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European Journal of Echocardiography 2008 9(1):88-91; doi:10.1016/j.euje.2007.02.010
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org.

Extensive dehiscence of a stentless bioprosthesis with only mild paravalvular regurgitation after replacement of a degenerated bicuspid aortic valve

Dirk Poppe*, Peter Blank, Uta Böge, Tatjana Kölzow, Jürgen Loh and Bernhard Schwaab

Curschmann-Klinik, Timmendorfer Strand, Germany

Received 2 February 2007; accepted after revision 14 February 2007; online publish-ahead-of-print 2 April 2007.

* Corresponding author. Curschmann-Klinik der Klinikgruppe Dr. Guth, Saunaring 6, D-23669 Timmendorfer Strand, Germany. Tel: +49 (0)4503 602 154; fax: +49 (0)4503 602 660. E-mail address: dr.poppe{at}drguth.de


    Abstract
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 Abstract
 Case report
 Discussion
 References
 
We report the case of a 54-year-old patient admitted for rehabilitation after implantation of a stentless bioprosthesis due to severe insufficiency of a degenerated bicuspid aortic valve. The patient could fully participate in a standard cardiac rehabilitation program without any signs of haemodynamic instability. Transthoracic echocardiography showed a small mobile subvalvular structure and only mild paravalvular reflux. Transesophageal echocardiography, however, revealed extensive dehiscence of the bioprosthesis with the need for urgent reoperation. We discuss the probable causes and encourage routine echocardiography after valve operations with generous application of transesophageal echocardiography in every suspicious case.

Keywords: Echocardiography; Transesophageal; Stentless; Valve; Surgery; Complication


    Case report
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 Abstract
 Case report
 Discussion
 References
 
In June, 2005, a 54-year-old male patient was admitted to our rehabilitation hospital 11 days after implantation of a stentless bioprosthesis (diameter 29 mm, PericarbonTM Freedom, Sorin Biomedica Cardio S. p. A., Saluggia, Italy) in aortic position due to severe insufficiency of a degenerated bicuspid aortic valve (BAV). In the operation report the use of continuous sutures for both the anulus and the commissures was described. Apart from a short episode of atrial fibrillation which was converted by amiodarone and electric cardioversion, the further postoperative course had been eventless.

On admission, the patient reported only slight postoperative chest pain and denied any palpitation, dyspnea, leg swelling, vertigo or syncope. Physical examination revealed normal body temperature, a regular heart rate of 78/min, a blood pressure of 120/70 mmHg and no signs of cardiorespiratory insufficiency. Auscultation revealed normal heart sounds with no systolic or diastolic murmurs. The lungs were clear with no rales or wheezing.

The electrocardiogram showed normal sinus rhythm with complete left bundle branch block. Laboratory tests revealed light postoperative anemia without elevated inflammatory parameters or lactate-dehydrogenase. Chest X-ray showed only a small left-sided pleural effusion.

On day one after admission to our institution, a standard 2-dimensional transthoracic echocardiography (TTE) was performed (Vivid 3 Expert, GE Healthcare Technologies, Waukesha, Wisconsin, USA) showing left ventricular (LV) hypertrophy (14–15 mm) and enlargement (enddiastolic/endsystolic diameters 66/48 mm, enddiastolic/endsystolic volume 245/130 ccm, respectively). LV ejection fraction was reduced to 45–50% (biplane Simpson's method) due to general hypokinesia and paradoxical septal movement. A circumferential pericardial effusion of less than 5 mm was present without compression of the right atrium or ventricle. In the TTE, morphology of the aortic bioprosthesis was normal. Below the valve, however, an echodense structure of 16 mm in length raised from the wall of the left ventricular outflow tract (LVOT) in systole and seemed to be attached to the anulus of the aortic valve prosthesis on the side of the right coronary cusp (RCC) (Figure 1). Color Doppler showed a mild paravalvular regurgitation in this area (Figure 2).


Figure 1
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Figure 1 Zoom of 5-chamber apical view. Mobile subvalvular structure raising from the wall of the left ventricular outflow tract during systole (arrow).

 


Figure 2
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Figure 2 Zoom of apical 5-chamber view. Color Doppler imaging showing a mild paravalvular regurgitation in the area of the mobile subvalvular structure shown in Figure 1.

 
In repeated TTE investigations, morphology of the aortic valve prosthesis, the subvalvular structure and the small paravalvular regurgitation remained unchanged; the pericardial effusion had disappeared. The patient, staying in stable physical condition with no signs of cardiorespiratory insufficiency, could fully participate in the routine rehabilitation program (maximum work load of 75 Watts during bicycle-ergometry, continuous bicycle training at 50 Watts over 20 min, participation in walking and gymnastics groups). Repeated laboratory tests showed no elevation of inflammatory parameters or lactate-dehydrogenase.

On day 14 after admission, a transesophageal echocardiography (TEE) was performed to identify the subvalvular structure and further clarify the mechanism of the paravalvular leakage. The most significant findings are shown in Figures 35: The bioprosthesis itself showed no signs of deterioration, the cusps were tender and showed normal mobility without any transvalvular regurgitation. The short axis view (40–50° rotation), however, showed an almost circular dehiscence between the anulus of the valve and the aortic wall with tight contact only at the commissures between the non-coronary cusp (NCC) and the left coronary cusp (LCC) as well as between NCC and RCC (Figure 3). In systole, the anulus bulged inwards on the level of the commissure between RCC/LCC giving space to a significant paravalvular systolic outflow in this area. In diastole, this part of the anulus moved back into close contact with the aortic wall thus allowing only little diastolic regurgitation (Figure 4). In the longitudinal axis (134° rotation) the subvalvular structure, undefined in TTE, could be identified as part of the aortic wall attached to the anulus of the valve (Figure 5) suggesting a circumscript dissection of the aortic wall in this area. Also in longitudinal axis, an echo-free space was detected between the tubular part of the prosthesis and the aortic wall, while the top of the prosthesis seemed to be closely fixed to the aortic wall (Figure 5). Figure 6 shows color Doppler imaging in longitudinal axis.


Figure 3
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Figure 3 Transesophageal echocardiography (TEE), short axis view (50°) in midesophageal level. Left: Extensive dehiscence between the anulus of the bioprosthesis and the aortic wall during systole, with tight contact only at the commissures between NCC and LCC (NL) as well as between NCC and RCC (NR). Right: In diastole, the anulus moves back into close contact with the aortic wall.

 


Figure 4
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Figure 4 TEE, short axis view (46°) in midesophageal level, color Doppler imaging. Left: In systole, flow can be seen through the center of the valve as well as through the space between anulus and aortic wall in the area of the commissure between LCC and RCC (arrow). Right: In diastole, only mild regurgitation is visible.

 


Figure 5
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Figure 5 TEE, long axis view (134°) in midesophageal level. Left: In systole, the subvalvular mobile structure (MS) and parts of the anulus of the bioprothesis raise from the aortic wall. Also, an echofree space (SP) is visible between the tubular part of the bioprosthesis and the aortic wall. Right: In diastole, these structures move back into close contact to the aortic wall.

 


Figure 6
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Figure 6 TEE, long axis view (134°) in midesophageal level, color Doppler imaging. Same view as in Figure 5, showing significant paravalvular forward flow during systole (left) with only mild regurgitation during diastole (right) (arrows).

 
On the basis of these TEE findings, significant dissolution or rupture of sutures for most parts of the proximal anulus, the commissure between RCC and LCC and probably part of the other commisures was diagnosed. Even though urgent reoperation was recommended, the patient hesitated and surgery was not performed until 2 months after the primary operation.

At time of reoperation the intraoperative inspection of the stentless bioprosthesis revealed intact sutures only in the area of the NCC/LCC commissure and the distal end of the tubular part of the prosthesis. The structurally intact bioprosthesis was removed in total, several lacerations on the inside of the ascending aorta were repaired and finally a mechanical valve was implanted. 14 months later, the patient has fully recovered and is in a good state of health.


    Discussion
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 Abstract
 Case report
 Discussion
 References
 
Stentless aortic bioprostheses are increasingly implanted due to better hemodynamic performance and patient survival1,2. Implantation procedure, however, is technically more demanding given the necessity of sewing not only the anulus but also the commissures and the distal end of the prosthesis to the aortic wall rigorously avoiding any geometric distortion35. Several techniques exist using interrupted or continuous sutures or a combination of both.

In our case, continuous sutures were used which may have contributed to the extensive dehiscence of the valve, as disruption of a continuous suture leads to larger areas of dehiscence than disruption of a single or several interrupted sutures.

The multiple lacerations of the aortic wall seen during reoperation lead attention to the underlying valvular disease. A degenerated bicuspid aortic valve (BAV) may be associated with several concomitant conditions, such as a persistent ductus arteriosus Botalli or aortic coarctation.6 In addition, characteristic histologic changes of the aortic wall could be found in patients with a BAV79that explain the association between this particular valve disease and ectasia or aneurysms of the ascending aorta as well as aortic dissections.10,11Although the patient presented exhibited no dilatation of the ascending aorta, a possible higher vulnerability of the aortic wall may have contributed to the lacerations seen. As no specimen of the aortic wall was saved during either operation, further histologic investigation was not performed.

Usually the amount of regurgitation as detected by transthoracic echocardiography is presumed to correspond to the morphological size of the paravalvular leakage. In the case presented, however, there was only a mild regurgitation, due to the close contact between the anulus of the aortic valve and the aortic wall during diastole. In addition, there were no clinical or laboratory signs of relevant aortic insufficiency and transthoracic echocardiography was not able to detect the true pathology. Only transesophageal echocardiography revealed the impending danger of complete disruption and dislocation of the aortic valve bioprosthesis which might have later resulted in a critical hemodynamic situation with possible lethal consequences.

In conclusion, transthoracic echocardiography (TTE) should be used rigorously and routinely in every patient early after valve surgery. Transesophageal echocardiography should generously be used in cases of impaired transthoracic viewing conditions and in every case of suspicious findings in TTE, even in the absence of clinical signs of valve dysfunction.


    References
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 Abstract
 Case report
 Discussion
 References
 

  1. Westaby S, Horton M, Jin XY, Katsumata T, Ahmed O, Saito S, et al. Survival advantage of stentless aortic bioprostheses. Ann Thorac Surg (2000) 70:785–90.[Abstract/Free Full Text]
  2. Akar AR, Szafranek A, Alexiou C, Janas R, Jasinski MJ, Swanevelder J, et al. Use of stentless xenografts in the aortic position: determinants of early and late outcome. Ann Thorac Surg (2002) 74:1450–7.[Abstract/Free Full Text]
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  7. Bauer M, Pasic M, Meyer R, Goetze N, Bauer U, Siniawski H, et al. Morphometric analysis of aortic media in patients with bicuspid and tricuspid aortic valve. Ann Thorac Surg (2002) 74:58–62.[Abstract/Free Full Text]
  8. Bonderman D, Gharehbaghi-Schnell E, Wolleneck G, Maurer G, Baumgartner H, Lang IM. Mechanisms underlying aortic dilatation in congenital aortic valve malformation. Circulation (1999) 99:2138–43.[Abstract/Free Full Text]
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