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Ann Thorac Surg 1998;66:603-604
© 1998 The Society of Thoracic Surgeons
a Department of Cardiac Surgery, University Hospital of Wales, Heath Park, Cardiff, CF4 4XW, United Kingdom
To the Editor
We read with interest the recent article by Mulay and associates [1]. Only a few papers reporting on a small number of patients have been published. There is still no consensus on the best strategy for the management of these lesions, particularly whether a one-stage or a two-stage approach should be used and, if a two-stage approach is chosen, whether the coarctation or the intracardiac lesion should be repaired first. A further issue is whether the approach should be different depending on whether the aortic or mitral valve is involved. In their 3 patients who had aortic coarctation associated with aortic valve disease, Mulay and associates chose a two-stage procedure and approached the intracardiac lesion first. The aortic coarctation was later dealt with surgically. The rationale for this approach is to prevent the acute change in coronary blood flow related to the sudden decrease in systemic vascular resistance that may occur when the aortic coarctation is relieved and may cause perioperative hemodynamic instability. In their experience, the obstruction at the site of the coarctation did not interfere with the weaning of patients from cardiopulmonary bypass. Adequate renal perfusion was maintained perioperatively and postoperatively by raising the mean arterial pressure.
Their excellent results would certainly support this surgical strategy. However, Mulay and associates do not indicate left ventricular function at time of the operation, although in reading between the lines it may be assumed that it was not significantly impaired.
In our opinion, in patients with severely compromised left ventricular function, relief of the aortic coarctation and off-loading of the left ventricle before the intracardiac procedure may be a safer option. We used this strategy in a 30-year-old man who had aortic coarctation, a small subaortic ventricular septal defect, and severe aortic regurgitation. For several years he refused operation because of a lack of symptoms. The onset of atrial fibrillation produced a sudden deterioration in his clinical condition. Echocardiography showed a grossly dilated, poorly contracting left ventricle; the right ventricle was also dilated, and the pulmonary pressure was raised. In addition, there was biochemical evidence of renal and hepatic dysfunction. The left ventricular function was considered to be too poor for an aortic valve replacement. The decision was made to repair the aortic coarctation and then, according to the response in left ventricular function to the reduced afterload, to proceed with either aortic valve replacement or cardiac transplantation. At operation, the coarcted segment of aorta was resected and a 22-mm Dacron graft was interposed. Unlike the experience of Rufilanchas and associates [2], the postoperative course was uneventful and the patient was discharged home a week later. Left ventricular function progressively improved, and renal and liver function returned to normal. Aortic valve replacement with an aortic homograft and closure of the ventricular septal defect was successfully performed 18 months later. Four and half years later the patient remains asymptomatic, in sinus rhythm, with a moderately impaired left ventricle on echocardiography.
The presence of aortic coarctation associated with mitral regurgitation also constitutes an important management problem. In these patients, a decrease in left ventricular systolic function caused by a combination of myocardial injury during the operation and the acute increase in afterload, in addition to the afterload related to the presence of aortic coarctation, may constitute a problem in the early postoperative period. In this clinical setting we have also used a two-staged approach, dealing first with the aortic coarctation. A 36-year-old man was admitted to the hospital with Streptococcus viridans endocarditis and severe mitral regurgitation. The presence of aortic coarctation was first detected at that time. Transesophageal echocardiography demonstrated the presence of vegetations on both leaflets and ruptured chordae to both leaflets of the mitral valve. The left ventricle was hyperdynamic and mildly hypertrophied. The aortic coarctation was imaged. Intravenous antibiotic therapy was commenced together with antifailure treatment. The patient remained hemodynamically stable and the infection was controlled. Four weeks later the coarctation was balloon-dilated with a reduction in gradient from 35 to 5 mm Hg, and after a week the mitral valve was successfully repaired. Six years later he remains well with no clinical evidence of recurrence of aortic coarctation or mitral regurgitation.
In conclusion, we believe that the staging of operation for aortic coarctation associated with major intracardiac pathology needs to be individualized, and in some cases, unlike the recommendation of Mulay and associates, the aortic coarctation should be dealt with first. The choice will be influenced by the degree of left ventricular dysfunction and the potential for the left ventricle to tolerate the altered loading conditions of the first operation. In this respect, in the presence of severe mitral regurgitation or impaired left ventricular function we believe that the aortic coarctation should be dealt with first.
References
This article has been cited by other articles:
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C. H. A. Jost, H. V. Schaff, H. M. Connolly, G. K. Danielson, J. A. Dearani, F. J. Puga, and C. A. Warnes Spectrum of Reoperations After Repair of Aortic Coarctation: Importance of an Individualized Approach Because of Coexistent Cardiovascular Disease Mayo Clin. Proc., July 1, 2002; 77(7): 646 - 653. [Abstract] [PDF] |
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