A single-center experience treating renal malperfusion after aortic dissection with central aortic fenestration and renal artery stenting
Article Outline
- Abstract
- Methods
- Results
- Discussion
- Conclusion
- Author Contriutions
- Appendix (online only).
- References
- Copyright
Objective:
Patients with aortic dissection were studied to define (1) anatomic and physiologic derangements in renal artery blood flow, (2) differences in clinically suspected renal malperfusion and true functional malperfusion, and (3) variations in endovascular interventions for the treatment of renal malperfusion.
Methods:
The cohort comprised 165 patients (mean age, 58 years) with dissections who were thought to have malperfusion sufficient to require arteriography. They were treated from 1996 to 2004 for acute (n = 115) or chronic (n = 50) aortic dissections (75 had type A, 90 had type B lesions). All patients had suspected peripheral vascular malperfusion (ie, cerebral, spinal, mesenteric, renal, or lower extremity vascular beds). Renal malperfusion was suspected in 88 patients secondary to worsening hypertension (n = 34), evolving renal insufficiency (n = 37), computed tomography evidence of impaired renal blood flow (n = 13), or a combination of factors (n = 4). Patients underwent angiographic and intravascular ultrasound studies. Renal malperfusion was confirmed with a systolic gradient between the aortic root and renal hilum (average, 44 mm Hg).
Results:
Right renal arteries arose exclusively from the true lumen in 115 patients (70%), the false lumen in 11 (7%), and both lumens in 37 (23%). Left renal arteries arose exclusively from the true lumen in 69 patients (42%), the false lumen in 32 (20%), and both lumens in 62 (38%). Angiographic confirmation of malperfusion existed in 59 patients (67%) of the 88 suspected of such, and in 31 patients (39%) of the 79 with suspected malperfusion of nonrenal tissues. Of the 90 patients with confirmed renal malperfusion, 71 underwent endovascular therapy, including isolated renal artery stenting (n = 31), as well as proximal aortic fenestration with or without aortic stenting (n = 24), or both renal and aortic intervention (n = 16). Residual pressure gradients averaged 8.1 mm Hg after these interventions. Five procedure-related complications (7%) occurred. The periprocedural postintervention mortality rate was 21% (n = 15), including multisystem organ failure (n = 7), false lumen rupture (n = 3), reperfusion injury (n = 2), cerebral ischemia (n = 1), cardiac arrest (n = 1), and unknown (n = 1).
Conclusions:
Percutaneous aortic fenestration and renal artery stenting are both technically feasible and associated with an acceptable complication rate. Most patients respond well symptomatically, obviating the need for immediate surgical relief of renal artery obstruction and allowing for renal malperfusion recovery.
Acute dissection is a common lethal aortic disease.1, 2, 3, 4, 5 Current literature suggests that aortic dissection results in visceral, renal, cerebral, spinal, or limb ischemia in 25% to 30% of cases and that peripheral vascular insufficiency increases overall patient morbidity and early mortality.1, 2, 6, 7, 8, 9, 10, 11, 12, 13 Specific treatment guidelines have yet to be established, and the optimal initial management of these patients remains controversial in terms of the use of a surgical vs endovascular approach, as well as the timing of central aortic repair. Objectives of the present study of patients with aortic dissection were to define specifically the (1) anatomic and physiologic derangements in renal artery blood flow, (2) how the clinical suspicion of renal malperfusion is related to true functional malperfusion, and (3) variations in endovascular interventions for the treatment of renal malperfusion.
Methods
Patients
A prospectively established electronic database consisting of consecutive patients presenting to the University of Michigan Section of Interventional Radiology with both acute and chronic aortic dissections for angiography between June 1996 and March 2004 was reviewed after approval from the University of Michigan Investigation Review Board (IRB# 2004-0500, “Aortic Dissection with Suspected Malperfusion”). These patients were referred for angiographic and manometric evaluation specifically for a pre-existing clinical suspicion of peripheral vascular malperfusion involving either the cerebral, spinal, mesenteric, renal, or lower extremity vascular beds. To further clarify, this cohort did not include all consecutive patients presenting with aortic dissection, but only those with suspected peripheral malperfusion.
All patients underwent angiographic and intravascular ultrasound (IVUS) studies and were subsequently classified as Stanford type A or B according to Daily et al.14 Criteria for the clinical suspicion of malperfusion included worsening hypertension, evolving renal insufficiency (oliguria or anuria, elevated serum creatinine ≥1.4 mg/dL, or both), or computed tomography (CT) evidence of impaired blood flow by asymmetric renal contrast uptake. True renal malperfusion was confirmed by a systolic gradient between the aortic root and the renal hilum of >10 mm Hg, which is the threshold at which renal artery stenosis is typically treated by the authors; failure of the artery to fill during injection of contrast in the true and false lumen of the aorta; or IVUS evidence of a “curtain-like” occlusion of the vessel origin or of the true lumen above its origin.
Endovascular treatment was undertaken at the discretion of the attending staff and included isolated renal artery stenting, central aortic fenestration with or without aortic stenting, or a combination of the two. Reasons for deferring intervention for a significant pressure gradient at the time of initial angiography included: (1) dissection extending into the lobar arteries or extensive thrombosis, such that renal artery cannulation or other intervention was thought to risk further renal compromise, technical failure, or inability to access accessory branches for stenting, and (2) a minimal pressure gradient that was thought to be “borderline” and likely clinically insignificant.
Outcomes at 30 days were noted and included the incidence of residual pressure gradients >15 mm Hg, death, inpatient renal replacement therapy requirements and hemodialysis needs at the time of discharge, renal insufficiency at the time of discharge (defined as serum creatinine >1.4 mg/dL with no previous history of renal insufficiency), renal artery thrombosis, subsequent open aortic reconstruction, and the average number of antihypertensive medications prescribed at the time of discharge.
Procedural details
Vascular access was gained typically through both common femoral arteries. The only exception to this approach was a woman accessed through the left brachial artery after numerous unsuccessful attempts at common femoral access. IVUS was performed with an 8.2F diagnostic ultrasound catheter with a 12.5-MHz transducer advanced through an 8F Balkan sheath (Cook, Bloomington, Ind). IVUS was performed from the ascending aorta to the iliac arteries to define the relationship of the dissection flap to branch arteries and to determine which lumen each major branch arose from (Fig 1, A and B, online only). Pressures in the SMA, bilateral renal arteries, and bilateral external iliac arteries were measured and compared to pressures in the aortic root. Bilateral renal and superior mesenteric arteriograms with hand injections of contrast were obtained to establish that the location of each measurement was peripheral to the distal extent of the false lumen. Aortic injections were rarely performed, thereby minimizing contrast load.
Renal artery obstructions, as established by aortorenal pressure gradients, were classified by the relation of the dissection flap to the branch origin as static, dynamic, or combined static and dynamic.15 In dynamic obstruction, the flap either prolapsed across the renal artery origin or the aortic true lumen was collapsed to a variable extent between the aortic root and the renal artery origin. In static obstruction, the flap entered the renal artery to a variable extent. Because aortorenal gradients are determined by the total obstructive lesion, treatment was directed initially at dynamic obstruction if present. In this case, fenestration was attempted close to the origin of the compromised vessel; for example, if a “curtain-type collapse” of the abdominal aorta was noted at the level of the renal arteries, a fenestration was performed near that level.
An Amplatz wire was typically advanced through a Cobra catheter. The catheter was then withdrawn over the wire and exchanged for a Rosch-Uchida introducer set (Cook) that was subsequently placed in the true lumen. The wire was removed, and the trocar, in its encasing 5F catheter, was advanced and thrust through the dissection flap using fluoroscopic and IVUS guidance. The trocar was exchanged for the Amplatz wire to allow balloon dilation of the flap and creation of the fenestration tear with a 14-mm-diameter balloon. Typically, little resistance was encountered during balloon dilation and very little “waist” was observed.
After creation of the tear, IVUS was used to observe the configuration of the two lumens. If the true lumen remains collapsed or, in questionable cases, if a gradient between the root and the abdominal aorta persisted, a 16- to 22-mm self-expanding stent was deployed in the aortic true lumen, taking care not to cover the renal or superior mesenteric artery origins (Fig 1, C, online only). Compromise of the superior mesenteric artery was treated before addressing compromise of the renal or iliac arteries. No covered stents and only one endograft were used in this series.
If static obstruction was evident, branch vessel stenting was attempted in standard fashion (Fig 1, D, online only; Fig 2, A to E). A self-expanding bare stent (Palmaz balloon-expandable stent, Cordis/Johnson & Johnson, Miami, Fla; Cook Zilver; Herculink, Abbott, Chicago, Ill; or Cordis S.M.A.R.T. stent) was then deployed under fluoroscopic and, in select cases, IVUS guidance. The stents were extended further into the aortic lumen (up to 5 to 10 mm) than is necessary when treating atherosclerotic stenoses. Early in our experience, we observed balloon-expanded stents being crushed even by small residual gradients between the true and false lumens, and we presently use self-expanding stents exclusively.
Fig 2.
A, Carbon dioxide angiogram of a patient with aortic dissection shows static left renal artery (LRA) obstruction and the true lumen (TL), false lumen (FL), and the dissection flap prolapsing into the left renal artery are well seen. Note that the catheter is in the false lumen. B, Carbon dioxide angiogram of the LRA after fenestration and LRA stenting. C and D, Three-dimensional reformats of the LRA stent (arrow). The true and false aortic lumens are identified. Note the stent extending through the aortic true lumen. E, Cross-sectional computed tomography image of the same patient at the 4-month follow-up. The arrow is directed at the previously placed LRA stent; note the bright and symmetric left renal contrast enhancement supporting adequate perfusion.
Reassessment with IVUS and pressure measurements were performed before the procedure was terminated, because occasionally, revascularization of a major vessel results in proximal collapse of the aortic true lumen with resultant dynamic obstruction. If dynamic obstruction results secondary to treating a branch artery narrowing, it is treated in standard fashion with fenestration and aortic stenting. Procedural success was supported by resolution of true lumen collapse and elimination of, or at least significant improvement in, aorta-branch-artery pressure gradients as determined by IVUS, branch arteriography, and manometry.
Results
The study cohort included 165 patients, 117 men (71%) and 48 women (29%) women with a mean age of 58 years (range, 29-81 years), who were treated from June 1996 to April 2004. Table I summarizes patient demographics, the incidence of acute and chronic type A and B aortic dissections, the etiology, and patient history. Type A dissections occurred in 75 patients (45%) and type B in 90 (55%). Almost 40% of acute dissection patients (n = 44) presented to an outside hospital before transfer to the University of Michigan. Angiographic findings (Fig 3) demonstrated that right renal arteries arose exclusively from the true lumen in 115 patients (70%), exclusively from the false lumen in 11 patients (7%), and from both lumens in 37 patients (23%). Left renal arteries arose exclusively from the true lumen in 69 patients (42%), exclusively from the false lumen in 32 (20%), and from both lumens in 62 (38%).
Table I. Patient demographics, including incidence of (A) acute and chronic type A and B aortic dissections, and (B) sex, etiology, and patient history
| A,Dissection | ||
|---|---|---|
| Dissection | Type A (N = 75), No. | Type B (N = 90), No. |
| Acute (n = 115) | 56 | 59 |
| Chronic (n = 50) | 19 | 31 |
| B,Sex, etiology, and patient history | |
|---|---|
| Demographics | No. (%) |
| Sex | |
| Female | 48 (29) |
| Male | 117(71) |
| Etiology, patient history | |
| Hypertension | 114(69) |
| Diabetes | 7(4.2) |
| Atherosclerosis | 29(17.6) |
| Marfan syndrome | 3(1.8) |
| Bicuspid aortic valve | 2(1.2) |
| Previous or coexisting AAA | 25(15.1) |
| Previous surgery | |
| Aortic (aneurysm/dissection) | 46(27.9) |
| Cardiovascular | 31(18.8) |
| CABG | 13(7.9) |
| AVR | 12(7.3) |
| MVR | 5(3.0) |
| TVR | 1(0.6) |
Fig 3.
Pie graphs illustrate angiographic findings. Top, Right renal arteries arose exclusively from the true lumen in 115 patients (70%), exclusively from the false lumen in 11 (7%), and from both lumens in 37 (23%). Bottom, Left renal arteries arose exclusively from the true lumen in 69 patients (42%), exclusively from the false lumen in 32 (20%), and from both lumens in 62 (38%).
All patients included in this cohort were referred for angiography with a clinical suspicion of peripheral vascular malperfusion. Evidence of mesenteric malperfusion was present in 70, lower extremity malperfusion in 33, spinal cord malperfusion in 6, and cerebral malperfusion in 1. Renal malperfusion was specifically suspected from clinical grounds in 88 patients after worsening hypertension in 34, evolving renal insufficiency in 37, CT evidence of impaired blood flow (asymmetric renal contrast uptake) in 13, or a combination of these factors in 4. Angiography confirmed renal malperfusion in 59 of the 88 (67%) in which it was suspected. Unsuspected renal malperfusion was demonstrated in 31of the 79 patients (39%) in whom renal malperfusion was not clinically suspected.
Renal perfusion pressure deficit between the aortic root and renal hilum averaged 44 mm Hg in this series (range, 12-103 mm Hg). Table II (online only) describes the classification of renal artery obstruction as dynamic or static, the specific endovascular treatment approach (central aortic fenestration with or without aortic stenting or renal artery stenting), and any residual pressure gradient >10 mm Hg after therapy.
Among the total of 90 patients with confirmed malperfusion, 71 underwent endovascular therapy, including isolated unilateral or bilateral renal artery stenting in 31, proximal aortic fenestration with or without aortic stenting in 24, or both renal artery stenting and proximal aortic fenestration with or without aortic stenting in 16. More specifically, these 71 patients had 104 renal arteries demonstrating obstructions that were further classified as 43 static, 30 dynamic, 22 static and dynamic, 2 fibromuscular dysplasia, and 2 stenosis secondary to atherosclerosis. A branch diagram summarizes the endovascular approach to the 71 patients (Fig 4). Incidentally, one endograft repair was done in this series, one patient received bilateral renal artery angioplasty for stenosis secondary to atherosclerosis, and the two patients with fibromuscular dysplasia were treated with either an aortic Wallstent (Boston Scientific, Natick, Mass) (n = 1) or a bare metal renal artery stent (n = 1).
Fig 4.
Branch diagram summarizes the endovascular treatment approach in this series of patients, which is related to unilateral or bilateral renal artery obstruction and the nature of such obstruction (ie, static, dynamic, or static + dynamic). Modalities used included isolated unilateral or bilateral renal artery stenting, proximal aortic fenestration with and without aortic stenting, or both renal artery stenting and proximal aortic fenestration with or without aortic stenting. Ao, Aortic; f/s, aortic fenestration. *Implies some additional therapy was used, such as thrombolysis or thrombectomy.
Reasons for deferring intervention at the time of initial angiography included dissections extending into the lobar arteries or extensive thrombosis such that renal artery cannulation or other intervention was thought to risk further renal compromise (n = 8), technical failure or inability to access accessory branches for stenting (n = 7), and an elevated pressure gradient that was thought to be “borderline” and likely clinically insignificant (n = 10). These same factors were also reasons why residual pressure gradients >10 mm Hg were not pursued therapeutically in some cases. Treatment failures were determined in part by residual pressure gradients after intervention, which averaged 81 mm Hg in this series.
Renal insufficiency (defined as a serum creatinine level >1.4 mg/dL at the time of discharge), need for renal replacement therapy, and difficult to control hypertension at the time of discharge were other factors considered. Of the seven patients (9.7%) who demonstrated a residual gradient of ≥15 mm Hg after intervention, five died early in their hospital course (<30 days), and three were discharged with a serum creatinine level >1.4 mg/dL and were taking an average of five antihypertensive medications at discharge. Of the seven patients (9.7%) that demonstrated a residual gradient of 11 to 14 mm Hg, two died, and four were discharged with a serum creatinine level >1.4 mg/dL and were taking an average of four antihypertensive medications at discharge. Of interest in this treatment cohort was that five patients were discharged with a serum creatinine level >1.4 mg/dL, with no history of renal insufficiency or evidence of residual gradient on manometry. The serum creatinine level averaged 1.6 mg/dL (range, 0.5-6.6 mg/dL) at admission and 1.7 mg/dL (range, 0.6-11.7) at discharge. Peak serum creatinine level in the treatment group averaged 3.3 mg/dL during hospitalization (range 0.8-11.7).
Five procedurally related complications were documented, including groin hematoma in 2, intraprocedural hypotension and bradycardia requiring atropine in 1, renal artery stent thrombosis requiring thrombolysis in 1, and endograft leak in 1. The periprocedural mortality rate (≤30 days) of the intervention cohort was 21% (n = 15). Cause of death included multisystem organ failure in 7, false lumen rupture in 3, reperfusion injury in 2, cerebral ischemia in 1, cardiac arrest in 1, and unknown in 1. Notably, of the patients with false lumen rupture, one was deemed a poor operative candidate for central aortic reconstruction, and the definitive surgical repair in another patient was delayed secondary to alcohol withdrawal and frank delirium tremens.
The obstruction type and endovascular approach distribution by aortic dissection type can be summarized (Fig 5). The 30-day outcomes of the 71 patients in the interventional group also can be summarized (Table III) by dissection type, including the incidence of residual pressure gradients >15 mm Hg, early death, necessary inpatient renal replacement therapy, and hemodialysis needs at the time of discharge, renal insufficiency at the time of discharge (defined as serum creatinine level >1.4 mg/dL), renal artery thrombosis, subsequent open aortic reconstruction, and the average number of antihypertensive medications prescribed at the time of discharge.
Fig 5.
A, Bar graph summarizes the incidence of renal artery obstruction by static or dynamic aortic dissection type, or both; other implies rare cases of fibromuscular dysplasia or atherosclerosis. B, The endovascular approach is summarized by aortic dissection type. Combo, is a combination of modalities; f/s, central aortic fenestration.
Table III. Thirty-day outcomes of intervention by aortic dissection type
| Outcome | Acute A | Acute B | Chronic A | Chronic B |
|---|---|---|---|---|
| Patient totals | 26 | 25 | 5 | 15 |
| Residual RA pressure gradient >15 mm Hg | 8 | 2 | 1 | 1 |
| Inpatient RRT required | 6 | 7 | 0 | 1 |
| At discharge | ||||
| Hemodialysis required | 0 | 1 | 0 | 0 |
| Renal insufficiencya | 7 | 5 | 0 | 2 |
| RA thrombosis | 2 | 2 | 0 | 0 |
| No. of antihypertensives, avg | 2.5 | 3.4 | 3.2 | 3.0 |
| Open aortic reconstruction ≤30 days | 10 | 1 | 1 | 1 |
| Early death (≤30 days) | 9 | 5 | 0 | 1 |
aDefined as serum creatinine >1.4mg/dL. |
In this series of dissections, 8 patients presenting with chronic type A dissection had a remote open surgical reconstruction, as did 7 patients with chronic type B, 3 patients with acute type B, and 1 patient with acute type A. A smaller proportion of the cohort patients were referred for angiographic evaluation for suspected malperfusion after open surgical reconstruction. This included six patients with acute type A dissection, three with chronic type A, and one with acute type B. Of these patients with suspected malperfusion after surgical aortic reconstruction, only four required an endovascular intervention for renal branch obstruction. Finally, open surgical reconstruction ≤30 days after angiography and endovascular intervention for branch obstruction was required in 21 patients with acute type A dissection, three with chronic type A, and two with acute type B. Recent cutdown of the femoral artery, such as when a patient underwent aortofemoral arterial bypass, did affect the endovascular approach. In this case, the affected femoral artery would be repaired in the surgery suite or the contralateral femoral artery would be punctured twice in tandem fashion.
Discussion
It should be noted that the angiographic evaluation of renal malperfusion is directed at finding and treating an ongoing anatomic renal artery obstruction. Patients who have renal artery obstruction early in the course of aortic dissection, but whose kidney spontaneously reperfuses, may have unilateral or bilateral acute tubular necrosis with no ongoing anatomic abnormality at the time of angiography. In putting numerous clinical articles in context, especially those reporting on nonoperated on type B dissections, “renal dysfunction” does not distinguish between simple acute tubular necrosis, mechanical obstruction by a static or dynamic mechanism, or a combination of both. In addition, we recognize that using residual pressure gradients to determine treatment success and failure is somewhat arbitrary and misleading, because, for example, improving an aortorenal gradient from 60 to 20 mm Hg would be construed as a treatment failure, yet by improving renal function, might represent a clinical success.
Individual patient outcome in our series (Table II online only) reflects a longstanding therapeutic approach to renal artery compromise, which is corroborated by the “aortic dissection treatment algorithm” Williams et al16 and Beregi et al17 set forth for acute malperfusion complicating acute aortic dissection.
Clinical experience has established that one-third of patients with acute aortic dissection will demonstrate peripheral vascular ischemia and that vascular insufficiency increases the risk of overall morbidity and early mortality.2, 6, 7, 8, 9, 10, 11 In addition, Miller et al18 identified both renal dysfunction and renal/visceral ischemia as significant independent predictors of operative death in both acute and chronic type A and B aortic dissections. What is not well established and remains controversial is the optimal treatment strategy for patients with aortic dissection complicated by peripheral vascular malperfusion. Some advocate immediate aortic reconstruction in the setting of an acute type A dissection. This is supported by the observation that up to 80% of peripheral malperfusions will resolve with restoration of blood through the true lumen.1, 2, 8, 11 Other practices advocate delaying surgery on acute type A dissections in preference for percutaneous correction of the peripheral vascular malperfusion to allow for recovery from reperfusion to reduce overall death.1, 7, 8, 15, 19, 20 Most will advocate medical management for acute type B dissections, reserving surgery (aortic graft replacement or extra-anatomic bypass) for patients with intractable pain, uncontrolled hypertension, severe aortic branch malperfusion, or aneurysm expansion.21
Studies have recognized that renal failure with anuria and bowel ischemia in the setting of acute aortic dissection have been associated with lethal multiorgan failure, making resolution of these symptoms a major priority.9, 15 Fann et al8, 22 demonstrated that impaired renal perfusion is associated with a high operative mortality rate of 50% with renal ischemia compared with 23% for those without compromised renal perfusion, and that both impaired renal perfusion and renal dysfunction were significant independent predictors of operative death.8, 22 In fact, these authors maintain that compromised renal perfusion was the only peripheral vascular complication that was a significant independent predictor of operative death.8
Shiiya et al23 recently recognized various mechanisms of malperfusion and found that although a central aortic operation alone successfully reversed 100% of aortic-type malperfusion in acute type A and B dissections, it was not effective for every branch-type malperfusion. They specifically noted that surgical fenestration successfully reversed branch-type renal malperfusion in only 15% (2 of 13 patients); however percutaneous stenting was successful in all vessels with branch-type malperfusion.23
Finally, Estrera et al24 have emphasized that end-organ malperfusion remains the most common cause of significant morbidity during the acute presentation of type B aortic dissection; presumably resulting from thrombosis, ischemia–reperfusion injury, or a systemic inflammatory response syndrome.2, 19 They also showed that low glomerular filtration rate was an independent risk factor for midterm death.24
Endovascular stent graft placement at the site of the aortic intimal tear is another evolving technique increasingly used in the approach to the dissected aorta in an effort to redirect flow into the true aortic lumen.1, 25, 26 In 1999, Dake et al25 reported 19 patients with aortic dissection, 37% of whom had symptomatic branch compromise. These authors demonstrated a 100% technical success rate in covering the aortic tear, resulting in resolution of peripheral ischemia in 76% of their cohort. The resolution of peripheral ischemia applied to 22 of 22 patients with dynamic obstruction and six of 15 patients with combined static and dynamic obstruction. Since this early report, several additional reports have supported the utility and safety of aortic stent grafts.25, 26 However, although stent grafting may be quite successful when directed at relieving a dynamic obstruction, the benefit in the setting of a branch-obstructing flap remains unclear.
Limitations associated with this study include its descriptive nature, the incomplete nature of electronic medical records for patients presenting before 1999, and the fact that a number of patients were lost to follow-up after hospital discharge. Also, the inclusion of chronic dissection patients with their associated previous surgical interventions and a sometimes atypical clinical presentation may only complicate this picture, and a focused investigation of strictly acute dissection is thought to be warranted. Longer follow-up and interrogation of more tangible outcomes of the aforementioned cohort, such as hospital length of stay, need for renal replacement therapy or renal transplant, and death, may better define the optimal initial therapeutic approach for those with aortic dissection and concomitant renal malperfusion.
Conclusion
This series of patients represents, to our knowledge, the largest reported cohort with renal malperfusion accompanying aortic dissection identified by IVUS, manometry, and selective renal arteriography, and treated by contemporary endovascular interventions. Percutaneous aortic fenestration and renal artery stenting in aortic dissections with renal artery obstruction has been shown to be technically feasible, adaptable to numerous clinical situations (preoperative or postoperative acute or chronic type A or type B dissection), and associated with an acceptable complication rate. Most patients respond well symptomatically, obviating the need for surgical relief of the obstruction, although additional measures such as stent implantation may be necessary for complete relief in some cases.10, 27
Author Contriutions
Appendix (online only)
Fig 1.
(online only). Intravascular ultrasound imaging (IVUS) of the thoracic aorta of a patient with an acute type B aortic dissection. A, The false lumen is hyperechoic and fully distended, obliterating the true lumen of the aorta except for a slit-like envelope anteriorly. B, In this image of the same patient's left renal artery, the left renal artery appears to arise from the false lumen, but selective arteriography demonstrated that the renal artery was narrowed, but remained tethered to the true lumen. C, IVUS imaging of the thoracic aorta after fenestration and placement of a Wallstent (Boston Scientific). The true lumen has been stented (arrow), with only some continued mild narrowing of the true lumen in the unstented region across the superior mesenteric and bilateral main renal arteries (not illustrated). After aortic fenestration and aortic stenting, a 17 mm Hg systolic gradient was measured across the renal artery origin, despite a re-entry tear at the origin. D, Final IVUS images of the bilateral renal arteries after aortic fenestration, aortic wall stent, and left renal artery stenting. Selective stenting of the left renal artery reduced systolic gradient to 6 mm Hg.
Table II. (online only). Classification of renal artery obstruction (dynamic vs static) and the specifications of endovascular treatments (central aortic fenestration vs renal artery stenting)
| Type of obstruction (pressure gradient, mm Hg) | Endovascular approach | Residual gradient (if >10 mm Hg) | |||||
|---|---|---|---|---|---|---|---|
| No. | RRA | LRA | F/S(+/−)a | RRA stent | LRA stent | RRA | LRA |
| 1 | Static(23) | . . . | Untreated | 23 | . . . | ||
| 2 | Dynamic(++)b | . . . | ✓(−) | . . . | |||
| 3 | Dynamic(63) | Static(20) | ✓(−) | ✓ | |||
| 4 | Static(58) | . . . | ✓ | . . . | |||
| 5 | Dynamic(44) | . . . | ✓(−) | . . . | |||
| 6 | Both(50)c | Both(50) | ✓(−) | ||||
| 7 | . . . | Static(91) | ✓ | . . . | |||
| 8 | . . . | Static(62) | ✓ | . . . | |||
| 9 | Dynamic(71) | Dynamic(71) | ✓(−) | ||||
| 10 | . . . | Static(++) | Untreated | . . . | ++ | ||
| 11 | Dynamic(14) | Both(26) | ✓(+) | Untreated | 26 | ||
| 12 | . . . | Static(15) | Untreated | . . . | 15 | ||
| 13 | Static(85) | . . . | ✓ | . . . | |||
| 14 | Dynamic(85) | Static(10) | ✓(−) | ✓ | |||
| 15 | Dynamic(54) | . . . | ✓(−) | . . . | |||
| 16 | . . . | Static(64) | ✓ | . . . | 15 | ||
| 17 | . . . | Static(++) | Untreated | . . . | ++ | ||
| 18 | Static(++) | . . . | Untreated | ++ | . . . | ||
| 19 | Dynamic(++) | Both(14) | ✓(+) | ✓ | |||
| 20 | Both(30) | Dynamic(27) | ✓(+) | ||||
| 21 | Static(16) | . . . | Untreated | . . . | 16 | . . . | |
| 22 | Dynamic(15) | Dynamic(15) | ✓(+) | ||||
| 23 | Both(48) | Static(48) | ✓(+) | ✓ | ✓ | ||
| 24 | Dynamic(++) | . . . | ✓(+) | . . . | |||
| 25 | Dynamic(12) | Dynamic(++) | ✓(+) | Untreated | ++ | ||
| 26 | . . . | Static(58) | ✓(+) | ✓ | . . . | ||
| 27 | Dynamic(44) | Static(58) | ✓(+) | Untreated | 58 | ||
| 28 | Static(60) | . . . | ✓ | 14 | . . . | ||
| 29 | . . . | Static(69) | Untreated | . . . | 69 | ||
| 30 | Static(38) | Static(38) | ✓(+) | ||||
| 31 | . . . | Static(52) | ✓ | . . . | |||
| 32 | Static(20) | Static(70) | ✓ | ✓ | 15 | ||
| 33 | Both(73) | Both(++) | ✓(+) | ✓ | ✓ | ++ | |
| 34 | . . . | Both(45) | ✓(−) | ✓ | . . . | ||
| 35 | Dynamic(45) | Both(17) | ✓(+) | ||||
| 36 | . . . | Static(81) | Untreated | . . . | 81 | ||
| 37 | Static(++) | Static(++) | Untreated | ++ | ++ | ||
| 38 | Dynamic(++) | . . . | ✓(+) | . . . | |||
| 39 | Static(47) | . . . | ✓ | 11 | . . . | ||
| 40 | . . . | Dynamic(21) | ✓(+) | . . . | |||
| 41 | Static(40) | Static(++) | Untreated | 40 | ++ | ||
| 42 | Static(14) | Static(25) | ✓ | ✓ | |||
| 43 | Static(9) | Static(19) | Untreated | 9 | 19 | ||
| 44 | . . . | Static(75) | ✓ | . . . | 13 | ||
| 45 | . . . | Other(44)d | ✓ | . . . | |||
| 46 | Both(70) | Both(15) | ✓ | ✓ | |||
| 47 | Dynamic(120) | Both(++) | ✓(+) | Untreated | 29 | ++ | |
| 48 | . . . | Static(77) | ✓ | . . . | |||
| 49 | . . . | Static(45) | ✓ | . . . | |||
| 50 | Dynamic(21) | . . . | Untreated | 21 | . . . | ||
| 51 | . . . | Static(24) | ✓ | . . . | |||
| 52 | . . . | Static(25) | ✓ | . . . | |||
| 53 | Static(41) | . . . | ✓ | . . . | |||
| 54 | Both(70) | Both(70) | ✓(+) | ||||
| 55 | . . . | Static(75) | ✓ | . . . | 14 | ||
| 56 | . . . | Both(33) | ✓(+) | ✓ | . . . | 14 | |
| 57 | Dynamic(++) | Dynamic(++) | ✓(+) | ||||
| 58 | Both(23) | Both(34) | ✓(+) | ||||
| 59 | Dynamic(15) | Dynamic(15) | Untreated | ||||
| 60 | . . . | Static(76) | ✓ | . . . | |||
| 61 | Static(71) | Static(71) | ✓(+) | ||||
| 62 | Dynamic(++) | Both(++) | ✓(+) | ✓ | 14 | ||
| 63 | Static(20) | . . . | ✓ | . . . | |||
| 64 | . . . | Static(22) | Untreated | 22 | |||
| 65 | Static(80) | Dynamic(80) | ✓(+) | ✓ | |||
| 66 | Dynamic(19) | . . . | ✓(−) | . . . | |||
| 67 | FMD(30) | Static(++) | ✓ | Untreated | ++ | ||
| 68 | . . . | Both(103) | ✓(+) | Untreated | . . . | ||
| 69 | Static(23) | . . . | ✓ | . . . | |||
| 70 | Both(59) | Dynamic(++) | ✓(+) | ✓ | |||
| 71 | Static(13) | Both(21) | ✓(−) | ✓ | 11 | 11 | |
| 72 | . . . | Static(++) | Untreated | . . . | ++ | ||
| 73 | . . . | Static(28) | ✓ | . . . | |||
| 74 | Both(20) | Dynamic(++) | ✓(+) | ✓ | |||
| 75 | . . . | Static(53) | ✓ | . . . | |||
| 76 | Dynamic(42) | Both(++) | ✓(+) | Untreated | ++ | ||
| 77 | . . . | Static(14) | Untreated | ||||
| 78 | . . . | Static(44) | ✓ | . . . | |||
| 79 | Dynamic(30) | . . . | ✓(+) | . . . | |||
| 80 | Static(81) | Static(++) | ✓(+) | ✓ | |||
| 81 | . . . | Static(++) | Untreated | . . . | ++ | ||
| 82 | Static(12) | Static(16) | Untreated | ||||
| 83 | Dynamic(83) | . . . | ✓(−) | ✓ | 15 | . . . | |
| 84 | Dynamic(54) | . . . | ✓(+) | ✓ | 25 | . . . | |
| 85 | Static(29) | . . . | ✓ | . . . | |||
| 86 | Static(118) | . . . | ✓ | . . . | |||
| 87 | Dynamic(83) | Static(15) | ✓(−) | 15 | |||
| 88 | Dynamic(11) | . . . | ✓ | . . . | |||
| 89 | Atherosclerotic(13) | Atherosclerotic(15) | ✓ | ✓ | |||
| 90 | Static(16) | Static(22) | Untreated | ||||
aAortic fenestration (F/S) with (+) or without (−) stenting of the aortic true lumen. |
b++ implies significant pressure gradient is present but is immeasurable. |
c“Both” implies both dynamic and static renal artery obstruction. |
d“Other” implies stenosis of a previously placed stent. |
References
- Contemporary management of aortic branch compromise resulting from acute aortic dissection. J Vasc Surg. 2001;33:1185–1192
- . Management strategies for type A dissection complicated by peripheral vascular malperfusion. Ann Thorac Surg. 2004;77:1309–1314
- . Acute aortic dissections. Ann Surg. 1976;42:395–404
- . Dissecting aneurysm of the aorta: a review of 505 cases. Medicine. 1958;37:217–219
- The International Registry of Acute Aortic Dissection (IRAD)–new insights into an old disease. JAMA. 2000;283:897–903
- Dissection and dissecting aneurysms of the aorta: twenty-year follow-up of five hundred twenty-seven patients treated surgically. Surgery. 1982;92:1118–1134
- . Aortic dissection: percutaneous management of ischemic complications with endovascular stents and balloon fenestration. J Vasc Surg. 1996;23:241–253
- Treatment of patients with aortic dissection presenting with peripheral vascular complications. Ann Surg. 1990;212:705–713
- Vascular complications associated with spontaneous dissection. J Vasc Surg. 1988;7:199–209
- Intravascular ultrasound-guided percutaneous fenestration of the intimal flap in the dissected aorta. Circulation. 1997;96:2124–2127
- Impact of organ malperfusion on mortality and morbidity in acute A aortic dissections. J Card Surg. 2006;21:363–369
- Acute limb ischemia associated with type B aortic dissection: clinical relevance and therapy. Surgery. 2006;140:532–539
- Acute aortic dissection presenting with primarily abdominal pain: a rare manifestation of a deadly disease. Ann Vasc Surg. 2005;19:367–373
- . Management of acute aortic dissections. Ann Thorac Surg. 1970;10:237–247
- The dissected aorta: part III. Anatomy and radiologic diagnosis of branch-vessel compromise. Radiology. 1997;203:37–44
- The dissected aorta: percutaneous treatment of ischemic complications—principles and results. J Vasc Interv Radiol. 1997;8:605–625
- Endovascular treatment of acute complications associated with aortic dissection: midterm results from a multi-center study. J Endovasc Ther. 2003;10:486–493
- . Independent determinants of operative mortality for patients with aortic dissections. Circulation. 1984;70:I153–I164
- Surgical delay for acute type A dissection with malperfusion. Ann Thorac Surg. 1997;64:1669–1675
- . Percutaneous balloon fenestration and stenting for life-threatening ischemic complications in patients with acute aortic dissection. J Thorac Cardiovasc Surg. 1999;117:1118–1127
- . Outcome of medical and surgical treatment in patients with acute type B aortic dissection. Ann Thorac Surg. 2005;79:790–794
- Surgical management of aortic dissection during a 30-year period. Circulation. 1995;92(9 suppl):II113–II121
- . Management of vital organ malperfusion in acute aortic dissection: proposal of a mechanism-specific approach. Gen Thorac Cardiovasc Surg. 2007;55:85–90
- Update on outcomes of acute type B aortic dissection. Ann Thorac Surg. 2007;83:S842–S845
- Endovascular stent-graft placement for the treatment of acute aortic dissection. N Engl J Med. 1999;340:1546–1552
- . Will stent-graft repair emerge as treatment of choice for acute type B dissection?. Semin Vasc Surg. 2006;19:40–47
- . The use of endovascular techniques for the treatment of complications of aortic dissection. J Vasc Surg. 1993;18:1042–1051
Additional material for this article may be found online at www.jvascsurg.org.
Competition of interest: none.
CME article
PII: S0741-5214(08)00015-3
doi:10.1016/j.jvs.2007.12.057
© 2008 The Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.
Refers to article:
- Invited commentary
Refers to erratum:
- Correction