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J Thorac Cardiovasc Surg 2002;124:628-629
© 2002 The American Association for Thoracic Surgery

Brief Communications

Sildenafil augments the effect of inhaled nitric oxide for postoperative pulmonary hypertensive crises

From the Division of Pediatric Cardiology,^a College of Pharmacy,^b and Division of Cardiothoracic Surgery,^c Medical University of South Carolina, Charleston, SC.

Received for publication Feb 26, 2002. Accepted for publication March 29, 2002. Address for reprints: Andrew M. Atz, MD, Director, Pediatric Cardiac Intensive Care, Children's Heart Program of South Carolina, Medical University of South Carolina, 165 Ashley Ave, PO Box 250915, Charleston, SC 29425 (E-mail: atzam@musc.edu).

The first 20% of the full text of this article appears below.

Pulmonary hypertension remains a major complication after surgical correction of congenital heart disease. Inhaled nitric oxide (NO) has been shown to reduce, but not eliminate, potentially life-threatening episodic pulmonary hypertensive crises. ¹ NO increases intracellular cyclic guanosine monophosphate (cGMP), resulting in smooth muscle vasodilation. Phosphodiesterase type 5 (PDE5) is responsible for cGMP breakdown in lung tissue. We hypothesized that sildenafil (Viagra; Pfizer Laboratories, New York, NY), a selective and potent inhibitor of PDE5, may augment pulmonary vasodilation with NO and reduce the risk of pulmonary hypertensive crises in an at-risk postoperative patient.

Clinical summary

A 9-month-old boy with congenital mitral stenosis underwent supra-annular valve replacement with a 16-mm Carbomedics prosthesis (Sulzer Carbomedics, Austin, Tex). Postoperative support included dopamine at 7 µg · kg^-1 · min^-1, milrinone at 0.75 µg · kg^-1 · min^-1, muscle relaxation with vecuronium at 0.1 mg · kg^-1 · h^-1, sedation with fentanyl at 20 µg · kg^-1 · h^-1. . . [Full Text of this Article]

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