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J Thorac Cardiovasc Surg 1998;115:484-485
© 1998 Mosby, Inc.

LETTERS TO THE EDITOR

Pulmonary artery banding in Eisenmenger complex

To the Editor:

The news article titled "Batista Strikes Again to Tackle Eisenmenger Complex," published in the May 1997 issue of The Lancet, has prompted us to review the strategies for surgical management of patients with Eisenmenger syndrome. As a primary step in the treatment of patients with Eisenmenger complex, Batista ¹ proposes pulmonary artery (PA) banding to dilate the pulmonary vascular bed by reducing PA oxygen saturation (Sao₂). Later, when PA and systemic pressures and arterial blood Sao₂ return to normal values, debanding of the PA and correction of congenital heart defects are indicated. ¹ This news brings to mind an article by Wagenvoort, Wagenvoort, and Draulans-Noë, ² in which the authors compared the morphologic changes in lung biopsy specimens of patients with congenital heart disease with a shunt and pulmonary hypertension before and after banding of the PA. These investigators reported that medial hypertrophy regressed after PA banding, and in plexogenic pulmonary arteriopathy, the earlier lesions, particularly cellular intimal proliferation, also regressed.

Although lung and heart-lung transplantation are the only definitive treatments for most adults with Eisenmenger syndrome, Hopkins and associates ^3,4 report that the natural survival of these patients is better than survival achieved with transplantation. In this regard, they have tried to identify means other than transplantation to improve their quality of life.

Because increased flow is an important pathogenic element in producing pulmonary hypertension, Dammann and colleagues ⁵ first performed PA banding to reduce pulmonary blood flow and PA hypertension and thereby therapeutically improve congestive heart failure. Serial biopsy specimens provided good evidence that PA banding was following by regression of the hypertensive changes in the lung vasculature. ⁵ Batista and associates ¹ postulate that high PA Sao₂, rather than hyperflow, is the main cause of PA vasoconstriction and PA vascular resistance. A review ⁶ of the experimental data concerning the effect of hypoxia on the pulmonary circulation does not support that hypothesis. Interestingly, in isolated pig lungs, Sylvester and associates ⁷ observed that reduction of the alveolar oxygen tension to a level of 50 to 30 mm Hg led to hypoxic pulmonary vasodilation.

Goldblatt and coworkers ⁸ presume that, in the presence of a right-to-left shunt, PA banding would increase cardiac embarrassment, both physiologically and hemodynamically. With a right-to-left shunt, the PA pressure is still increased, but the pulmonary blood flow is not. ⁸ It is important to decide how much the PA pressure can be reduced without compromising the heart's ability to perfuse a highly resistant pulmonary arteriolar bed in Eisenmenger complex. ⁸ In the course of PA banding, systemic Sao₂ was reduced from 97% to 60% or 75% and pulmonary Sao₂ from 87% to about 20% ¹ in patients with right-to-left shunt without compromising the heart (no respiratory acidosis developed, per a personal communication with Dr. Randas Batista).

Brammell and colleagues ⁹ suggest that if the pulmonary vascular bed is reactive, PA banding is not contraindicated in Wood's definition of Eisenmenger syndrome. To avoid a catastrophic outcome, before operating, one can evaluate the reactivity of the pulmonary vascular bed to PA banding by partially occluding the PA with a balloon-tipped catheter during preoperative catheterization.

What options remain when lung or heart-lung transplantation is not possible or even advisable, ^3,4 especially for patients from a poor socioeconomic condition who have pulmonary vasculature changes of Heath-Edwards grade IV-VI? The choices may be PA banding, with all supportive measures, or death.

Department of Cardiovascular SurgeryAkita University School of Medicine1-1-1 Hondo, Akita 010, Japan References

1. Batista strikes again to tackle Eisenmenger complex (News). Lancet 1997;349:1605.
   
2. Wagenvoort CA, Wagenvoort N, Draulans-Noë Y. Reversibility of plexogenic pulmonary arteriopathy following banding of the pulmonary artery. J Thorac Cardiovasc Surg 1984;87:876-86.[Abstract]
   
3. Hopkins WE. Severe primary pulmonary hypertension in congenital heart disease: a review of Eisenmenger syndrome. Curr Opin Cardiol 1995;10:517-23.[Medline]
   
4. Hopkins WE, Ochoa LL, Richardson GW, Trulock EP. Comparison of the hemodynamics and survival of adults with severe primary pulmonary hypertension or Eisenmenger syndrome. J Heart Lung Transplant 1996;15:100-5.[Medline]
   
5. Dammann JF Jr, McEachen JA, Thompson WM, Smith R, Muller WH Jr. The regression of pulmonary vascular disease after the creation of pulmonary stenosis. J Thorac Cardiovasc Surg 1961;42:722-34.
   
6. Fishman AP. Hypoxia on the pulmonary circulation: how and where it acts. Circ Res 1976;38:221-31.[Free Full Text]
   
7. Sylvester JT, Harabin AL, Peake MD, Frank RS. Vasodilator and constrictor responses to hypoxia in isolated pig lungs. J Appl Physiol 1980;49:820-5.[Abstract/Free Full Text]
   
8. Goldblatt A, Bernhard WF, Nadas AS, Gross RE. Pulmonary artery banding: indications and results in infants and children. Circulation 1965;32:172-84.[Free Full Text]
   
9. Brammell HL, Vogel JH, Pryor R, Blount SG Jr. The Eisenmenger syndrome: a clinical and physiologic reappraisal. Am J Cardiol 1971;28:679-92.[Medline]
   

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