4. Discussion
To the best of our knowledge, this is the first clinical study for TAD up to date. In our study, we found that TAD is distinct from NTAD. Compared to patients with NTAD, TAD are younger and have a lower proportion of hypertension, a shorter length of dissection and shorter preoperative duration, etc. During the long-term follow-up, the TAD group exhibited a lower incidence of complications and long-term mortality rates following TEVAR than the NTAD group.
Aortic blunt injury frequently results from external forces applied to the chest during traffic accidents or falls from heights, leading to aortic trauma of varied severity [
11]. Aortic trauma can lead to AD through intimal tears; however, the exact mechanism remains unknown. In contrast, NTAD, or spontaneous AD, is caused by high blood pressure acting on the aortic wall, leading to intimal tears. Risk factors for NTAD include genetics, smoking, hypertension, and atherosclerosis [
12,
13,
14]. Hypertension is a significant risk factor for predisposing to AD by subjecting the aortic wall to increased shear stress [
15]. The International Registry of Acute Aortic Dissection (IRAD), which is a consortium of 58 research centers in 13 countries, was established in 1996 and evaluates the management and outcomes of acute aortic dissection and intramural hematoma, assessing etiological factors, clinical features, treatment, and post-discharge outcomes globally, reported that 74.4% of them had a history of hypertension at least [
13,
16]. Hypertension contributes to NTAD by triggering spontaneous aortic intimal tears, indicating an underlying pathological condition or their own vascular characteristics, such as type III aortic arch, a radiological feature known to increase the risk of type B aortic dissection (TBAD) [
17]. Meanwhile, age is also a significant factor in the occurrence of aortic dissection. Data from IRAD suggests that the average age of patients with acute type B aortic dissection is 63.6 ± 14.1 years, another data from Germany over 9 years reported an average age of 66 [IQR 56–74] years for patients with TBAD [
16,
18]. Our results showed an age of 55 [IQR 47–61] years for patients with NTAD and 50 [IQR 40–59] years for the TAD group, Chinese patients are younger, which is consistent with previous research findings [
19]. Meanwhile, as a risk factor for aortic dissection, aortic root diameter increases with age [
20]. Animal experiments have demonstrated that aortic medial degeneration leads to age-dependent aortic dilation and, under hypertensive stress, results in aortic dissection [
21]. In our study, patients with TBAD who underwent TEVAR surgery in the NTAD group had a higher prevalence of smoking, hypertension type III aortic arch, and an enlarged ascending aorta compared to the TAD group.
Patients with NTAD had a longer dissection length and a larger maximum diameter of the ascending aorta compared to the TAD group, with a significant proportion (up to 48.96%) having a maximum ascending aorta diameter of >40 mm. Similarly, more aortic zones were involved in the NTAD group than in the TAD group. Our results corroborate findings from the IRAD, which reported a high prevalence (40.2%) of ascending aorta diameters >40 mm in patients with NTAD. However, the all-cause mortalities did not differ based on the diameter size of the ascending aorta in their study [
22]. The differences in ascending aorta diameter are likely attributed to the long-term effects of hypertension or arteriosclerosis. In evaluating the dissection features in the TAD group, we analyzed the prevalence of dissection on the lesser curvature side, multiple channels, the maximum diameter of the true/false lumen, and complicated aortic dissection. Contrastingly, we found that TAD more frequently extended from the lesser curvature of the aortic arch, while NTAD was more prone to having multiple tears. The anatomic features of the aorta could explain these differences. The relatively mobile aortic arch and the fixed descending aorta create a vulnerable aortic isthmus between them, which is more susceptible to various mechanical forces. Therefore, the PETs are ideally positioned in the aortic isthmus, particularly in the lesser curvature. This finding aligns with previous research [
23]. The inherent vulnerability of the aorta to any injury in NTAD induces blood to strike the arterial wall, causing tears in the aortic isthmus between the aortic arch and the descending aorta. Blood from the aortic lumen enters the aortic media through these intimal tears, resulting in perfused channel formation in the aortic media. These channels expand along the long axis of the aorta, creating a new lumen within the aortic wall [
24].
Interestingly, no significant difference was observed in the distance between the LSA and the PET between the two groups, indicating that the most common site for the primary tear is at the junction of the arch and descending aorta, where the curvature alters its direction, affecting the blood flow shear. This anatomical and structural vulnerability renders the aorta susceptible to injuries from external and internal forces. However, a significantly higher proportion of dissections originate on the lesser curve, possibly suggesting differences in internal and external forces and the anatomical characteristics of the aortic arch.
With recent advancements in endovascular technology, TEVAR has emerged as a favorable treatment option for blunt thoracic aortic injury (BTAI) compared to open aortic repair [
25]. Regarding perioperative outcomes, our study found no significant differences between the two groups regarding surgical duration, the mean number of stents implanted per patient, and TEVAR-assistive techniques. However, the optimal timing for intervention remains uncertain. The 2011 clinical practice guidelines from the SVS suggest urgent repair (≤24 h) for stable aortic trauma unless accompanied by other non-aortic serious injuries [
26]. However, a retrospective observational study involving 548 patients compared early (≤24 h) versus delayed (>24 h) TEVAR for BTAI. The study indicated that delayed TEVAR was associated with a lower mortality risk, even after adjusting for the aortic injury grade [
27]. As for TAD, there is currently no recommended optimal timing for intervention. According to a recent meta-analysis, TEVAR has shown a favorable long-term prognosis for blunt aortic trauma, with rare instances requiring reinterventions [
28]. The American College of Cardiology (ACC) and the American Heart Association (AHA) 2022 guidelines for the Diagnosis and Management of Aortic Disease indicate that the timing of surgical intervention remains unclear [
6]. In our center, the intervention time is based on hemodynamical stability and an unstable state with signs of aortic rupture necessitating an urgent intervention. For others, we follow a conventional treatment strategy for NTAD, with a mean preoperative duration of 11 days. Although the patients with TAD had a four-day shorter preoperative waiting time, we did not observe significant differences in complications, all-cause mortality, and survival time. However, the proportion of complications and deaths in the TAD group was lower, with mortalities primarily resulting from non-aortic-related causes.
Table 6 presents the incidence risks of complications and mortalities in the TAD and NTAD populations. Although there was no significant difference in early mortality between the two groups, the TAD group showed significantly better in terms of mid-to-long-term outcomes. We primarily attribute this outcome to the trauma associated with the TAD group, while the differences in long-term complications and mortality rates may be due to factors such as the extensive involvement of the dissection in the NTAD group and a higher proportion of complex dissections.
D-dimer concentration strongly correlates with AD and has been suggested as a parameter to predict outcomes and rule out or confirm AD in patients [
29,
30,
31]. In our study, patients in the TAD group had significantly higher median D-dimer levels. We hypothesize that the elevated D-dimer levels in the TAD group may be attributed to trauma-induced imbalances between plasminogen activators and inhibitors. Therefore, we conclude that D-dimers could not fully predict the clinical outcome in this study. Meanwhile, the TAD group experienced significant reductions in RBC and HGB levels, possibly due to blood loss directly related to the trauma. The reduction in Hb level and also the higher level of D-dimer might be related not only to TAD. Being TAD is usually related to other trauma, the blood loss and D-dimer might reflect also other sites of injury. Plasma levels of Hcy are independent risk factors for severe cardiovascular involvement and AD [
32]. Our study confirmed that the plasma homocysteine level was significantly lower in the TAD group compared to the NTAD group. As NTAD is closely associated with hypertension and is also suspected of having underlying structural defects, this partly explains why the maximum diameter of the false lumen and the total diameter of the false lumen plus the true lumen is larger in NTAD than in TAD, as observed in our study.
Our study has several limitations: a small number of patients in the TAD group, which limits the generalizability of our prognostic study. Additionally, this is a single-center, retrospective study, there may be a selection bias, leading to a non-random and non-comprehensive sample, which also raises concerns about low external validity; retrospective studies rely on patient recall or medical records. Additionally, there may also be a recall bias.