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Ann Thorac Surg 1996;61:1724-1726
© 1996 The Society of Thoracic Surgeons


Original Article: Cardiovascular

Perioperative Complications in Combined Aortic Valve Replacement and Extraanatomic Ascending-Descending Bypass

Klaus Pethig, MD, Thorsten Wahlers, MD, Salis Tager, MD, Hans-Georg Borst, MD

Division of Thoracic and Cardiovascular Surgery, Surgical Center, Hannover Medical School, Hannover, Germany

Accepted for publication February 5, 1996.


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Background. In adult patients, the combination of severe aortic valve stenosis and coarctation is rare. Surgical options comprise either a two-stage approach with valve replacement and subsequent repair of the coarctation or a one-stage repair involving valve replacement and insertion of an extraanatomic bypass graft from the ascending to the descending aorta.

Methods. We report the cases of 2 adult patients with this combined lesion who underwent simultaneous aortic valve replacement and transpericardial bypass of the coarctation.

Results. Weaning from extracorporeal circulation and restoration of spontaneous circulation required resuscitative measures. By increasing mean arterial perfusion pressure using norepinephrine, the observed hemodynamic instability could be controlled effectively.

Conclusions. Changes in the hemodynamics of the thoracic vascular bed resulting in coronary malperfusion are discussed to be the major cause of heart failure and life-threatening ventricular arrhythmias seen in our patients after aortic valve replacement and insertion of an ascending-descending aorta bypass graft. Awareness of the complications described is considered important for successful management of these high-risk patients.


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Coarctation of the aorta combined with aortic valve stenosis is a congenital cardiovascular disorder that is rarely first diagnosed in adulthood [1]. Severe arterial hypertension and heart failure caused by the severe left ventricular (LV) pressure overloading resulting from this tandem stenosis characterize the natural course. Therefore, surgical therapy is indicated for symptomatic and prognostic reasons [2]. A two-stage approach involving standard valve replacement and subsequent coarctation repair through a posterolateral thoracotomy can be used. Alternatively, both lesions can be managed simultaneously through a median sternotomy with valve replacement and insertion of a transpericardial bypass graft from the ascending to the descending aorta [35]. For the latter procedure, a low rate of complications and good functional results have been reported [3, 6, 7]. We observed an unexpectedly complicated early postoperative course after this procedure in 2 adult patients. The causes of the severe hemodynamic disturbances as well as their recognition and treatment are discussed.


    Material and Methods
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We present here the case reports of the 2 adults.

Patient 1
A 47-year-old woman with a 20-year history of severe arterial hypertension was admitted for operation for aortic valve stenosis and coarctation of the aorta. Echocardiography and left heart catheterization revealed a severely hypertrophied left ventricle and a sclerosed and calcified aortic valve (ejection fraction, 0.71; mean transvalvular gradient, 75 mm Hg; mean gradient across the coarctation, 106 mm Hg). It was decided to perform a one-stage repair including aortic valve replacement and insertion of a bypass graft between the ascending and descending thoracic aorta.

After cannulation of the ascending aorta and the femoral artery, the aortic valve was replaced with a 21-mm St. Jude Medical prosthesis (St. Jude Medical, Minneapolis, MN). With the heart still arrested, a 12-mm Dacron graft was inserted transpericardially between the ascending aorta and the supradiaphragmatic portion of the descending aorta. Antegrade intermittent cold blood cardioplegic arrest lasted for 95 minutes.

Shortly after discontinuation of extracorporeal circulation, severe hypotension with low cardiac output was observed. Recurrent episodes of ventricular fibrillation and persistent hemodynamic instability required repeated periods of extracorporeal reperfusion. During short runs of sinus rhythm, transesophageal echocardiography revealed a well-contracting left ventricle.

Despite the administration of sotalol hydrochloride (40 mg intravenously), several efforts to wean the patient from extracorporeal circulation were followed by renewed episodes of ventricular fibrillation. After the administration of amiodarone hydrochloride (150 mg intravenously) and norepinephrine to raise the mean arterial pressure to 100 mm Hg, the patient was weaned from bypass without further arrhythmias. After 48 hours, norepinephrine was discontinued in stepwise fashion. Postoperative echocardiography showed normal LV function and a patent extraanatomic bypass graft.

Patient 2
A 45-year-old man was seen with severe arterial hypertension (200/120 mm Hg despite medical therapy), coarctation of the aorta (Fig 1Go), aortic valve stenosis, and aneurysmal dilatation of the ascending aorta (diameter, 5 cm). Left heart catheterization revealed single-vessel disease with 80% stenosis of the right coronary artery and normal systolic LV function. Mean gradients across the aortic valve and the coarctation were 65 mm Hg and 80 mm Hg, respectively.



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Fig 1. . Three-dimensional computed tomographic scan demonstrating aneurysmal enlargement of ascending aorta, hypoplastic terminal arch, and coarctation.

 
Because of these findings, the patient underwent concomitant replacement of the ascending aorta with a valved conduit (29-mm Carbo-Seal; CarboMedics, Inc, Austin, TX) and intrapericardial bypass grafting from the ascending aortic prosthesis to the descending aorta. A saphenous vein graft was placed from the prosthesis to the main right coronary artery. Cold blood cardioplegic arrest time was 142 minutes.

As in patient 1, after successful weaning from bypass, severe depression of blood pressure complicated by ventricular fibrillation was noted, despite adequate left heart filling pressures. Amiodarone administration abolished the tendency for ventricular fibrillation. Although the sinus rhythm was stable, the transesophageal echocardiogram showed intermittent dramatic reductions in the initially normal LV ejection fraction in conjunction with each period of hypotension.

As a result, an attempt was made to elevate preload and afterload by volume loading and by administering norepinephrine with the aim of maintaining a mean arterial pressure of 110 mm Hg. These measures resulted in stabilization of the patient's hemodynamics. The further postoperative course was complicated by an episode of sepsis, which resulted in a prolonged postoperative course. Three months later, the patient was in stable condition with adequate function of both ventricles and a substantial decrease in LV hypertrophy as assessed by echocardiography. Both the valve and the bypass graft were functioning adequately.


    Comment
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Heart failure or life-threatening ventricular arrhythmias after extraanatomic bypass grafting, as observed in our 2 patients, is an unusual complication. This may be due to the fact that excessive overloading of the left heart created by a tandem stenosis nowadays is rarely encountered in adults. Both of our patients came from areas where up-to-date diagnostic equipment is not available. Efforts to analyze the pathophysiologic background seem justified because of possible therapeutic consequences in similar situations in future.

Although hemodynamics were initially stable after weaning from bypass, frequent episodes of ventricular fibrillation in 1 patient and abrupt development of LV failure (documented online by transesophageal echocardiography) in the other were major findings. In our opinion, the most probable common denominator of these events was global myocardial ischemia resulting from an impaired coronary blood supply. Changes in the hemodynamics of the thoracic vascular bed after aortic valve replacement and placement of an ascending-descending aorta bypass graft have to be taken into account. While preoperatively, because of the gradient across the coarctation, the hypertrophied left ventricle had adapted to high perfusion pressures, relief of isthmic stenosis resulted in a major drop in pressure in the ascending aorta postoperatively. This ``normalization'' of blood pressure appears to be inadequate to maintain sufficient myocardial perfusion in hypertrophied left ventricles. However, administration of high doses of norepinephrine with the resulting increase in arterial perfusion pressure led to stabilization of the hemodynamics, a finding supporting this theory of coronary malperfusion. Future surgical strategies and perioperative drug management should be influenced by these observations.

The principal advantages of single-stage repair in combined aortic valve and isthmic stenosis in terms of the number of surgical procedures and the length of hospital stay must be weighed against the potentially increased intraoperative risk. If a single-stage approach is chosen, measures to increase preload and afterload in the period after weaning from extracorporeal circulation appear mandatory. Awareness of the pathophysiologic background of the complications observed is considered important for the successful management of these high-risk patients.


    Footnotes
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 Abstract
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 Material and Methods
 Comment
 References
 
Address reprint requests to Dr Pethig, Klinik für Thorax-, Herz- und Gefäßchirurgie, Medizinische Hochschule Hannover, D-30623 Hannover, Germany.


    References
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 Footnotes
 Abstract
 Introduction
 Material and Methods
 Comment
 References
 

  1. Child JS, Perloff JK. Natural survival patterns. In: Perloff JK, Child JS, eds. Congenital heart disease in adults. Philadelphia, London, Toronto: WB Saunders, 1991:21-59.
  2. Campbell M. Natural history of coarctation of the aorta. Br Heart J 1970;32:633–40.[Abstract/Free Full Text]
  3. Wukasch DC, Cooley DA, Sandiford FM, Nappi G, Reul GJ Jr. Ascending aorta-abdominal aorta bypass: indications, technique, and report of 12 patients. Ann Thorac Surg 1977;23:442–8.[Abstract/Free Full Text]
  4. Robicsek F, Hess PJ, Vajtai P. Ascending-distal abdominal aorta bypass for treatment of hypoplastic aortic arch and atypical coarctation in the adult. Ann Thorac Surg 1984;37:261–3.[Abstract/Free Full Text]
  5. Sweeney MS, Walker WE, Duncan JM, Hallman GL, Livesay JJ, Cooley DA. Reoperation for aortic coarctation: techniques, results, and indications for various approaches. Ann Thorac Surg 1985;40:46–9.[Abstract/Free Full Text]
  6. Edie RN, Janani J, Attai LA, Malm JR, Robinson G. Bypass grafts for recurrent or complex coarctations of the aorta. Ann Thorac Surg 1975;20:558–66.[Abstract/Free Full Text]
  7. Pasic M, Carrel T, Tönz M, et al. Der extraanatomische aszendenzsuprazöliakale Aortenbypass in der Behandlung der komplexen oder rezidivierenden Aortenisthmusstenosen. Helv Chir Acta 1993;60:447–50.[Medline]



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