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Ann Thorac Surg 2008;86:2025-2026. doi:10.1016/j.athoracsur.2008.06.044
© 2008 The Society of Thoracic Surgeons

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Correspondence

Arterial Switch Operation, Aortic Root Dilation, and Long-Term Aortic Valve Competence

Tomaso Bottio, MD, PhDa, Gaetano Thiene, MDb, Vincenzo Tarzia, MDa, Giulio Rizzoli, MDa, Gino Gerosa, MDa

a Cardiovascular Surgery Institute, University of Padua Medical School, Via Giustiniani, 2, Padova, Padua, 35100 Italy
b Cardiovascular Pathology Institute, University of Padua Medical School, Via Giustiniani, 2, Padova, Padua, 35100 Italy

(Email: tbottio{at}gmail.com).

To the Editor:

We have a concern regarding the report by Bové and colleagues [1] on midterm outcomes of patients undergoing arterial switch operation (ASO). In their study, 93 patients were subdivided into two groups according to presence or absence of ventricular septal defect (VSD) and were treated by ASO and echocardiography. Only 1 patient suffered from symptomatic aortic regurgitation and needed a late surgical repair. Freedom from aortic regurgitation was significantly lower for patients with a concomitant VSD, but the Z-score in VSD patients was higher than in those without VSD. The authors observed that after ASO the neoaortic root is larger in comparison with a normal population and that this observation is more pronounced when both VSD closure and moderate aortic valve incompetence occurs after the procedure, or when only one of these occurs. Lalezari and colleagues [2] speculate that morphologic and functional deterioration occurring in the neoaortic root may explain this phenomenon.

Lalezari and colleagues [2] compared the sinus walls taken from 20 patients with untreated great artery transposition (9 with VSD and 11 without) and 9 age-matched patients with a normal heart. They observed downregulation of all smooth-muscle cell markers in the pulmonary artery media of older patients, and concluded that this may be the explanation for neoaortic root dilation.

Recently, we examined the aortic and pulmonary roots of three different groups of patients. Group A included patients with a normal heart (4 patients, age 0 to 12 months; 4 patients, 1 to 5 years old; 7 patients, 13 to 21 years); group B included 10 patients with diagnosis of transposition of the great arteries without VSD (age, 1 to 23 days); and group C included 10 patients (age, 12 to 52 years) with a diagnosis of chronic pulmonary hypertension who had undergone a heart-lung transplant. These patients included a 12-year-old who had a longlasting pulmonary hypertension due to VSD. In all others, pulmonary hypertension developed in adulthood. Both aortic and pulmonary sinus walls of patients with transposition of the great arteries were identical in terms of configuration, elastic units density, and elastic units count, although the pulmonary media was thicker than the aorta. Among the pulmonary hypertensive patients, the pulmonary configuration in the 12-year-old child was absolutely identical to that of aorta, although the pulmonary wall was thinner than the aorta (ratio, 0.8), and the elastic unit count and density in the pulmonary sinus were higher than the aorta (ratio, 1.5). In contrast, the aortic sinuses and pulmonary sinuses of the other 9 patients all showed pulmonary and aortic media thickening compared with the media of adult normal hearts, but the pulmonary wall configuration was identical to that of the normal adult pulmonary wall.

The ASO transfers the pulmonary root and valve into systemic flow. Smooth-muscle cells increase in the pulmonary wall after the Ross-procedure [3] and after pulmonary hypertension disease [4], but decrease in the pulmonary media of patients with untreated great-artery transposition [2]. In contrast, we observed that the elastic components of the pulmonary wall (which are chronically exposed to systemic pressure) are comparable to the aorta.

Summarizing we speculate that the pulmonary sinus wall of patients aged 0 to 12 months has the same histologic potential as the aorta, and when exposed to systemic pressure an aortic-like configuration develops. Therefore, the first postoperative pulmonary dilation may be explained by greater elasticity than the aorta, and is not due to a nonspecified downregulation. In the long-term, the pulmonary root exposed to systemic pressure may actively grow to acquire the same histologic properties of the aorta.


    References
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 References
 

  1. Bové T, De Meulder F, Vandenplas G, et al. Midterm assessment of the reconstructed arteries after the arterial switch operation Ann Thorac Surg 2008;85:823-830.[Abstract/Free Full Text]
  2. Lalezari S, Hazekamp MG, Bartelings MM, Schoof PH, Gittenberger-de Groot AC. Pulmonary artery remodeling in transposition of the great arteries: relevance for neo-aortic root dilation J Thorac Cardiovasc Surg 2003;126:1053-1060.[Abstract/Free Full Text]
  3. Schoof PH, Gittenberger-de Groot AC, de Heer E, et al. Remodeling of the porcine pulmonary autograft wall in the aortic position J Thorac Cardiovasc Surg 2000;120:55-65.[Abstract/Free Full Text]
  4. Owens G. Influence of blood pressure on development of the aortic medial smooth muscle hypertrophy in spontaneously hypertensive rats Hypertension 1987;9:178-187.[Abstract/Free Full Text]



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