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Ann Thorac Surg 1998;66:1679-1683
© 1998 The Society of Thoracic Surgeons

Experimental confirmation of effectiveness of fenestration in acute aortic dissection

David L.S. Morales, MDa, Jacquelyn A. Quin, MDa, John H. Braxton, MDa, Graeme L. Hammond, MDa, Richard J. Gusberg, MDa, John A. Elefteriades, MDa

a Section of Cardiothoracic Surgery, Yale University School of Medicine, New Haven, Connecticut, USA

Accepted for publication May 27, 1998.

Address reprint requests to Dr Elefteriades, Section of Cardiothoracic Surgery, Yale University School of Medicine, 121 FMB, 333 Cedar Street, New Haven, CT 06520
e-mail: (John Elefteriades{at}qm.yale.edu)


   Abstract
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 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. Aortic fenestration is used clinically to treat organ ischemia in acute descending aortic dissection. However, fenestration has not been studied experimentally. This study does so using an animal model.

Methods. Descending aortic dissection was created in six dogs, with subsequent fenestration of the infrarenal aorta. Blood flow (femoral, cephalic, and renal), blood pressure (femoral and carotid), and aortic distensibility were measured at baseline, after dissection, and after fenestration. Values were compared using paired t tests.

Results. Baseline femoral, cephalic, and renal arterial flows were 53 ± 37, 78 ± 65, and 83 ± 52 mL/min, respectively. Baseline femoral and carotid pressures were 82 ± 13 and 81 ± 11 mm Hg, respectively. After dissection, femoral, cephalic, and renal arterial flow decreased to 20 ± 21 (p < 0.05), 38 ± 26, and 56 ± 36 mL/min, respectively. Femoral blood pressure decreased to 28 ± 17 mm Hg (p < 0.05). With fenestration, femoral, cephalic, and renal flows increased to 60 ± 37 (p < 0.05), 78 ± 51, and 80 ± 48 mL/min, respectively. Femoral blood pressure increased to 85 ± 28 mm Hg (p < 0.05). Carotid pressure remained unchanged with dissection and fenestration (77 ± 17 mm Hg, 82 ± 17 mm Hg, respectively). Baseline aortic distensibility (21%) decreased significantly after dissection (to 1.4%, p < 0.05) and increased after fenestration (to 12%, p < 0.05).

Conclusions. Experimental aortic fenestration restored blood pressure and flow to hypoperfused organs in acute descending aortic dissection. The continued clinical application of fenestration is supported.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
Aortic dissection is a common occurrence with an estimated incidence of 2,000 cases per year in the United States [1]. Outcome depends largely on the type of dissection. Ascending aortic dissections are frequently fatal as a result of rupture, aortic valvular insufficiency, coronary artery occlusion, or pericardial tamponade. Most of these deaths occur in hours to days [2]; thus treatment of ascending aortic dissections requires prompt surgical correction.

Dissection of the descending aorta carries a better prognosis. It is increasingly agreed that distal dissections may be treated medically using afterload reduction with operations undertaken selectively for complications including rupture, extension, or, most commonly, end-organ ischemia [3].

We previously reported successful clinical application of aortic fenestration for patients with organ ischemia from acute aortic dissection [4]. Despite this clinical application in a small number of patients, the effects of the fenestration procedure have not been investigated specifically in the laboratory. In the present study, we used an established experimental model of acute aortic dissection to evaluate the effectiveness of aortic fenestration in restoration of organ perfusion and decompression of the false lumen in descending aortic dissection.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
Animal preparation
Seven male mongrel dogs, weighing 40 to 50 lb, were studied. The animals were given humane care in compliance with the "Guide for the Care and Use of Laboratory Animals" (NIH publication 85-23, revised 1996). Anesthesia was induced with 25 mg/kg intravenous phenobarbital and was maintained using inhalational oxygen and isoflurane. Six dogs underwent fenestration; one additional dog served as a control to confirm the model of aortic dissection.

Operative procedure
The method of induction of aortic dissection follows that described by Blanton and associates [5] and by Carney and associates [6]. A left thoracotomy was performed in the fourth intercostal space. The descending aorta was exposed for 5 cm and isolated between two cross-clamps. Local intercostal branches were ligated. A bolus of 5,000 units of intravenous heparin was given and the aorta clamped. A transverse aortotomy, encompassing 50% of the aortic circumference, was made. An aortic intimal flap was created distal to the incision and was loosely attached to the opposite aortic wall to ensure creation of a false passage. The aortotomy was closed with a running 4-0 polypropylene suture; the aorta was unclamped and hemostasis obtained. Heparin reversal (ie, protamine) was not given. Intravenous epinephrine and isoproterenol were administered briefly to augment blood pressure and thus encourage distal propagation of the dissection.

Placement of monitoring catheters and probes was performed using a midline abdominal incision from xiphoid to pubis (Fig 1). In dogs, the equivalent of the superior mesenteric artery is termed the cephalic artery. Doppler flow probes (Crystal Biotech, Northboro, MA) were placed onto this artery (4-mm probe) and onto the left renal and femoral arteries (5-mm probe) for quantitative flow measurements. Indwelling 18-gauge arterial pressure catheters were placed into the right femoral and carotid arteries. A crystal thickening probe (Crystal Biotech, Northboro, MA) was secured to the aortic wall below the level of creation of dissection.



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  		Fig 1. Hemodynamic monitoring apparatus. Doppler flow probes are placed on the cephalic, femoral, and renal arteries. Pressure transducers are placed in the femoral and carotid arteries. An aortic strain probe is placed on the aorta distal to the created dissection.

 
The technique of fenestration as performed clinically is illustrated in Figure 2 [4]. In the experimental animal model, aortic exposure was obtained through the midline abdominal incision. The distal infrarenal aorta was clamped and completely transected. Proximally, the intimal layer, which had dissected from the aortic wall, was removed; the distal intimal layer was reapproximated to the adventitia by using a continuous running 4-0 polypropylene suture. The transected aorta was anastomosed with a running 4-0 polypropylene suture, and the adventitial upper aorta was sewn to the reconstituted lower aorta. Upon completion of the experimental protocol, animals were sacrificed and the aortas removed for pathologic examination.



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  		Fig 2. Fenestration procedure showing the incision (A), exposure of the aorta (B), transection of the aorta with the double lumen visible and resection of the intima proximally (C), and suturing of the adventitial aorta above to the reconstituted distal aorta below (D). This diagram schematizes the procedure as performed in human patients. In the experimental model, fenestration was performed similarly, except for exposure, which was obtained by midline laparatomy. (Reproduced with permission from Elefteriades and associates [4].)

 
Aortic imaging
A baseline echocardiographic image of the native aorta was obtained (UM9 Echo with a 5 MHz phased array probe, Advanced Technology Laboratories, Bellingham, WA). After creation of the aortic dissection, presence of a false lumen was confirmed in all cases before proceeding to aortic fenestration. Final images of the aortic lumen were taken after fenestration.

Pressure and flow measurements
Arterial flow (femoral, cephalic, and renal) and pressure (femoral and carotid) were measured at baseline and 30 minutes after creation of the aortic dissection. After the fenestration procedure, measurements were repeated at 10-minute intervals for 30 minutes, after which the interval was increased to 15 minutes for the remaining 90 minutes of the experiment. Pressure and flow measurements were stored in a computer software package for analysis (Dataflow, Crystal Biotech, Northboro, MA).

Aortic distensibility
Aortic wall thickness was measured at end-systole and end-diastole. Aortic distensibility in this experimental model, reported as a percentage, is defined as the difference in aortic wall thickness between diastole and systole, divided by the aortic wall thickness at the end of diastole; ie, (TD - TS)/TD, where TD and TS represent thickness in diastole and systole, respectively. As such, a decrease in aortic distensibility indicates a smaller change in aortic wall thickness between systole and diastole. Absolute measurements of aortic wall thickness were loaded into a computer software package (Dataflow, Crystal Biotech) and internally analyzed for distensibility calculations.

Statistical analysis
Descriptive analyses of the mean and standard deviation were performed directly from pressure and flow measurements for all six dogs. Differences in pressure and flow as a result of dissection and after fenestration were analyzed for significance using paired t tests, where each animal served as its own control. Statistical analysis was performed using a computerized software package (SAS Institute, Cary, NC).


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
Measurements for flow, mean blood pressure, and aortic distensibility at baseline, 30 minutes after aortic dissection, and 90 minutes after fenestration are given in Table 1 for the six animals that underwent the experimental protocol. After dissection, femoral mean arterial flow decreased significantly, from 53 ± 37 mL/min to 20 ± 21 mL/min (p < 0.05). Cephalic and renal mean arterial flow decreased from 78 ± 65 and 83 ± 52 mL/min to 38 ± 26 and 56 ± 36 mL/min, respectively; these decreases approached statistical significance (p = 0.07 and 0.06, respectively). After the fenestration procedure, femoral, cephalic, and renal flow returned to baseline values (60 ± 37, 78 ± 51, and 80 ± 48 mL/min, respectively); the increases in femoral and cephalic flow were significant (p < 0.05).


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  		Table 1. Flow, Pressure, and Aortic Distensibility Measurements in Six Dogs

 
After dissection, mean femoral arterial pressure significantly decreased from 82 ± 13 mm Hg to 28 ± 17 mm Hg (p < 0.05); the return in pressure to baseline after fenestration was also significant (85 ± 28 mm Hg, p < 0.05). There were no significant changes in carotid arterial pressure as a result of dissection or fenestration, which is consistent with creation of a descending aortic dissection distal to the carotid and subclavian arteries.

Aortic distensibility at baseline was 21%. This value decreased significantly to 1.4% (p < 0.05) after creation of the dissection and increased to 12% (p < 0.05) after the fenestration procedure.

Echocardiographic imaging demonstrated impingement of the true aortic lumen by the false lumen after dissection; contour of the true lumen was restored after fenestration (Fig 3).



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  		Fig 3. Echocardiographic examination of the dissected aorta before (A and C) and after (B and D) fenestration. Panels A and B show the cross- sectional aorta and panels C and D show the aorta in longitudinal view. A decrease in the size of the false lumen is seen after fenestration.

 
After completion of the experimental protocol, the aorta was removed, and aortic dissection was confirmed by pathologic examination. Dissections were antegrade and lateral or spiral in nature. Fenestration effected decompression of the false lumen, with no demonstrated thrombus.

One animal served as a control to confirm the model of dissection. Respective blood flows for the femoral, cephalic, and renal arteries were 110, 106, and 29 mL/min (Table 2). Baseline mean femoral and carotid arterial pressures were 120 and 86 mm Hg, respectively. Thirty minutes after creation of the dissection, blood flow decreased dramatically to 19, 58, and 21 mL/min for the femoral, cephalic, and renal arteries, respectively. Femoral mean arterial pressure also decreased to 27 mm Hg after 30 minutes; carotid mean arterial pressure did not decrease markedly until 60 minutes after creation of the dissection (from 86 mm Hg at baseline to 41 mm Hg). After 75 minutes, the animal died of bradycardia and severe hypotension. Postmortem examination confirmed descending aortic dissection and disclosed intestinal and bilateral renal infarction. This lethal outcome without fenestration contrasted with the survival and good condition of the fenestrated animals.


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  		Table 2. Flow, Pressure, and Aortic Distensibility in Control Animal

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
This experimental protocol provides documentation of the effectiveness of the fenestration procedure in reversing the peripheral complications of acute descending aortic dissection.

Peripheral ischemia is the predominating complication of distal aortic dissection, with overall clinical incidence of 30% to 50% [7]. Extremity ischemia occurs most commonly; other organs that might be affected include the kidneys, brain, spinal cord, and abdominal viscera. This clinical distribution of organ ischemia appears to be replicated satisfactorily by the current experimental model. Femoral arterial flow and mean pressure significantly decreased as a result of the dissection. Renal and cephalic flow and pressure also decreased dramatically, closely approaching statistical significance. Carotid arterial flow and pressure did not change significantly during the experiment, which is consistent with a dissection limited to the descending aorta.

This experimental investigation supports the hypothesis that fenestration successfully restores blood flow through the true aortic lumen and its branches by decompression of a tense false lumen that would otherwise impinge on the ostia of such branch vessels [8]. The present study demonstrates that fenestration improves perfusion both above (cephalic and renal) and below (femoral) the aortic level at which the actual fenestration is performed. Decompression of the false lumen was demonstrated in the experimental model both by echocardiography (Fig 3) and by postmortem examination of the aorta.

In this investigational protocol, aortic distensibility was also studied; it was defined as the difference in aortic wall thickness between end-diastole and end-systole divided by the thickness of the aorta at the end of diastole. A high aortic distensibility implies a compliant, easily distensible aorta; wall thickness differs markedly between diastole and systole. Conversely, a stiff, noncompliant aorta has a lower distensibility. In the experimental model, the baseline percentage distensibility of the aorta dropped from 21% to 1.4% after creation of the dissection. The aorta might have lost a large part of its elasticity secondary to impingement by a false lumen distended with blood, maximal distention even in diastole, or loss of the elastic layers from the outer wall of the dissection. After fenestration, the aortic distensibility improved significantly, which suggests an improvement in the intrinsic mechanics of the aortic wall. One caveat in interpreting the results of the study is that the aorta in the experimental animal was presumably normal, as opposed to the atherosclerotic, diseased aorta, which is encountered clinically.

Fenestration is not a new technique. It was first described by Gurin and associates [9] in 1935 and used successfully by DeBakey and associates [10] in 1955. Additional studies of its sporadic clinical application in aortic dissection have been published [11–13].

We previously examined the role of fenestration as part of our complication-specific approach to patients who present with descending aortic dissection [4]. Patients with descending aortic dissection who had no immediate indication for operation were treated expectantly for complications. Impending rupture or enlargement was treated by direct aortic replacement, or, rarely, thromboexclusion. Patients with peripheral ischemia were treated using fenestration.

In our initial series of 12 patients who presented with ischemic complications secondary to aortic dissection, fenestration restored distal flow in 11 patients. Of the 10 patients with limb ischemia, normal pulses were reestablished in 9. The only unsuccessful case was one in which fenestration was performed after lower-extremity and renal ischemia had persisted for 2 weeks. We emphasize that fenestration is effective clinically only when performed early in the course of the descending aortic dissection; optimally, it should be undertaken within 24 hours of onset. As time progresses, the false lumen thromboses, after which fenestration is ineffective.

On long-term follow-up of 14 patients who have undergone fenestration, our 3- and 5-year survival rates were 77% and 53%, respectively [3]. Heinemann and colleagues [14] subsequently confirmed our findings regarding the safety and efficacy of fenestration in a similar clinical series with descending aortic dissection.

Conventional descending aortic replacement carries a high risk in the patient with acute descending aortic dissection. In the study by Fann and associates [7] of 40 patients with acute descending aortic dissections who were treated surgically, the overall mortality rate was 40%. Eleven of the 40 patients had peripheral vascular complications, of whom 7 (64%) died. The fenestration procedure represents a quick, simple, safe alternative surgical therapy.

Replacement of a small portion of the proximal descending aorta, commonly performed for acute descending aortic dissection, might not correct the end organ ischemia. The potential advantages of fenestration over descending aortic replacement include avoidance of thoracotomy, avoidance of paraplegia, avoidance of perfusion adjuncts for spinal cord protection, and use of only native tissue. Fenestration does not require circulatory support for spinal cord protection and distal perfusion. Finally, fenestration directly addresses limb ischemia, whereas ischemia might persist after standard graft replacement.

This investigation confirmed the effectiveness of the fenestration procedure in restoring blood flow and pressure to the extremities and visceral organs in an experimental model of aortic dissection. These findings add support for the continued clinical application of fenestration for patients with acute descending aortic dissection with visceral or extremity ischemia.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Demos T.C., Posniak H.V., Marsan R.E. CT of aortic dissection. Semin Roentgenol 1989;24:22-37.[Medline]
  2. Svensson L.G., Crawford E.S. Aortic dissection and aortic aneurysm surgery: clinical observations, experimental investigations, and statistical analyses. Part II. Curr Prob Surg 1992;29:913-1057.[Medline]
  3. Elefteriades J.A., Hartleroad J., Gusberg R.J., et al. Long-term experience with descending aortic dissection: the complication-specific approach. Ann Thorac Surg 1992;53:11-20.[Abstract]
  4. Elefteriades J.A., Hammond G.L., Gusberg R.J., Kopf G.S., Baldwin J.C. Fenestration revisited: a safe and effective procedure for descending aortic dissection. Arch Surg 1990;125:786-790.[Abstract]
  5. Blanton F.S., Miller W.H., Jr, Warren W.E. Experimental production of dissecting aneurysms of the aorta. Surgery 1959;45:81-90.[Medline]
  6. Carney W.I., Rheinlander H.F., Cleveland R.J. Control of acute aortic dissection. Surgery 1975;78:114-120.[Medline]
  7. Fann J.I., Sarris G.E., Mitchell R.S., et al. Treatment of patients with aortic dissection presenting with peripheral vascular complications. Ann Surg 1990;212:705-713.[Medline]
  8. Crawford S., Crawford J. Diseases of the aorta. Baltimore, MD: Williams & Wilkins, 1984.
  9. Gurin D., Bulmer J.W., Derby R. Dissecting aneurysm of the aorta: diagnosis of operative relief of acute arterial obstruction due to this cause. N Y State J Med 1935;35:1200-1202.
  10. DeBakey M.E., Cooley D.A., Creech O. Surgical consideration of dissecting aneurysm of the aorta. Ann Surg 1955;142:586-612.[Medline]
  11. Beckwith J.R., Muller W.H., Warren W.D., Wood A.E. Acute dissecting aneurysm of the aorta: diagnosis and selection of patients for surgery. Arch Intern Med 1959;104:217-225.[Abstract/Free Full Text]
  12. Rob C., Kenyon J.R. Dissecting aneurysm. BMJ 1960;1:1384-1388.[Medline]
  13. Hume D.M., Porter R.R. Acute dissecting aortic aneurysm. Surgery 1963;53:122-154.
  14. Heinemann M.K., Beuhner B., Schaefers H.J., Jurman M.J., Laas J., Borst H.G. Malperfusion of the thoracoabdominal vasculature in aortic dissection. J Card Surg 1994:748-757.



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