Asian Cardiovasc Thorac Ann 2001;9:48-50
© 2001 Asia Publishing EXchange Pte Ltd
Acute Dissection of Ascending Aorta After Aortic Valve Replacement
enol Yavuz, MD,
Mehmet Adnan Celkan, MD,
Mustafa Mavi, MD,
Tamer Türk, MD,
Mehmet Tu
rul Göncü, MD,
brahim Ayhan Özdemir, MD
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Department of Cardiovascular Surgery Bursa Yüksek htisas Hospital Bursa, Turkey
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For reprint information contact: enol Yavuz, MD Tel: 90 224 360 5055 Fax: 90 224 360 2928 email: syavuz64{at}yahoo.com Department of Cardiovascular Surgery, Bursa Yüksek htisas Hospital, Duaçinari, Bursa 16330, Turkey.
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Abstract
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A 57-year-old man who had aortic insufficiency with mild dilatation (36 mm) of the ascending aorta but no evidence of aortic wall degeneration, developed acute dissection of the ascending aorta 6 months after aortic valve replacement. He underwent successful Dacron graft replacement of the ascending aorta.
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Introduction
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Acute ascending aortic dissection following open heart surgery, particularly in patients with dilatation of the aortic root or cystic medial necrosis, is a rare but potentially fatal complication.1–3 It is unclear whether aortic valve replacement (AVR) is a predisposing factor. Concomitant replacement of the ascending aorta may be required with AVR, although the optimal surgical treatment of such patients has not been resolved. Such a problem arose in a patient who developed acute dissection of the ascending aorta 6 months after AVR.
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Case Report
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A 57-year-old man underwent AVR at our center because of grade-4 aortic regurgitation. His arterial blood pressure was 140/90 mm Hg at that time. He was not diabetic. At surgery, there was mild dilatation of the ascending aorta (36 mm) and aortic regurgitation. No degeneration of the ascending aortic wall was observed. The aortic valve was a tricuspid structure. A 23-mm Carpentier-Edwards bioprosthesis (Baxter Healthcare Corp., Irvine, CA, USA) was implanted because of his socioeconomic status. The postoperative course was uncomplicated. The patient was discharged from hospital on the eighth postoperative day and made a full recovery.
Six months later, he was referred to a local hospital with severe chest pain radiating to his back and blood pressure of 210/110 mm Hg. He was hospitalized for one day because of enlargement of the mediastinal shadow on chest radiography. He was noted to be oliguric and was transferred to our hospital for further investigation. On admission, his arterial blood pressure was 210/100 mm Hg. His pulse was 88 beats•min- and regular. The peripheral pulses were palpable. His blood pressure was controlled with nitroprusside and a low-dose dopamine infusion was initiated for diuresis. Transesophageal echocardiography revealed type A aortic dissection starting from the ascending aorta with an intimal flap arising just above the aortic valve prosthesis. Neither aortic regurgitation nor pericardial effusion were detected. The diameter of the ascending aorta was measured as 55 mm. The aortic valve prosthesis was functioning normally.
The patient underwent emergency reoperation. The subclavian artery was prepared for arterial cannulation. A redo median sternotomy was performed, recent adhesions were divided, and bicaval venous cannulation was set up. The ascending aorta was found to be dilated to 55 mm in diameter. Cardiopulmonary bypass was instituted with antegrade direct coronary artery and retrograde coronary sinus perfusion with cold blood cardioplegia. An aortotomy was performed after crossclamping at the level of the innominate artery. A supracoronary intimal tear involving the venting site was observed 3 cm above the valve prosthesis. The intimal flap was thin and friable, indicating that the dissection had occurred recently. The native coronary orifices were not involved. There were no pathological findings on the bioprosthetic valve (Figure 1
), which was left in place. The proximal aortic cuff was reconstructed with a strip of Teflon felt placed between the intima and adventitia, and reinforced externally with a second Teflon strip. The proximal anastomosis was performed during aortic crossclamping. The ascending aorta was then replaced with a 30-mm Dacron tube graft (Meadox Medicals, Inc., Oakland, NJ, USA), using 4/0 Prolene (Ethicon Ltd., Edinburgh, Scotland, UK) continuous sutures. The patient was cooled down to 22°C, during circulatory arrest (for 23 minutes), and the crossclamp was removed. Retrograde cerebral perfusion was applied (for 21 minutes) with oxygenated blood at 10°C and a flow rate of 300 mL•min-1 via the superior vena cava to the internal jugular vein, while the patient was in a head-down position. The superior vena caval pressure was kept at less than 25 mm Hg. The distal anastomotic line of the graft was defined. The arcus vessels were kept constant while the graft was adjusted to allow hemi-arcus replacement. With Teflon strips reinforcing the distal aortic cuff, the distal end of the graft was sewn with 4/0 Prolene continuous sutures. The circulation was then restored and the patient was rewarmed. Weaning from cardiopulmonary bypass was uneventful, using a low-dose inotropic infusion. Histology of the excised aortic wall showed atherosclerotic degeneration. The postoperative course was smooth and the patient was discharged on the 10th postoperative day. He was found to be well 3.3 years later but did not report for computed tomographic evaluation.
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Discussion
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The incidence of acute ascending aortic dissection after AVR has been reported as 0.6% or less.1,4 Suggested predisposing factors include AVR in patients with aortic regurgitation, or aortic stenosis accompanied with aortic regurgitation in middle-aged men, systemic hypertension, and an ascending aortic diameter exceeding 50 mm.4 In this case, aortic venting may have been involved because of the intimal tear at the venting site. In patients with aortic valve disorders, it is still a matter of debate whether hemodynamic stress or a congenital or acquired weakness of the aortic wall might be responsible for dilatation. Poststenotic dilatation is well known in patients with aortic stenosis where poststenotic turbulent flow plays an important role. This has been verified by the observation that surgical correction of the valvular lesion prevents further enlargement of the ascending aorta. Nevertheless, aortic dissection may also develop after surgery for aortic stenosis.5
Aortic regurgitation and root dilatation may occur despite elimination of hemodynamic stress by AVR. Structural alterations at the aortic wall may lead to further dilatation.4,6,7 Dissection is more frequent in patients with a bicuspid aortic valve.7 Milano and colleagues5 suggested that AVR alone may not prevent progression of aortic root enlargement nor reduce the risk of future dissection in patients with aortic regurgitation and ascending aortic ectasia. The importance of the type of prosthesis in the risk of dissection has not been defined. Pieters and colleagues4 found aortic dissection more often in patients with mono-disc prosthetic valves. The flow pattern of this type of prosthesis resembles that of a bicuspid aortic valve, having a laterally directed jet. In our patient, neither structural valve alterations nor paravalvular leakage were observed.
Surgery is essential for ascending aortic dilatation accompanied by aortic valvular disorders. Presbitero and colleagues2 suggested that replacement of the ascending aorta should be considered if marked dilatation of the aortic root is found during AVR. Surgical strategies in patients with a mild degree of dilatation are still undefined but a high mortality rate is associated with reoperation for aortic dissection, so it is essential to identify those at high risk.2,4,6,8 In this case, ascending aortic replacement was not considered at the initial operation as there was no apparent degeneration of the aortic wall. Experiences reported over the last few years have led us to adopt a diameter of 45 mm as the criterion for treatment of aortic dilatation. The simplest treatment is aortoplasty, although there is a high rate of recurrence on long-term follow-up.8 Ascending aortic replacement in addition to AVR, may be preferred in patients with supracoronary aortic dilatation accompanied by aortic stenosis. On the other hand, in annuloaortic ectasis, the Bentall procedure or its modifications are more appropriate.9
Patients with a mildly dilated aortic root should be followed up by echocardiography at regular intervals after AVR. Elective ascending aortic replacement must be considered if progression of dilatation is detected. As found in this case, dissection may develop in patients with systemic hypertension even though no significant progression has been noted during follow-up studies.4 Therefore, careful preoperative evaluation must be carried out in patients undergoing AVR. In those with a thin ascending aorta and mild dilatation that does not require intervention during AVR, progression of the dilatation should be followed by echocardiography every 6 months postoperatively. Dilatation in excess of 60 mm mandates elective ascending aortic replacement to avoid dissection. Consequently, treatment of ascending aortic dilatation should be given special consideration during AVR.
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References
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Pieters FA, Widdershoven JW, Gerardy AC, Geskes G, Cheriex EC, Wellens HJ. Risk of aortic dissection after aortic valve replacement. Am J Cardiol 1993;72:1043–7.[Medline]
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Abstract
Introduction
