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November 2023
Where Do We Stand on Truly Uncomplicated TBAD? It’s Complicated
The management of uTBAD remains controversial—mostly due to difficulty identifying patients with truly uTBAD.
By Sophia Khan, MD, and Rana O. Afifi, MD
Acute aortic dissection remains one of the most complex and life-threatening aortic disorders, with type B aortic dissection (TBAD) accounting for approximately one-third of dissections. Historically, the management and prognosis of TBAD patients depended on complications at the time of initial diagnosis. Based on the most recent 2022 American College of Cardiology (ACC)/American Heart Association (AHA) guideline for the diagnosis and management of aortic disease, TBAD is defined as complicated TBAD (cTBAD) if rupture or malperfusion exists and if there is an extension of dissection; progressive enlargement of the true lumen, false lumen (FL), or both in the acute phase; intractable pain; and uncontrolled hypertension (HTN).1 The guidelines include a recommendation for intervention in addition to optimal medical treatment (OMT). If the previously mentioned complications do not exist, dissection is defined as uncomplicated TBAD (uTBAD), and OMT is recommended as initial management for reducing heart rate and blood pressure to decrease aortic wall stress.1
Treatment of cTBAD has evolved over the past 2 decades, as thoracic endovascular aortic repair (TEVAR) has become the standard of care due to improved outcomes compared to open surgical repair.2-5 However, the management of uTBAD remains controversial, mostly due to the difficulty of identifying patients with truly uTBAD.
NATURAL HISTORY OF uTBAD
The number of patients presenting with uTBAD varies from 60% to 75% of all patients with acute TBAD.6-8 Most patients with uTBAD are treated medically with blood pressure and anti-impulse control, with 3% to 10% early mortality. Nearly 40% of uTBAD patients will require a late intervention, mostly due to aneurysmal degeneration, with long-term survival of 50% to 60%.7,9-15 With this natural history and the significant improvement of outcomes of patients with cTBAD treated with TEVAR, there has become an increased interest in TEVAR for uTBAD.3,5,16
ROLE OF TEVAR IN uTBAD
The INSTEAD trial randomized 140 patients with subacute uTBAD into cohorts of elective TEVAR with OMT to OMT alone and found no significant difference in mortality at 2 years between the groups; however, the TEVAR group was associated with aortic remodeling and FL thrombosis.16 When they extended the follow-up to 5 years in the INSTEAD XL trial, they found significant improvement in aortic-related mortality and improved aortic remodeling in the TEVAR plus OMT group compared to OMT alone.17
The ADSORB trial compared TEVAR plus OMT to OMT in uTBAD.18 It showed no difference in early mortality between the groups, with one death in the TEVAR plus OMT group at 1-year follow-up. ADSORB also demonstrated significantly improved aortic remodeling, with FL thrombosis and FL diameter decrease in the TEVAR plus OMT group compared to OMT alone.18 One major criticism of those studies is the lack of data on high-risk features.
“HIGH-RISK” FEATURES OF uTBAD
In recent years, many have tried to identify features of uTBAD that would predict the development of late complications. Despite the inconsistency and difficulty in reproducibility of those results, the 2022 ACC/AHA guideline gave a weak recommendation that TEVAR may be considered if any of the following high-risk factors are present: maximal aortic diameter > 40 mm; FL diameter > 20 to 22 mm; entry tear > 10 mm; entry tear on the lesser curvature; increase in total aortic diameter of > 5 mm between serial imaging studies; bloody pleural effusion; imaging-only evidence of malperfusion; refractory HTN despite more than three different classes of antihypertensive medications at maximal recommended or tolerated doses; and refractory pain persisting > 12 hours despite maximal recommended or tolerated doses and need for readmission.1
Does this mean that the truly uTBAD are those that lack any of the above high-risk factors? Can we make this decision based on moderate-quality data? Can we determine organ malperfusion based solely on static cross-sectional imaging? What would happen if we started treating all those patients with TEVAR? Will we prevent future aortic degeneration?
Famularo et al performed a systematic review assessing medium- and long-term outcomes after TEVAR for the treatment of TBAD.19 They showed that patients after TEVAR still had a significant risk for developing aneurysmal degeneration in the thoracic aorta, which was similar to the risk in patients treated with OMT. In addition, the risk for aneurysmal degeneration in the abdominal aorta was shown to be higher than in the thoracic aorta.19 All this shows that we are still far from fully understanding this complex disease.
RISK PREDICTORS FOR DELAYED COMPLICATIONS IN PATIENTS WITH uTBAD: WHAT ARE WE MISSING?
Currently, the recommended initial imaging is CT, with MRI and echocardiography as alternatives.1 Our protocol must evolve to include more technologies that can examine flow dynamics, such as dynamic CT, computational fluid dynamics, and four-dimensional flow MRI. An increasing number of publications correlate different flow patterns in the FL to different risk levels for delayed complications.20-24 Including dynamic imaging studies in evaluating uTBAD will help overcome the complexity and heterogeneity of the disease. In addition, incorporating those technologies during follow-up with all aortic dissection patients will allow us to understand the changes in the flow and pressure in the FL and true lumen over time as the acute dissection becomes chronic, and even more after an intervention and placement of a stent graft or performing graft replacement of the aorta.
The World Health Organization describes social determinants of health (SDOH) as the conditions in which people are born, grow, work, live, and age, as well as the wider set of forces and systems shaping the conditions of daily life. These nonclinical and nonbiologic factors, including HTN control, can profoundly impact health outcomes.
Factors associated with uncontrolled HTN include medication costs, health care access, medication complexity, patient beliefs and perceptions, educational achievement, socioeconomic status, depression and demoralization, perceived racism and discrimination, social networks and support, physician prescribing practices, and neighborhood segregation.25-32 HTN is the major clinical risk factor for dissection and death due to aortic dissection. In fact, up to 10% of patients with hypertensive emergencies develop aortic dissection—and > 70% of patients admitted to the hospital due to aortic dissection have HTN.33 Studies have demonstrated the importance of controlling HTN and heart rate in preventing delayed aortic complications and improving outcomes in patients with aortic dissection.34-37 Yet, none of those SDOH factors are considered in most studies investigating the long-term outcomes of uTBAD.
CONCLUSION
Where do we stand on truly uTBAD? Unfortunately, we are back to square one. We still don’t know who are the truly uTBAD patients. We must be able to define our patients into acute cTBAD, delayed cTBAD, and truly uTBAD. Our task should be to focus on identifying the patients who will develop delayed cTBAD, which requires a large, randomized trial comparing TEVAR plus OMT to OMT alone. To do this, we must first reproduce and validate some of the high-risk features that are currently suggested as indications for intervention in uTBAD. More importantly, we must rethink the data that we collect. This means that, in addition to the usual clinical, demographic, and radiologic data, we need to add new imaging technologies that can provide information about flow dynamics, dynamic behavior of the dissection flap, and wall stress measurements. We must then incorporate SDOH data and try to understand how health care insecurities influence the outcomes of patients with uTBAD and ensure that our patients are compliant with OMT and document the effectiveness of that management as well as identify the barriers to compliance if they exist.
If we can do these things, our future predictive risk models for identifying delayed cTBAD will look different. Future interventions might require more than surgical interventions—they could require building a safety net for our patients to ensure they have access to long-term follow-up, adequate blood pressure control, and chronic aortic dissection treatment. Only then will we know where we stand with truly uTBAD and, more importantly, if they can still be defined that way.
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