Author + information
- Alan B. Lumsden, FACS⁎ ( and )
- Michael J. Reardon, FACS
- ↵⁎Reprint requests and correspondence:
Dr. Alan B. Lumsden, Department of Cardiovascular Surgery, 6560 Fannin Street, Suite 1006, Houston, Texas 77030.
The challenge of the acute type B dissection remains as formidable now as it did 28 years ago (1) when DeBakey and Crawford began to classify and intervene on this challenging problem. The average physician dreads the transfer of these patients because of the unpredictability of the clinical course and the unforgiving nature of its complications.
In the absence of prospective randomized trials of medical therapy versus open surgery versus stent grafting, clinicians are guided by the best available data. The investigators of this report (2) and the founders of the International Registry of Acute Aortic Dissection (IRAD) are to be congratulated on their vision and creation of the IRAD and for providing us with these “best available data.” This information is currently being utilized to guide and power clinical trials specifically addressing therapy of acute type B aortic dissection.
The weakness of IRAD consists of data collection in both a prospective and retrospective manner, absence of randomization, vagaries of referral patterns, lack of long-term follow-up; its clear strength is in the consecutive large numbers (571 cases) and propensity scoring in this article. That the data was pooled from 20 aortic centers and 9 countries further enhances the prestige of the database. The multidisciplinary founders of IRAD and the investigators of this report have come to be recognized as being among the most knowledgeable physicians in the aortic dissection arena and have made invaluable contributions in this field.
What Are the Therapeutic Goals in Type B Dissection?
The goal of medical therapy is “short-term complication avoidance.” It does not resolve the dissection; indeed, under the best-case scenario, it commits the patient to life-long aggressive antihypertensive therapy and life-long surveillance in most cases with computed tomography scanning with its attendant radiation and contrast exposure. Subsequent intervention is required in 25% to 30% of patients (3) for aneurysm expansion, progressive dissection, and other complications from the unresolved dissection process. While in-hospital blood pressure control can often be precisely achieved, there are little data on patient compliance and no data on 24-h blood pressure control on the outcome of dissections once the patient is in the outpatient setting (4). Adequacy of blood pressure control at follow-up has been reported as predictive of reintervention for type B dissections (5) and after type A repair (6). Good blood pressure control remains the rationale for advocating continued medical therapy for dissections. In the medical therapy group, “once dissected, always dissected.” Avoidance of short-term complications, life-long blood pressure control, life-long imaging and surgical intervention for up to 30% of the failures is currently the gold standard!
One of the appealing aspects of stent grafting is the elusive paradigm of dissection healing—false lumen thrombosis and remodeling of the aortic wall (7,8). This is a very powerful observation and treatment goal, which raises more questions than it currently answers. Reapposition of the true and false lumen has in many cases produced complete disappearance (at least by contemporary imaging standards) of the dissection. This typically occurs along the length of the stent graft, with reappearance of the dissection in our experience at the end or immediately proximal to the end of the device. The dissection then persists distally. These preliminary multiauthor observations tantalize us with the recognition that:
1) Endovascular devices can initiate false lumen thrombosis.
2) False lumen thrombosis can result in aortic wall healing.
3) Absence of the device leads to reperfusion of the false lumen in most cases.
Clearly these preliminary observations raise the concept that bare stents beyond the covered portion may result in additional wall healing. This is the premise of the TX-2 trial currently underway in Europe (9). This scenario then raises another entire list of intriguing questions:
1) Is the healed wall resistant to redissection?
2) Are the presumed device-related complications sufficiently low to accept this aggressive endoluminal treatment strategy?
3) Does this reduce long-term dissection morbidity?
4) Does this reduce or ameliorate the need for long-term antihypertensive control and imaging follow-up?
These are tantalizing questions that beg analytical and quantitative answers, which currently do not exist. In the abdominal aortic aneurysm environment, sac shrinkage and, in some cases, complete resolution is observed, but does not appear to result in sac healing and fibrosis. Consequently, stabilization of the aortic wall in the absence of stent graft integrity does not develop, rapid re-expansion occurs if repressurization occurs. A contemporary report from Beijing (10) in 63 patients treated with stent grafts for type B dissection reported a 3.2% mortality rate and complete thrombosis of the false lumen in 98.4% at 12-month follow-up. If validated by other centers, this would be yet another piece of evidence that supports the observations in this manuscript supporting the role for stent grafting in type B dissections.
Malperfusion Drives Morbidity and Mortality
Although in this series the morbidity for fenestration (connecting true and false lumen to equilibrate pressure on each side, thereby restoring flow to visceral vessels) was low, fenestration does nothing to stabilize the aneurysm, protect against future expansion, and, in some cases, fails to restore organ flow. In our institution, “primary” fenestration has largely been abandoned in favor of “primary stent grafting” and secondary fenestration if the stent graft fails to restore vital organ perfusion. The rationale for this approach is as stated by the investigators (2):
1) Redirection of flow back into the true lumen by stent grafting usually results in organ reperfusion.
2) The stent graft also has a direct influence on the dissection (stabilization, induction of thrombosis).
Although physicians agonize over identifying which lumen perfuses which visceral vessels, in an effort to predict the beneficial or deleterious effects of stent grafting, in practice this is usually irrelevant. The reason for this irrelevance is that the intima torn out of a renal artery orifice often returns to that spot when the stent graft is inserted. Rarely is supplemental renal stenting even required, but when necessary is a relatively small incremental procedure. We believe that this is the reason stent grafting restored visceral perfusion in 16 of 17 patients in this study compared with 9 of 18 with fenestration and only 4 of 14 with open surgery.
Recognition and Therapy for Acute Aortic Pathologies
Recently a broad group of conditions referred to as “acute aortic syndromes” has been defined (11). Many of these may represent stages in evolution of the same process: intramural hematoma; dissection; aneurysm formation, penetrating ulcer; saccular aneurysm. Nevertheless, they all represent life-threatening aortic pathology especially in the acute presentation. The poster child for this acuity is the type A (ascending) aortic dissection) where mortality is measured as 1% per hour. Misdiagnosis of these pathologies usually because of confusion with myocardial ischemia has led to untimely deaths and high profile lawsuits. Because of the success of national standards for expediting the care of patients with acute myocardial infarction (door-to-balloon time 60 min) and acute ischemic stroke (lysis with 3 h of event), we believe that similar standards should be evolved for acute aortic emergencies. With this in mind, we have created an Acute Aortic Treatment Center that focuses on public education, education of emergency room physicians and cardiologists on identification of the patient with atypical chest pain (12). The rapid transportation of these patients to an appropriate facility and the rapid triage and institution of appropriate therapy of these diverse pathologies. The establishment of an “acute aortic treatment center,” we believe, is the next step in furthering the goal of IRAD to reduce morbidity and mortality from acute aortic disease.
↵⁎ Editorials published in JACC: Cardiovascular Interventions reflect the views of the authors and do not necessarily represent the views of JACC: Cardiovascular Interventions or the American College of Cardiology.
- American College of Cardiology Foundation
- Kahn S.L.,
- Dake M.D.
- Ahmad F.,
- Cheshire N.,
- Hamady M.
- Lumsden A.B.,
- Crawford D.J.,
- Peden E.K.,
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