|Year : 2020 | Volume
| Issue : 1 | Page : 15-20
The beneficial enlightenment of thoracic endovascular aortic repair for traumatic Type B aortic dissection with long-term follow-up: A single-center experience sharing
Yongfu Xie, Shiying Wang, Qingsheng Lu
Department of Vascular Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China
|Date of Submission||11-Jan-2020|
|Date of Decision||16-Feb-2020|
|Date of Acceptance||20-Feb-2020|
|Date of Web Publication||30-Mar-2020|
Dr. Qingsheng Lu
Department of Vascular Surgery, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433
Source of Support: None, Conflict of Interest: None
Backgroud: Traumatic Aortic Dissection is a emergency that patients will face soon death, even there is no enough time to transport patient to the hospital. In this study we retrospectively analyze the long-term therapeutic effects of endovascular treatment of traumatic Type B aortic dissection to get some inspiration for the next step treatment and to provide a useful guidance.
Method: 21 patients with Stanford type B aortic dissection caused by trauma endovascular treatment after strict condition assessment in our vascular center from December 1999 to May 2012 was recruited into this retrospective study. The overall diameter of the aorta, the number of tears and the extent of the dissection were observed based on three-dimensional reconstruction of the CTA during the follow-up. The recurrence of the operation and the 2-year and 5-year survival rates were recorded.
Conclusion: Endovascular treatment of traumatic aortic dissection increases the survival rate of these patients who cannot tolerate traditional open surgery. This survival benefit sustained throughout the long-term follow-up.
Keywords: Aortic dissection, aortic repair, endovascular
|How to cite this article:|
Xie Y, Wang S, Lu Q. The beneficial enlightenment of thoracic endovascular aortic repair for traumatic Type B aortic dissection with long-term follow-up: A single-center experience sharing. Vasc Invest Ther 2020;3:15-20
|How to cite this URL:|
Xie Y, Wang S, Lu Q. The beneficial enlightenment of thoracic endovascular aortic repair for traumatic Type B aortic dissection with long-term follow-up: A single-center experience sharing. Vasc Invest Ther [serial online] 2020 [cited 2020 Nov 30];3:15-20. Available from: https://www.vitonline.org/text.asp?2020/3/1/15/281599
| Introduction|| |
Traumatic aortic dissection, defined as aortic true and false lumen separation, is caused by blood flow through the injured aortic intima rupture into the central membrane. Traumatic aortic dissection is a special case of traumatic aortic injury. When the injury factors damage the whole layer, causing arterial rupture, patients will face soon death, even there is no enough time to transport patient to the hospital. Literature has introduced characteristics and effects of traumatic aortic dissection treatment, however, the long-term efficacy of this intracavitary treatment has rarely been reported. In this study, we retrospectively analyzed the long-term therapeutic effects of endovascular treatment of traumatic Type B aortic dissection to get some inspiration for the next-step treatment and to provide a useful guidance.
| Materials and Methods|| |
Patients with Stanford Type B aortic dissection caused by trauma endovascular treatment after strict condition assessment at our vascular center from December 1999 to May 2012 were recruited into this retrospective study. All patients underwent aortic computed tomography angiography (CTA) examination. It clearly showed the scope of the aortic dissection; the initial tear and the remaining tear position; linear, semi-curved, or V-shaped intramedullary membrane; true and false cavity; and branch artery blood supply. Aortic dissection patients were classified according to the current internationally popular Stanford classification with the support of generalized CTA image interpretation. The inclusion criterion was traumatic causes. Patients with the following conditions were excluded: (a) coronary artery involvement; (b) acute myocardial infarction; (c) cardiac tamponade or echocardiography recorded history of severe aortic regurgitation (Grade 3 or 4); (d) potentially life-threatening history of ventricular arrhythmias; and (e) accidental death. The end point for follow-up was May 1, 2017, and did not count any accidental deaths such as car accident, suicide, known malignancy, and other noncardiovascular resulted death as final follow-up outcome. All patients came to our center 3 months after operation for the first follow-up. The first follow-up was performed with enhanced CTA of the entire aorta. The second follow-up were performed 6 months after the operation, and annually thereafter. The overall diameter of the aorta, the number of tears, and the extent of the dissection were observed based on three-dimensional reconstruction of the CTA during the follow-up. The recurrence of the operation and the 2- and 5-year survival rates were recorded.
All these patients underwent procedures with general anesthesia. The femoral artery was transplanted through the groin, a 0.035” soft guide wire with a pig tail tube was used to ascend aortic angiography, and the dissection of the gap position was confirmed again. The graft was guided by the femoral artery with the support of a super-hard wire, and was located at the main gap [Figure 1]. We used thoracic aortic stent graft systems from the Medtronic talent and valiant series, MicroPort scientific corporation Hercules, and Cook Zenith series. The model was chosen in line with the aorta size (the proximal diameter ranges from 28 to 44 mm, with the length ranging from 160 to 200 mm). The size of the graft was selected based on the size of the aortic anchorage zone. The magnification was about 10%–15% of the inner diameter. On the three-dimensional reconstructed image, the diameter of the major axis of the cross-section that was perpendicular to the central streamline was selected as the measured value of inner aortic diameter.
|Figure 1: (a and b) Preoperative three-dimensional images, true and false lumen, are visually difficult to distinguish; (c and d) the three-dimensional image 3 months after operation, postoperative branch artery development is visually good, and dissection is isolated and the blood inside is cut back|
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In the study, the mean values (± standard deviation) and median were used to describe the continuous variables, and the categorical variables were expressed as a percentage. Categorical variables were analyzed using Fisher's exact test or Chi-square test, and continuous variables were analyzed by unpaired t-test or single-factor analysis of variance. All variables were adjusted simultaneously in one step. The survival and time–event curves were calculated by the Kaplan–Meier method and compared by log-rank test. P < 0.05 was considered statistically significant. SPSS software version 18.0 (SPSS, Inc., Chicago, Illinois, USA) was used in all analyses.
| Results|| |
The clinical features of patients who underwent endovascular repair are summarized in [Table 1]. The average age of 21 traumatic Type B aortic dissection patients was 42.3 years (range: 19–67 years). Men accounted for 85.7% (18/21). Nearly 80.9% (17/21) of the dissections were caused by car accident, three were due to falling accident from high places, and one patient was defined a Stanford Type B aortic dissection after sudden chest pain while rowing a boat. The median time from onset to treatment was 7 days (range: 1–73 days). There were 16 cases (<14 days) in the acute phase, 2 cases (15–60 days) in the subacute phase, and 3 cases (>60 days) in the chronic phase. There was no patient in super acute phase in the study group (0–24 h). It should be noted that five patients in the nonacute phase only received medication for various reasons in the initial treatment and smoothly went through the acute phase. They turned to our center for further treatment because of persistent symptoms or the sign of dissection lesion which needs to be intervened. [Table 2] concludes the perioperative study and follow-up outcomes, and postoperative vascular remodeling was rigorously assessed. In this study, the perioperative mortality rate was 9.52% (2/21). Patient No. 9 died 27 days after surgery due to multiple organ failure caused by postoperative lung infection. Patients No. 14 experienced intraoperative blood pressure sharp decline, cardiac arrest, and died after invalid rescue. Perioperative pulmonary infection was found in two cases (9.52%) and multiple organ failure in one case (4.76%). The median follow-up time was 94 (range: 1–205) months. Patient 8 died of advanced lung cancer at 53 months after operation, and the remaining patients continued to participate in the follow-up. During the follow-up period, there were two cases of complications; no mezzanine was newly developed in any patients. Patient 17 at the 3rd month after the surgery was found to have left renal atrophy accompanied with a slight increase in serum creatinine to 204 μmol/L; after left renal artery stenting, the affected layer of blood flow was recovered, and the creatinine level gradually decreased and stabilized. Patient 4 was examined at the 6th month after the surgery and found with endoleak around the graft, while there was no significant expansion of the aortic segment. There was a limited amount of blood flow around the graft, and the blood flow originated from the gap between the proximal part of the graft and the minor curvature at the junction of the aortic arch, which resulted in the attachment of the graft to the aorta. In the case of the absence of obvious contrast agent leakage into the cavity and obvious symptoms, the patient was subjected to conservative drug treatment and close follow-up. The 2- and 5-year survival rates of the study were 90.48% and 85.71%, respectively. During the follow-up, there was no occurrence of stent-graft shift, and none of the patients developed limb ischemia, transient ischemic attack, spinal cord ischemia, or stroke.
| Discussion|| |
The occurrence of aortic dissection is closely related to hypertension; in addition, diabetes, hyperlipidemia, and cardiovascular disease history are also risk factors for aortic dissection. The exact pathogenesis of traumatic aortic dissection is not clear, but it is believed to be a direct or indirect effect of multiple forces. The lesion is mainly seen in the distal aorta of the left subclavian artery, and the ascending aorta is adjacent to the open mouth of the head. The incidence of aortic arch and descending aorta is low.,,, The main reason is probably the presence of intercostal arteries, pleura, and arterial ligament which around root of left subclavian artery is fixed, while the aortic isthmus below is relatively free. The slowdown wound induced during the horizontal deceleration period is caused by the shear stress, which is the result of the difference in the inertia between the isthmus and adjacent blood vessels.
[Table 1] shows that most of the traumatic Type B aortic dissections resulted from car accident injuries (80.9%, 17/21). In other cases, three were high falling injuries and one was aortic dissection triggered by a sudden thoracic pain while rowing a boat. A report showed that, motor vehicle accident-related aortic dissection accounted for 96.7% and falling accident-related aortic dissection accounted for the remaining 3.3%. It has also been reported that, some violent physical activity, including weight lifting and back impact, can induce the onset of acute aortic dissection as well, which could be caused by the rapid increase in hemodynamic stress.
Acute aortic dissection is still an emergent life-threatening cardiovascular disease, and posttreatment morbidity and mortality are high, yet traumatic aortic dissection is usually fatal. It has been reported that the 1st day of traumatic aortic dissection has a hospital mortality rate of 32%, followed by 61% in the 1st week and 74% in 2 weeks. In addition, according to the literature, survived patients with no operative acute phase had a risk of rupture of 30% due to advanced traumatic thoracic aortic aneurysms. Most of the traumatic Type B aortic dissections in this study were treated in the acute phase, implying that our endovascular technique has potential value in reducing the risk of traumatic Type B aortic dissection in patients with high risk. Methods of treating traumatic Type B aortic dissection include open surgery, hybrid surgery, and endovascular treatment. In our study, the perioperative mortality of endovascular treatment of traumatic Type B aortic dissection was 9.52% (2/21). This result is similar to the meta-analysis conducted by Tang et al. and Kasirajan et al., and is significantly better than traumatic aortic dissection surgery which has 28% mortality and 16% paraplegia., Compared to open surgery, it appears that this alternative treatment increases the survival rate of specific patients and reduces the incidence of major complications associated with surgery, and moreover this survival benefit is sustained in long-term follow-up. The beneficial aspects include minimal invasion, rapid recovery, and early out-of-bed activity.
At the same time, out of 509 cases of nontraumatic Stanford Type B aortic dissection, who were studied at our center, 21 cases died during the perioperative period and the perioperative mortality rate was 4.13%. [Table 3] summarizes the perioperative death of two groups of patients with Chi-square test (χ2 = 1.416, P = 0.234, >0.05), and no significant difference in mortality rate was seen, suggesting that the cause of the disease is not a determinant in choosing whether endovascular treatment is required or not.
|Table 3: Comparison of perioperative mortality between traumatic and nontraumatic groups|
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The perioperative death of traumatic patients is mainly due to the general poor physical condition of the patients. In one case, intraoperative blood pressure plummeted, autopsy results suggested aortic dissection led to hemorrhage, and in the other case, postoperative pulmonary infection led to systemic failure and death. This suggests that we should pay attention to the treatment of complications in patients with traumatic aortic dissection. We should not only deal with life-threatening aortic wall dissection, but also craniocerebral trauma, fractures, pulmonary contusions, and other complications, which can have serious consequences if not treated properly. A large-scale study showed that acute aortic dissection patients with syncope had a worse prognosis than those without syncope, which reminded us of the importance of treating complications in a timely manner.
[Table 2] rigorously assesses patients' postoperative vascular reconstruction conditions. Observing the false lumen thrombosis, we can see that thoracic endovascular aortic repair for traumatic Type B aortic dissection can effectively promote aortic remodeling, and the remodeling results in turn reflect the prognosis of endovascular treatment; moreover, patients in the trauma group confirmed good long-term survival. This result suggested that our endovascular treatment of traumatic Stanford Type B aortic dissection can achieve good long-term clinical benefits.
[Figure 2] shows the survival curves of two groups of patients admitted to our hospital over the same period. It can be seen that the 2-year survival rate of the trauma group was 90.48% and the 5-year survival rate was 85.71% (18/21), and in the nontraumatic group, the 2-year survival rate was 94.11% and the 5-year survival rate was 92.93%. The log-rank test showed that there were no statistically significant differences between the two survival curves (χ2 = 1.093, P = 0.296, >0.05). This outcome suggested that the long-term clinical benefit similar to that of nontraumatic Type B aortic dissection can be achieved by intracavitary treatment of traumatic Type B aortic dissection.
Endoleak is considered to be an important complication after endovascular treatment. The formation of endoleak is related to the smaller radius of curvature at the junction of the aortic arch and the shorter anchorage area of the graft. However, the difference in configuration between the straight-tube graft and the curved proximal aortic arch, the impulse of the aorta, and the impact of the aorta pulsating blood flow can impair the early benefit and eventually lead to an implant endoleak and even late migration of the graft. It has been reported that in Type B aortic dissection cavity treatment, the incidence of mid-term leakage was reported as high as 8.1%. In our study, only a limited endoleak occurred in the trauma group during the follow-up procedure, with mid-term leakage rate of 4.76% (1/21), suggesting that our intracavitary treatment in the postoperative complications of traumatic Stanford Type B aortic dissection can achieve better clinical expectations.
It is worth to notice that the majority of patients with traumatic Type B aortic dissection were trying to get treatment in the acute phase, where good results could be achieved after treatment. However, not all patients can be diagnosed in the acute phase, or come to the hospital for the treatment. There were two subacute cases (15–60 days) and three chronic-phase cases (>60 days). Two among the three cases of chronic patients had a history of trauma; the diagnosis was confirmed after repeated conservative treatment of medical symptoms and further aortic CTA angiography. One case of chronic trauma was diagnosed 73 days after trauma; while there was no obvious pain and the patient was hesitant, the endovascular treatment was prolonged. Two subacute cases were diagnosed with traumatic chest injury and craniocerebral injury, hence thoracic surgery and neurosurgery were performed sequentially, mediastinum widening was found in CT scan, and aortic dissection was diagnosed in further CTA examination before transferring to our center. All of the above suggest us to pay attention to the diagnosis of traumatic aortic dissection and to prevent the misdiagnosis due to the excessive focus on the complications. When chest pain appears after trauma, especially car or falling accident, we need to pay attention to the exclusion of the aortic dissection, so as to avoid the serious consequences caused by the delay in diagnosis.
| Conclusion|| |
Endovascular treatment of traumatic aortic dissection increases the survival rate of these patients who cannot tolerate traditional open surgery because of their poor physical conditions and high surgical risks. This survival benefit sustained throughout the long-term follow-up. In contrast, compared with nontraumatic Type B aortic dissection, traumatic Type B aortic dissection patients who received endovascular treatment benefited from the long-term clinical outcomes, which provides a guidance for future clinical treatment of this type disease.
Financial support and sponsorship
This study was financed by the Shanghai training project for medical leaders (2019 LJ7).
Conflicts of interest
There are no conflicts of interest.
| References|| |
Richens D, Field M, Neale M, Oakley C. The mechanism of injury in blunt traumatic rupture of the aorta. Eur J Cardiothorac Surg 2002;21:288-93.
Arajärvi E, Santavirta S, Tolonen J. Aortic ruptures in seat belt wearers. J Thorac Cardiovasc Surg 1989;98:355-61.
Rabinsky I, Sidhu GS, Wagner RB. Mid-descending aortic traumatic aneurysms. Ann Thorac Surg 1990;50:155-60.
Parmley LF, Mattingly TW, Manion WC, Jahnke EJ Jr. Nonpenetrating traumatic injury of the aorta. Circulation 1958;17:1086-101.
Feczko JD, Lynch L, Pless JE, Clark MA, McClain J, Hawley DA. An autopsy case review of 142 nonpenetrating (blunt) injuries of the aorta. J Trauma 1992;33:846-9.
Yilmaz O, Arbatli H, Sirin G, Arpaz M, Yagan NE, Numan F, et al
. Endovascular treatment of traumatic thoracic aortic aneurysms: report of five cases and review of the literature. Ulus Travma Acil Cerrahi Derg 2010;16:575-8.
Lee WA, Matsumura JS, Mitchell RS, Farber MA, Greenberg RK, Azizzadeh A,et al
. Endovascular repair of traumatic thoracic aortic injury: Clinical practice guidelines of the society for vascular surgery. J Vasc Surg 2011;53:187-92.
Propper BW, Clouse WD. Thoracic aortic endografting for trauma: A current appraisal. Arch Surg 2010;145:1006-11.
Hatzaras I, Tranquilli M, Coady M, Barrett PM, Bible J, Elefteriades JA. Weight lifting and aortic dissection: More evidence for a connection. Cardiology 2007;107:103-6.
Ipek E, Ermis E, Demirelli S, Yildirim E, Yolcu M, Sahin BD. Traumatic coronary artery dissection in a young woman after a kick to her back. Korean J Thoracic Cardiovascr Surg 2015;48:281-4.
Orihashi K. Acute type a aortic dissection: For further improvement of outcomes. Ann Vasc Dis 2012;5:310-20.
Jang MO, Kim JH, Oh SK, Lee MG, Park KH, Sim DS, et al
. Endovascular stent in traumatic thoracic aortic dissection. Korean Circ J 2012;42:341-4.
Finkelmeier BA, Mentzer RM Jr., Kaiser DL, Tegtmeyer CJ, Nolan SP. Chronic traumatic thoracic aneurysm. Influence of operative treatment on natural history: An analysis of reported cases, 1950-1980. J Thorac Cardiovasc Surg 1982;84:257-66.
Tang GL, Tehrani HY, Usman A, Katariya K, Otero C, Perez E, et al
. Reduced mortality, paraplegia, and stroke with stent graft repair of blunt aortic transections: A modern meta-analysis. J Vasc Surg 2008;47:671-5.
Kasirajan K, Heffernan D, Langsfeld M. Acute thoracic aortic trauma: A comparison of endoluminal stent grafts with open repair and nonoperative management. Ann Vasc Surg 2003;17:589-95.
Kwolek CJ, Blazick E. Current management of traumatic thoracic aortic injury. Semin Vasc Surg 2010;23:215-20.
Patel HJ, Hemmila MR, Williams DM, Diener AC, Deeb GM. Late outcomes following open and endovascular repair of blunt thoracic aortic injury. J Vasc Surg 2011;53:615-20.
Nallamothu BK, Mehta RH, Saint S, Llovet A, Bossone E, Cooper JV, et al
. Syncope in acute aortic dissection: Diagnostic, prognostic, and clinical implications. Am J Med 2002;113:468-71.
Bossone E, Evangelista A, Isselbacher E, Trimarchi S, Hutchison S, Gilon D, et al
. Prognostic role of transesophageal echocardiography in acute type A aortic dissection. Am Heart J 2007;153:1013-20.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3]