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J Thorac Cardiovasc Surg 2006;132:1501-1502
© 2006 The American Association for Thoracic Surgery

Letter to the Editor

Nitric oxide precursors and congenital cardiac surgery: A randomized controlled trial of oral citrulline. Definition of pulmonary hypertension in Fontan circulation?

Maurice Beghetti, MD, Yacine Aggoun, MD, Eduardo Da Cruz, BSc, MD

Unité de Cardiologie Pédiatrique, Hopital des Enfants, Genève, Switzerland

(Email: Maurice.Beghetti{at}hcuge.ch).

To the Editor:

We read with great interest the article from Smith and colleagues1Go describing the effect of citrulline supplementation in reducing postoperative pulmonary hypertension. This is very appealing therapy because it is reported to be effective and without any side effects.

Nevertheless, we have a concern with the definition of pulmonary hypertension. The authors have used the accepted definition of pulmonary hypertension as a mean pulmonary arterial pressure of at least 25 mm Hg2Go or exceeding 50% of the mean systemic artery pressure. Although acceptable for patients presenting with ventricular or atrioventricular septal defect, as well as transposition of the great arteries, this definition is more questionable for bidirectional Glenn and Fontan procedures.

A prerequisite for a successful bidirectional Glenn or Fontan procedure would be a mean pressure of less than 15 mm Hg. In addition, a pressure of more than 12 mm Hg in a Fontan circulation would be considered a suboptimal result.

Taking 25 mm Hg as a limit to describe high pulmonary pressure in this group induces a significant bias to our point of view. Assuming that we use 15 mm Hg as the limit for the Glenn and Fontan group, all patients (11/11) presented with pressure of more than 15 mm Hg in the placebo group, and 9 of 10 patients presented with this pressure in the citrulline group. Taking 20 mm Hg as a superior limit, 4 of 11 in the placebo group presented with pressure over the limit compared with 4 of 10 in the citrulline group, respectively.

On this basis, we think that groups with shunt lesions and biventricular repair versus single-ventricle physiology should not be evaluated similarly with regard to pulmonary hypertension.

Another concern, and this is applicable to both shunt lesions or single-ventricle circulation, is that nothing is reported with regard to postoperative care, and several confounding factors can increase or decrease pulmonary arterial pressures in this period, such as pH, PO 2, sedation, ventricular function, pulmonary wedge or atrial pressures, and inotropic/vasodilatory support for 48 hours.3Go

We think these points are of major importance because citrulline levels might not have been the sole responsible variable for reducing pulmonary arterial pressure.

References

  1. Smith HA, Canter JA, Christian KG, Drinkwater DC, Scholl FG, Christman BW, et al. Nitric oxide precursors and congenital heart surgery: a randomized controlled trial of oral citrulline. J Thorac Cardiovasc Surg 2006;132:58-65.[Abstract/Free Full Text]
  2. Simonneau G, Galie N, Rubin LJ, Langleben D, Seeger W, Domenighetti G, et al. A Clinical classification of pulmonary hypertension. J Am Coll Cardiol 2004;43(suppl):5S-12S.[Abstract/Free Full Text]
  3. Adatia I. Pathophysiology of postoperative pulmonary hypertension. In: Beghetti M, Barst RJ, Naeije R, Rubin LJ, editors. Pulmonary arterial hypertension related to congenital heart disease. 1st ed.. Munich: Elsevier GmbH; 2006. pp. 75-91.




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