13-15 or studies evaluating poor outcomes and complications by open surgery and endovascular treatment.6,7 According to previous studies, the incidence of MCAD varied from 4.9% to 9%.5-7,13-15 We observed dissections with more than two adjacent FLs in 54 (8.4%) of 644 patients treated with TEVAR. This incidence was similar to that in previous reports, suggesting that the condition may occur frequently and is of great concern. Ando et al6 noted three-channeled AD in 31 (7.3%) of 426 patients with AD who underwent surgical treatment, and the incidence was higher in patients with Marfan syndrome (58% [18 of 31]). However, Sueyoshi et al7 found no significant differences between MCAD and DCAD in terms of clinical characteristics, including the presence of Marfan syndrome. In our study, the percentage of patients who had both Marfan syndrome and MCAD was 11.1% (6 of 54). Because the morbidity of type B AD in patients diagnosed with Marfan syndrome was not high (9%), it is unclear whether multichanneled morphologic features are associated with vasculitis diseases.16,17
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Fig 4. Aneurysmal dilation of multichanneled aortic dissection (MCAD) with full true lumen (TL) collapse after thoracic endovascular aortic repair (TEVAR) and chimney stent in left subclavian artery (LSA). Computed tomography (CT) images at 26 months showed that the false lumens (FLs) near the proximal entry tear were completely thrombosed and the chimney stent was patent (A and B). The “true-false-false” lumen configuration still appeared in the distal endograft (C and D). The FLs, with an increased blood flow from TL through the distal re-entry tears, were expanding into dissecting aneurysms.
Fig 5. Overall survival of multichanneled aortic dissection (MCAD) patients with and without full true lumen (TL) collapse.
In all the previous reports, however, the most important question remains unanswered: Why does MCAD have a significantly poorer survival rate than DCAD? The results of this study suggest that the morphologic features of the TL and FLs contributed to the mixed causes,
including fragility of the aortic wall and multiple-lumen configuration as the pathologic background and complicated AD hemodynamics as the most important provocative aspect. Fragility of the aortic wall and multiple-lumen configuration may be deemed the most basic factors contributing to the high mortality rate found in our study. A secondary FL may develop on the lateral wall of the first TL, which has a “true-false-false” or “false-false-true” lumen configuration. In our study, this multichanneled morphology was more common in patients without full TL collapse (Fig 3). A secondary FL may also exist on the other side of the TL, which has a “false-true-false” lumen configuration. This morphology may often cause full TL collapse (Fig 2). DCAD was complicated by additional new FLs that usually had no re-entry formation. Then, an increase in inflow and low or no outflow increased the pressure in the FLs and caused the TL to collapse.18 In addition, because the lateral wall of the FLs and dissection flaps were fragile and pliable as a result of the two layers of dissection, the patients’ risk of rupture
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Table V. Univariate and multivariate analysis for 30-day major adverse events Univariate analysis Parameter Malperfusion syndrome
Multivariate analysis
HR
95% CI
P value
HR
95% CI
P value
3.867
1.049-14.248
.042
1.933
0.422-8.856
.396
12.000
1.125-127.969
.040
2.717
0.196-37.650
.456
Maximum diameter of the affected aorta
1.081
1.019-1.147
.009
1.038
0.967-1.114
.300
Full TL collapse
7.179
1.687-30.552
.008
3.994
0.821-19.431
.086
Quadruple channeled
CI, Confidence interval; HR, hazard ratio; TL, true lumen.
Table VI. Univariate and multivariate analysis for aortic dissection (AD)-related deaths Univariate analysis
Multivariate analysis
HR
95% CI
P value
Signs of aortic rupture
46.000
5.048-419.440
.001
Quadruple channeled
22.000
1.959-247.056
.012
1.188
1.075-1.313
.001
22.000
2.484-194.876
.005
Parameter
Maximum diameter of the affected aorta Malperfusion syndrome
HR
95% CI
P value
1.176
1.015-1.362
.031
CI, Confidence interval; HR, hazard ratio.
was increased.6 Sueyoshi et al7 demonstrated that the presence of MCAD was the most powerful predictor of AD-related deaths. The literature also indicates that the aortic wall may suffer from medial degeneration and cystic medial necrosis.6,15 These factors may be the pathologic background for propagation of MCAD. As is well known, hemodynamics plays a major role in the initiation, acute propagation, and chronic development of dissections.19 A transmural pressure gradient between the TL and FLs is generated across the dissection flap and moves it. If the dissection flap does not balance the pressures of different channels, acute propagation causes signs of aortic rupture or hemodynamic instability. The primary strategy of intervention is closure of the primary entry tear to decompress the TL, to restore distal perfusion by expanding the TL, and finally to stabilize segments with impending rupture (Video, online only).20,21 Full TL collapse causes a series of detrimental effects and increases the risk of aortic rupture. In our study, there was a significant difference in the perioperative mortality rate between patients with full TL collapse (17.4%) and patients without full TL collapse (0%; P ¼ .028). In clinical practice, however, there were no tools available to identify hemodynamic instability in a timely and effective manner unless there were signs of instability. Thus, we suppose the morphology of full TL collapse may be an indicator of hemodynamic instability because we could not conclusively determine the reason for the observed disparity. To date, few studies have examined the role of natural history and factors affecting the effectiveness of TEVAR for treating MCAD. Sueyoshi et al7 reported that of 20 MCAD patients, 9 patients suffered from AD-related
death (45%), including aortic rupture (8 of 20) and redissection (1 of 20), whereas the mortality rate in patients with DCAD was much lower (17.4%; P ¼ .0002). Ando et al6 found that recurring pain in patients with chronic AD was a strong indicator of three-channeled dissection. Similarly, in this study, the overall mortality rate for patients with MCAD was 16.7% perioperatively and during the follow-up period. Therefore, clinical observation of MCAD was of importance during either interpretation of the initial CTA findings or the follow-up period. MCAD patients with full TL collapse should alert their physicians of the possibility of hemodynamic instability and the necessity of urgent intervention. In our cohort, the morbidity of 30-day major adverse events was 20.0% (10 of 50), and a significant difference was found between the two groups (36.8% vs 9.7%; P ¼ .030). Apart from acute malperfusion and hemodynamic redistribution after TEVAR, endograft-related aortic wall injury may be another important risk factor for the adverse events, especially retrograde dissection.22 Cheng et al15 reported that a patient with triple-channeled AD developed retrograde type A AD during endograft repair. Identifying the possible risk factors for AD-related deaths and future adverse events would improve the management of patients with multichanneled morphologic features. Several studies have suggested that saccular formation of FLs, number of intimal tears, large entry tears ($10 mm), location of the primary entry tear, and configuration of the FL may influence the aortic growth rate during the follow-up period.23-25 In this study, however, the maximum diameter of the affected aorta was the only independent predictor of AD-related deaths. These findings suggested that increased inflow due to a large entry tear and damaged FL media may
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result in hemodynamic redistribution and acute dissection propagation. Study limitations. First, this study was performed as an observational study in our study population. The number of cases of MCAD was relatively small; thus, the results should be limited to hypothesis deriving. Second, nongated CT technology was used, and not all patients were examined with CT in the follow-up, which might have biased our results. Third, we did not compare the DCAD with the study cohort; therefore, it has unfortunately not been investigated whether TL collapse in general (MCAD and DCAD) yields worse outcome. However, we attempted to highlight this kind of type B AD with multichanneled morphology as a high mortality was observed in clinical practice.
CONCLUSIONS Of patients with type B AD, 8.4% presented with multichanneled morphology. Urgent or elective TEVAR was indicated in all our patients with MCAD. In patients with MCAD, full TL collapse was associated with worse outcomes, and this finding may represent an adjunct for physicians to stratify patients at high risk of complications and indicate the need for more urgent or emergent repair. Further studies are necessary to determine the optimal therapeutic strategy for this type of dissection. We thank Professor Xiao Yun Xu (Department of Chemical Engineering, Imperial College London, South Kensington Campus, London, UK) for her support in the hemodynamic discussion of aortic dissection.
AUTHOR CONTRIBUTIONS Conception and design: BG, DG, WF Analysis and interpretation: BG, KH, XX, PL, WF Data collection: KH, ZS, YS, PL Writing the article: BG, DG Critical revision of the article: BG, DG, XX, ZS, WF Final approval of the article: BG, KH, DG, XX, ZS, YS, PL, WF Statistical analysis: BG, YS Obtained funding: Not applicable Overall responsibility: WF
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