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Case 42: Aortic Homograft Anastomotic Dehiscence and Pseudoaneurysm Formation¹

¹ From the Department of Radiology, National Naval Medical Center, Bethesda, Md (M.L.G.); and Department of Cardiac Surgery, St Joseph Hospital, Bellingham, Wash (E.R.Z.). Received June 27, 2000; revision requested July 28; revision received September 20; accepted October 2. Address correspondence to M.L.G., Department of Radiology, United States Naval Hospital, Roosevelt Roads, Puerto Rico, PSC 1008, Box 3007, FPO AA 34051 (e-mail: mlgrebenc@rroads.med.navy.mil).

Index terms: Aorta, grafts and prostheses, 568.4523, 568.4528, 568.4558 • Connective tissue, diseases, 40.1711, 568.1971 • Diagnosis Please • Grafts • Marfan syndrome, 40.1711, 568.1971

	HISTORY

TOP HISTORY IMAGING FINDINGS DISCUSSION REFERENCES

 
A 27-year-old man with Marfan syndrome was referred for cardiac magnetic resonance (MR) imaging for evaluation of an aortic root homograft that had been placed 9 months earlier. He had retrosternal chest pressure but no clinical evidence of infection. He had a history of progressive annuloaortic ectasia and aortic insufficiency that had been documented previously by means of serial echocardiograms and MR images, and he eventually required surgical replacement of the aortic root and arch with a prosthetic composite graft. This first surgical procedure was complicated by endocarditis with an aortic root abscess that necessitated surgical removal of the graft and replacement with an aortic root homograft. At the time of referral, the patient underwent MR imaging with a 1.5-T system (Signa Cvi; GE Medical Systems, Milwaukee, Wis).

	IMAGING FINDINGS

TOP HISTORY IMAGING FINDINGS DISCUSSION REFERENCES

 
Transverse (10-mm-thick) and coronal (8-mm-thick) double inversion-recovery fast spin-echo and coronal oblique cine fast spoiled gradient-recalled echo MR images of the heart (Figs 1–3) demonstrated an approximately 6-cm-diameter anastomotic pseudoaneurysm. The pseudoaneurysm arose from the aortic annulus and extended superiorly and to the right, between the aortic root homograft and the superior vena cava. While the double inversion-recovery fast spin-echo MR images displayed flow void within the pseudoaneurysm, signal intensity was heterogeneous because of turbulent blood flow (Figs 1, 2). The pseudoaneurysm compressed the superior vena cava; however, no significant obstruction of venous return was demonstrated with cine MR imaging. The superior aspect of the left atrium also was slightly compressed.

View larger version (106K): [in this window] [in a new window] [Download PPT slide]   Figure 1a. Transverse cranial to caudal electrocardiographically gated double inversion-recovery fast spin-echo MR images (repetition time msec/echo time msec, 1,714/43.8 [effective]) of the heart at the level of the aortic root and proximal ascending aorta display. * = pseudoaneurysm, S = superior vena cava. (a) Area of heterogeneous intermediate signal intensity between the aortic homograft (Ao) and the superior vena cava represents the superior aspect of the pseudoaneurysm. The proximal left coronary artery (arrow) is demonstrated and appears normal. LV = left ventricle, PA = pulmonary artery. (b, c) The pseudoaneurysm is interposed between the aortic root homograft and the superior vena cava. The heterogeneous signal intensity in the pseudoaneurysm is caused by turbulent blood flow. Note the slight compression of the superior vena cava. The area of heterogeneous intermediate to hyperintense fluid collection (long arrow), which has characteristics of a perigraft hematoma, is present between the homograft and right ventricle (RV). The three commissures of the aortic valve delineate the sinuses of Valsalva (1 = right coronary sinus, 2 = left coronary sinus, 3 = noncoronary sinus). Short arrow depicts the left pulmonary veins entering the left atrium (LA). (d) The pseudoaneurysm arises from the left ventricular outflow tract (LVO). A fluid collection with heterogeneous signal intensity (long white arrow), likely representing a small perigraft hematoma, is seen anterior to the left ventricular outflow tract. Note the flow void of the right coronary artery (black arrow). The right inferior pulmonary vein (short white arrow) is shown entering the left atrium (LA). RV = right ventricle.

View larger version (110K): [in this window] [in a new window] [Download PPT slide]   Figure 1b. Transverse cranial to caudal electrocardiographically gated double inversion-recovery fast spin-echo MR images (repetition time msec/echo time msec, 1,714/43.8 [effective]) of the heart at the level of the aortic root and proximal ascending aorta display. * = pseudoaneurysm, S = superior vena cava. (a) Area of heterogeneous intermediate signal intensity between the aortic homograft (Ao) and the superior vena cava represents the superior aspect of the pseudoaneurysm. The proximal left coronary artery (arrow) is demonstrated and appears normal. LV = left ventricle, PA = pulmonary artery. (b, c) The pseudoaneurysm is interposed between the aortic root homograft and the superior vena cava. The heterogeneous signal intensity in the pseudoaneurysm is caused by turbulent blood flow. Note the slight compression of the superior vena cava. The area of heterogeneous intermediate to hyperintense fluid collection (long arrow), which has characteristics of a perigraft hematoma, is present between the homograft and right ventricle (RV). The three commissures of the aortic valve delineate the sinuses of Valsalva (1 = right coronary sinus, 2 = left coronary sinus, 3 = noncoronary sinus). Short arrow depicts the left pulmonary veins entering the left atrium (LA). (d) The pseudoaneurysm arises from the left ventricular outflow tract (LVO). A fluid collection with heterogeneous signal intensity (long white arrow), likely representing a small perigraft hematoma, is seen anterior to the left ventricular outflow tract. Note the flow void of the right coronary artery (black arrow). The right inferior pulmonary vein (short white arrow) is shown entering the left atrium (LA). RV = right ventricle.

View larger version (111K): [in this window] [in a new window] [Download PPT slide]   Figure 1c. Transverse cranial to caudal electrocardiographically gated double inversion-recovery fast spin-echo MR images (repetition time msec/echo time msec, 1,714/43.8 [effective]) of the heart at the level of the aortic root and proximal ascending aorta display. * = pseudoaneurysm, S = superior vena cava. (a) Area of heterogeneous intermediate signal intensity between the aortic homograft (Ao) and the superior vena cava represents the superior aspect of the pseudoaneurysm. The proximal left coronary artery (arrow) is demonstrated and appears normal. LV = left ventricle, PA = pulmonary artery. (b, c) The pseudoaneurysm is interposed between the aortic root homograft and the superior vena cava. The heterogeneous signal intensity in the pseudoaneurysm is caused by turbulent blood flow. Note the slight compression of the superior vena cava. The area of heterogeneous intermediate to hyperintense fluid collection (long arrow), which has characteristics of a perigraft hematoma, is present between the homograft and right ventricle (RV). The three commissures of the aortic valve delineate the sinuses of Valsalva (1 = right coronary sinus, 2 = left coronary sinus, 3 = noncoronary sinus). Short arrow depicts the left pulmonary veins entering the left atrium (LA). (d) The pseudoaneurysm arises from the left ventricular outflow tract (LVO). A fluid collection with heterogeneous signal intensity (long white arrow), likely representing a small perigraft hematoma, is seen anterior to the left ventricular outflow tract. Note the flow void of the right coronary artery (black arrow). The right inferior pulmonary vein (short white arrow) is shown entering the left atrium (LA). RV = right ventricle.

View larger version (102K): [in this window] [in a new window] [Download PPT slide]   Figure 1d. Transverse cranial to caudal electrocardiographically gated double inversion-recovery fast spin-echo MR images (repetition time msec/echo time msec, 1,714/43.8 [effective]) of the heart at the level of the aortic root and proximal ascending aorta display. * = pseudoaneurysm, S = superior vena cava. (a) Area of heterogeneous intermediate signal intensity between the aortic homograft (Ao) and the superior vena cava represents the superior aspect of the pseudoaneurysm. The proximal left coronary artery (arrow) is demonstrated and appears normal. LV = left ventricle, PA = pulmonary artery. (b, c) The pseudoaneurysm is interposed between the aortic root homograft and the superior vena cava. The heterogeneous signal intensity in the pseudoaneurysm is caused by turbulent blood flow. Note the slight compression of the superior vena cava. The area of heterogeneous intermediate to hyperintense fluid collection (long arrow), which has characteristics of a perigraft hematoma, is present between the homograft and right ventricle (RV). The three commissures of the aortic valve delineate the sinuses of Valsalva (1 = right coronary sinus, 2 = left coronary sinus, 3 = noncoronary sinus). Short arrow depicts the left pulmonary veins entering the left atrium (LA). (d) The pseudoaneurysm arises from the left ventricular outflow tract (LVO). A fluid collection with heterogeneous signal intensity (long white arrow), likely representing a small perigraft hematoma, is seen anterior to the left ventricular outflow tract. Note the flow void of the right coronary artery (black arrow). The right inferior pulmonary vein (short white arrow) is shown entering the left atrium (LA). RV = right ventricle.

View larger version (120K): [in this window] [in a new window] [Download PPT slide]   Figure 2a. Coronal oblique electrocardiographically gated double inversion-recovery fast spin-echo MR images (1,714/43.8 [effective]) of the aortic root. * = pseudoaneurysm, LV = left ventricle, PA = main pulmonary artery, RA = right atrium. (a) The pseudoaneurysm is adjacent to but not compressing the aortic root homograft (Ao). A hyperintense fluid collection (arrow) shown to the left of the aortic valve has characteristics consistent with a perigraft hematoma. (b) Image acquired posterior to a shows the pseudoaneurysm arising from the outflow tract of the left ventricle and compressing the superior vena cava (arrow). The increased signal intensity in the pseudoaneurysm is caused by turbulent blood flow. AA = aortic arch.

View larger version (143K): [in this window] [in a new window] [Download PPT slide]   Figure 2b. Coronal oblique electrocardiographically gated double inversion-recovery fast spin-echo MR images (1,714/43.8 [effective]) of the aortic root. * = pseudoaneurysm, LV = left ventricle, PA = main pulmonary artery, RA = right atrium. (a) The pseudoaneurysm is adjacent to but not compressing the aortic root homograft (Ao). A hyperintense fluid collection (arrow) shown to the left of the aortic valve has characteristics consistent with a perigraft hematoma. (b) Image acquired posterior to a shows the pseudoaneurysm arising from the outflow tract of the left ventricle and compressing the superior vena cava (arrow). The increased signal intensity in the pseudoaneurysm is caused by turbulent blood flow. AA = aortic arch.

View larger version (137K): [in this window] [in a new window] [Download PPT slide]   Figure 3a. Coronal oblique electrocardiographically gated cine fast spoiled gradient-recalled echo MR images (8.7/4.6) of the aortic root were acquired at the same location during (a) systole and (b) diastole. PA = main pulmonary artery, RA = right atrium. The elevation of the aortic root homograft (Ao) above the aortic annulus (white arrows) is demonstrated. The left ventricle (LV) supplies blood into the pseudoaneurysm (*) and aortic homograft. Note the small regurgitant jet (black arrow in b) from the aortic valve during diastole.

View larger version (138K): [in this window] [in a new window] [Download PPT slide]   Figure 3b. Coronal oblique electrocardiographically gated cine fast spoiled gradient-recalled echo MR images (8.7/4.6) of the aortic root were acquired at the same location during (a) systole and (b) diastole. PA = main pulmonary artery, RA = right atrium. The elevation of the aortic root homograft (Ao) above the aortic annulus (white arrows) is demonstrated. The left ventricle (LV) supplies blood into the pseudoaneurysm (*) and aortic homograft. Note the small regurgitant jet (black arrow in b) from the aortic valve during diastole.

Preoperative MR imaging of the thoracic aorta was performed before the first surgical procedure and demonstrated a fusiform aneurysm of the aortic root, which was 5.7 cm in maximal diameter (Fig 4). The normal sinotubular ridge was effaced, and the ascending aorta abruptly returned to normal caliber before the aortic arch. Two months after the initial aneurysm repair, the patient presented with fever. The white blood cell count was increased, and blood cultures were positive for Staphylococcus organisms. Contrast material–enhanced chest computed tomography (CT) demonstrated heterogeneously enhancing tissue anterior and to the right of the aortic root, which represented an aortic root abscess. A small low-attenuating focus consistent with air within the abscess was noted (Fig 5).

View larger version (118K): [in this window] [in a new window] [Download PPT slide]   Figure 4. Sagittal oblique electrocardiographically gated cine fast spoiled gradient-recalled echo MR image (8.9/4.5) of the thoracic aorta before the first surgical procedure shows marked aneurysmal dilatation (A) of the aortic root and proximal ascending aorta. The aneurysm was 5.7 cm in maximal diameter. Note the abrupt return to normal caliber (arrows) before the aortic arch, which is characteristic of aneurysms in patients with Marfan syndrome.

View larger version (148K): [in this window] [in a new window] [Download PPT slide]   Figure 5. Transverse contrast material-enhanced chest CT scan (mediastinal window) obtained after the first and before the second surgical procedure at the level of the aortic root shows prosthetic graft endocarditis. Heterogeneously enhancing tissue (long arrow) is seen anterior and to the right of the aorta, representing an aortic root abscess. The origin (arrowhead) of the right coronary artery is demonstrated. A small low-attenuating focus (short arrow) is consistent with air within the abscess.

	DISCUSSION

TOP HISTORY IMAGING FINDINGS DISCUSSION REFERENCES

Currently, the preferred surgical procedure for aortic root replacement is the insertion of a composite valve-graft, which consists of a prosthetic valve sewn to a synthetic graft (3). The coronary arteries are attached directly to the graft by using surrounding buttons of native aortic tissue and are buttressed by using prosthetic washers to prevent the formation of coronary ostial aneurysms (4,6,7). A former surgical practice of wrapping the native aneurysmal aortic wall around the site of repair to control bleeding is no longer used. This method was associated with an increased rate of complications, such as anastomotic leakage, continued aneurysmal dilatation of the aortic wrap, and false aneurysm formation at the coronary ostial graft suture line (6).

Patients with mechanical heart valves require lifelong anticoagulation therapy with warfarin sodium to decrease the probability of thromboembolic complications. Aortic valve–sparing surgical procedures, which preclude the need for anticoagulation therapy, are performed in patients with Marfan syndrome at some institutions, with good long-term results (8). However, the aortic valves resected in patients with Marfan syndrome demonstrate abnormal elastin-associated microfibrils at histologic examination, and the native aortic valve left in situ may undergo continued degeneration and functional failure. For this reason, valve-sparing procedures are not generally advocated in these patients (7). Elective aortic root replacement surgery in patients with Marfan syndrome has a surgical risk of less than 2% and a good long-term survival of 88% at 5 years, 81% at 10 years, and 75% at 20 years (5).

While aortic root cadaveric homografts may be used for the original replacement of the aortic root to obviate lifelong anticoagulation therapy, they are generally used for the treatment of prosthetic valve endocarditis that has been complicated by aortic root destruction (7,9–11). This entails the removal of the infected prosthesis and necrotic tissue, insertion of the homograft, and direct reimplantation of the coronary arteries onto the homograft (12). Prior to implantation, the homografts are sterilized with antibiotics and stored in a tissue culture medium at 4°C (cryopreservation) (10). These grafts display a greater resistance to infection when compared with mechanical valves (9).

Pseudoaneurysm formation secondary to anastomotic dehiscence has been described as a relatively common finding in patients treated for active prosthetic valve endocarditis with homograft replacement surgery (13). A report by Oechslin and colleagues (11) reveals that small (1.5 cm) anastomotic pseudoaneurysms were observed with echocardiography in 73% of patients. The presence of friable periannular tissue in these patients contributes to anastomotic failure (11,14). MR imaging of a pseudoaneurysm demonstrates a contained area of extraluminal blood flow that is characterized by signal void at spin-echo MR imaging and intracavitary flow of bright blood at cine gradient-recalled echo MR imaging (15).

The risks associated with pseudoaneurysms are not well documented. One article, which describes the results of periodic surveillance of anastomotic pseudoaneurysms with MR imaging, shows that the majority of small (<4 cm) pseudoaneurysms remained unchanged, decreased in size, or completely thrombosed, while the majority of those 4 cm or larger enlarged (15). Large pseudoaneurysms may compress an adjacent native vascular structure, cardiac chamber, or aortic graft and may obstruct blood flow. Thromboembolism or rupture with fatal hemorrhage are other potential complications.

The differential diagnosis of a perigraft cavity or collection observed after aortic root replacement surgery includes pseudoaneurysm from an aortic graft or coronary artery anastomotic dehiscence, infectious pseudoaneurysm, periannular abscess, and perigraft hematoma. Demonstration of intact coronary arterial origins will help to exclude coronary dehiscence as a diagnostic possibility. Infectious pseudoaneurysms, perfused cavities that result from ruptured endocarditis-related abscesses, may appear similar to anastomotic pseudoaneurysms at MR imaging (16,17). Patients with infectious pseudoaneurysms usually present with clinical evidence of infection (9), which was not present in this patient at the time of cardiac MR imaging. In addition, the cultures of the resected homograft were sterile. Visualization of the entry site of blood from an area of dehiscence into a pseudoaneurysm will help to differentiate it from an unperfused collection, such as an unruptured abscess or extraluminal hematoma. Imaging findings in this case demonstrate the separation of the homograft from the aortic annulus with an associated perfused cavity and establish an anastomotic pseudoaneurysm as the most likely diagnosis.

In summary, MR imaging is beneficial in the pre- and postoperative evaluation of the thoracic aorta in patients with Marfan syndrome. In this case, MR images depicted features of a large pseudoaneurysm associated with subtotal anastomotic dehiscence of an aortic root homograft, a serious complication of aortic root surgery. Familiarity with the surgical therapies used for patients with Marfan syndrome and with the potential postoperative complications is the key to providing an accurate diagnostic evaluation.

	FOOTNOTES

 
The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Departments of the Navy or Defense.

Part 1 of this case appeared 4 months previously and may contain larger images.

	REFERENCES

TOP HISTORY IMAGING FINDINGS DISCUSSION REFERENCES

 

1. Reddy GP, Higgins CB. MR imaging of the thoracic aorta. Magn Reson Imaging Clin N Am 2000; 8:1-15.
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3. Gott VL, Greene PS, Alejo DE, et al. Replacement of the aortic root in patients with Marfan’s syndrome. N Engl J Med 1999; 340:1307-1313.
4. Finkbohner R, Johnston D, Crawford ES, Coselli J, Milewicz DM. Marfan syndrome: long-term survival and complications after aortic aneurysm repair. Circulation 1995; 91:728-733.
5. Baumgartner WA, Cameron DE, Redmond JM, Greene PS, Gott VL. Operative management of Marfan syndrome: the Johns Hopkins experience. Ann Thorac Surg 1999; 67:1859-1860.
6. Svensson LG, Crawford ES, Coselli JS, Safi HJ, Hess KR. Impact of cardiovascular operation on survival in the Marfan patient. Circulation 1989; 80(suppl I):I233-1242.
7. Gott VL, Laschinger JC, Cameron DE, et al. The Marfan syndrome and the cardiovascular surgeon. Eur J Cardiothorac Surg 1996; 10:149-158.
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11. Oechslin E, Carrel T, Ritter M, et al. Pseudoaneurysm following aortic homograft: clinical implications. Br Heart J 1995; 74:645-649.
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13. Federmann M, von Segesser LK, Ritter M, Jenni R. Spontaneous obliteration of a pseudo-aneurysm complicating an aortic homograft. Eur J Cardiothorac Surg 1996; 10:705-706.
14. Yamashita C, Tsuji Y, Yoshimura M, Kozawa S, Okada M. Successful surgical treatment of a pseudoaneurysm after composite graft replacement of the aortic valve and ascending aorta: report of two cases. Surg Today 1994; 24:1019-1022.
15. Dagenais F, Cartier R, Paquet E, Hudon G, Castonguay Y, Leclerc Y. Pseudoaneurysm after Bentall repair: magnetic resonance imaging assessment. Can J Cardiol 1993; 9:869-872.
16. Winkler ML, Higgins CB. MRI of perivalvular infectious pseudoaneurysms. AJR Am J Roentgenol 1986; 147:253-256.
17. Akins EW, Stone RM, Wiechmann BN, Browning M, Martin TD, Mayfield WR. Perivalvular pseudoaneurysm complicating bacterial endocarditis: MR detection in five cases. AJR Am J Roentgenol 1991; 156:1155-1158.

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Marcelo Bordalo Rodrigues, São Paulo, Brazil

Martín Campi, MD, Mar del Plata, Argentina

James W. Cole, MD, Cincinnati, Ohio

Thuan Dang, MD, Colton, Calif

Kemal Demir, MD, Ataköy, Istanbul, Turkey

Milton R. Fuentealba, MD, General Roca, Rio Negro, Argentina

Akira Fujikawa, Tokyo, Japan

Dr. Marcelo B. G. Funari, São Paulo, SP, Brazil

Douglas Gardner, MD, Windsor, Ontario, Canada

John D. Grizzard, Midlothian, Va

Glenn Krinsky, New York, NY

S. Lachanis, MD, Athens, Greece

Mario Laguna, West Allis, Wis

Frank J. McKowne, MD, Vancouver, Wash

Manabu Minami, MD, Tokyo, Japan

Carlos J. Nassar, MD, Humacao, Puerto Rico

Sanford M. Ornstein, MD, Phoenix, Ariz

Shawn P. Quillin, MD, Charlotte, NC

Enrique Remartinez Escobar, MD, Melilla, Spain

Matt Shapiro, MD, Lowell, Mass

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This Article Figures Only Full Text (PDF) All Versions of this Article: 2221001152v1 222/1/139    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Grebenc, M. L. Articles by Zech, E. R. Search for Related Content PubMed PubMed Citation Articles by Grebenc, M. L. Articles by Zech, E. R.