Point/Counterpoint: Is TEVAR required for all Type B aortic dissections?

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Yes, TEVAR is clearly indicated.

Aortic dissection is a devastating condition afflicting an estimated two to eight per 100,000 people annually and comprises a large portion of the clinical entity known as the acute aortic syndromes. Patients presenting with an uncomplicated type B acute aortic dissection (TBAD) generally have low in-hospital mortality rates (2.4%-9%) when managed appropriately with anti-impulse therapy. However, survival continues to decrease with follow-up, with survival ranging between 80% and more than 95% at 1 year, progressing to approximately 75% at 3-4 years, and 48%-65% at 10 years. In late follow-up, the development of a new dissection with complications is estimated to occur in 20%-50% of patients. Complicated aortic dissections affect between 22% and 47%, and when present, mortality reaches more than 50% within the first week. TEVAR in these patients has been shown to be clearly indicated in a variety of studies with marked improvements in early mortality and late survival. Thus, one can see that aortic dissection is a disease that needs to be managed lifelong, and is associated with a high risk of mortality for the next 10 years after the initial presentation.1,2,3

The long-term effects of a patent false lumen have been well documented. Several studies following patients with chronic TBAD have documented progressive enlargement in aortic diameter with a patent false lumen. The mean increase in maximum aortic diameter ranges from 3.8 to 7.1 mm annually with any flow in the false lumen (FL) versus 1-2 mm per year with a thrombosed FL. Patients with a patent FL had 7.5 times increased risk of a dissection-related death or need for surgery as compared to patients with thrombosis of the FL. Dissection-related death or need for surgery occurred at a significantly earlier follow-up period in the patients with a patent FL.1,2,3

The aortic diameter may also influence the patency of the FL at presentation. In a review of 110 patients presenting with acute uncomplicated TBAD, 44% were identified to have a patent FL on initial imaging. Thirty-one percent of these patients had a maximum aortic diameter of 45 mm or more versus 14% of patients with a thrombosed FL (P = .053). Incidentally, patients with FL patency were on average 4 years younger than their thrombosed counterparts (62 vs. 66 years, P = .009).

Moreover, it appears that the long-term risks associated with a patent FL are further augmented by aortic dilatation at presentation. When combining both risk factors (FL patency and aortic diameter of 40 mm or more), only 22% of patients are dissection-related event–free at 5-year follow-up.Onitsuka et al.4 substantiated this finding on multivariate analysis. Interestingly, 10 of the 76 patients included in that study met both conditions, and seven of those patients (70%) experienced a dissection-related death or surgical conversion. Certainly patients meeting both criteria merit close follow-up for the development of aortic enlargement or symptoms of impending rupture.

The natural history of TBAD lends itself to at least some thrombus formation within the FL and is a common finding as the dissection becomes chronic. But in fact, partial thrombosis of the FL is associated with higher mortality in patients discharged from the hospital with stable TBAD at 1- and 3-year follow-up (15.4% and 31.6%, respectively). Matched patients with a patent FL had a 5.4% and 13.7% rate of mortality at 1 and 3 years, and patients with complete FL thrombosis were found to have mortality rates of 0% and 22.6% at the same follow-up.

Aortic remodeling after TEVAR

Placement of a thoracic endograft under these acute circumstances can often significantly alter the preoperative morphology of the true and false lumen. Schoder and colleagues5 followed changes in the TL and FL diameter in 20 patients after TEVAR for acute complicated dissection. Ninety percent of patients were found to have complete FL thrombosis of the thoracic aorta at 1 year, with a mean decrease in FL diameter of 11.6 mm. Two patients with a patent FL showed a mean increase in the maximal aortic diameter of 4.5 mm. In a similar study, Conrad et al.6 documented aortic remodeling of 21 patients in the year following TEVAR, 88% of whom had thrombosis of the FL. Most often the mobile septum is easily displaced by the radial force of the stent graft, with minimal limitation of expansion to the design diameter. Thus, endograft selection should be directed by the diameter of the normal unaffected aorta with minimal oversizing commonly limited to 5%-10%. Balloon profiling is not typically necessary.

Dr. Frank J. Arko III

The INSTEAD trial7 evaluated the management of uncomplicated type B aortic dissection and compared optimum medical therapy (OMT) to OMT with TEVAR. A total of 140 subjects were enrolled at seven European sites with 68 patients enrolled in OMT and 72 in OMT with TEVAR. In patients treated with TEVAR there was 90.6% complete FL thrombosis with a maximum true lumen diameter of 32.6 mm as compared to 22% and 18.7 mm in those treated with medical therapy alone. Furthermore, there was a 12.4% absolute risk reduction in aortic specific mortality and a 19.1% absolute risk reduction in disease progression in patients treated with TEVAR.

It is clear that patients that present with complicated type B aortic dissections mandate intervention with TEVAR and potentially other interventions to alleviate the complications at presentation. INSTEAD demonstrates that elective TEVAR results in favorable aortic remodeling and long-term survival, reinterventions were low, and it prevents late expansion and malperfusion. TEVAR was also associated with improved 5-year aortic-specific survival. TEVAR appears to be beneficial in those patients who present initially with a false lumen diameter of greater than 22 mm and an aortic diameter of greater than 40 mm with a patent false lumen.

References

1. Circ. Cardiovasc. Interv. 2013;4:407-16.

2. J. Vasc. Surg. 2012;55:641-51.

3. J. Vasc. Surg. 2011;54:985-92

4. Ann. Thorac. Surg. 2004;78:1268-73.

5. Ann. Thorac. Surg. 2007;83:1059-66.

6. J. Vasc. Surg. 2009;50:510-17.

7. Circulation 2009;120:2519-28.

Dr. Arko is with the Aortic Institute, Sanger Heart & Vascular Institute, Charlotte, N.C. He reported no relevant conflicts.

No, evidence supports careful choice of patients.

While the role of TEVAR has been proven to treat complications of acute type B dissections,1 its value as a prophylactic treatment in uncomplicated cases remains controversial. Optimal medical treatment (OMT) with strict blood pressure (SBP less than 120 mm Hg) and heart rate control is associated with a low morbidity and mortality, despite the risk of progressive aortic dilation. On the other hand TEVAR can result in early death and significant neurologic complications; other devastating complications of TEVAR include retrograde aortic dissection and access vessel rupture with a high associated mortality.

A meta-analysis of the published literature reported a high technical success of TEVAR for uncomplicated type B dissection and a relatively high conversion rate (20%) for patient treated with OMT, however the results did not identify an advantage for TEVAR with respect to 30-day and 2-year mortality.2

Dr. Murray L. Shames

An expert panel review of the world literature also did not find significant data to support use of TEVAR for uncomplicated type B dissection.3 In the only randomized prospective trial to examine the role of TEVAR for uncomplicated type B dissection, the INSTEAD trial randomized 140 patients to OMT vs. OMT and TEVAR.4 The study results also did not support the use of TEVAR for the treatment of uncomplicated type B dissection, there was no survival advantage at 2 years, while TEVAR was associated with a 11.1% overall mortality and 4.3% neurologic complication rate, compared with 4.4% and 1.4% in the OMT group. The initial study did however report improved aortic remodeling at 2 years with TEVAR. The results of INSTEAD have been challenged because critical analysis of the INSTEAD trial has determined that the results were underpowered and that there was a 21% crossover in the OMT group and four patients received TEVAR that should have been excluded.5

Subsequent long-term analysis of the INSTEAD XL data do demonstrate a significant survival benefit and freedom from aortic adverse events in the TEVAR group after the initial 2-year analysis.6 At the 5-year follow up only 27 patients remained without a TEVAR. Fortunately there were no adverse events in the patients that crossed over to TEVAR from the OMT group demonstrating the safety of delayed TEVAR in this group. The high rate of aortic associated adverse events may favor early TEVAR. The INSTEAD XL study did identify a large primary tear (more than 10 mm) and an initial aortic diameter of 40 mm as risk factors to crossover suggesting a more aggressive approach in this subset of patients.

So while the INSTEAD XL trial now supports the use of TEVAR for uncomplicated type B dissections this was a relatively small trial that was underpowered in its initial analysis. Expert review of the world literature still supports medical management in the initial phase of treatment. Obviously in cases of failure of medical management TEVAR provides an effective treatment to restore the true lumen and visceral perfusion with possible sustained remodeling of the false lumen.

Given the not insignificant morbidity associated with TEVAR placement, routine treatment of all acute, uncomplicated type B dissections cannot be supported with the current evidence. However, a strategy of selective treatment based on size of the entry tear, extent of dissection, false lumen diameter and extent of thrombosis, effectiveness of antihypertension medications, ability to comply with medical therapy, and surveillance may be implemented. Furthermore treatment at centers of excellence with extensive TEVAR experience based on established protocols favor improved patient outcomes.

References

1. N. Engl. J. Med. 199;340:1546-52

2. Vasc. Endovascular. Surg. 2013 Oct 12;47(7):497-501. Epub 2013 Jul 12.

3. J. Am. Coll. Cardiol. 2013;61(16):1661-78.

4. Circulation 2009;120:2519-28.

5. Circulation 2009;120:2513-14.

6. Circ. Cardiovasc. Interv. 2013;6:407-16.

Dr. Shames is professor of surgery and radiology and program director of vascular surgery at the University of South Florida, Tampa. He reported no relevant conflicts.

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