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J Thorac Cardiovasc Surg 1998;115:875-882
© 1998 Mosby, Inc.
SURGERY FOR CONGENITAL HEART DISEASE |
Supported by The Children's Hospital Research Institute Career Development Award (D.D.I., J.P.K.), the National Institutes of Health (H241012 and 46481; S.H.A.), the March of Dimes Birth Defects Foundation (D.D.I., J.P.K.), the Bugher Physician-Scientist TrainingProgram (D.D.I., J.P.K.), and the American Heart Association Established Investigator Award (S.H.A.). Also supported by grant M01RR00069 General Clinical Research Centers, National Centers For Research Resources, National Institutes of Health.
Received for publication July 18, 1997. Revisions requested Sept. 15, 1997; revisions received Dec. 3, 1997. Accepted for publication dec. 9, 1997. Address for reprints: D. Dunbar Ivy, MD, Department of Cardiology, Box B100, The Children's Hospital, 1056 East 19th Ave., Denver, CO 80218.
Objective: Inhaled nitric oxide therapy causes selective and sustained pulmonary vasodilation in patients with pulmonary hypertension; however, attempts to discontinue inhaled nitric oxide therapy may be complicated by abrupt life-threatening events. Dipyridamole, a cyclic guanosine monophosphate–specific phosphodiesterase inhibitor, blocks the hydrolysis of cyclic guanosine monophosphate in vascular smooth muscle cells.
Methods: We studied 23 consecutive children who were treated with inhaled nitric oxide because of clinically significant pulmonary hypertension after surgery for congenital heart disease. Inhaled nitric oxide therapy was withdrawn before and after dipyridamole treatment of children in whom sustained elevations of pulmonary artery pressure developed for over 30 minutes.
Results: In 7 of 23 children, inhaled nitric oxide withdrawal caused a 40% increase in pulmonary artery pressure, a 17% decrease in systemic venous oxygen saturation, and a 46% increase in the ratio of mean pulmonary artery pressure to aortic pressure. Compared with children who had no significant increase in pulmonary artery pressure, children who experienced the development of prolonged pulmonary hypertension after inhaled nitric oxide therapy withdrawal had higher mean pulmonary artery pressure immediately before inhaled nitric oxide withdrawal (22 ± 1 mm Hg versus 27 ± 2 mm Hg; p = 0.04) and received inhaled nitric oxide for a longer duration (2 ± 1 days versus 4 ± 1 days; p = 0.01). Dipyridamole therapy attenuated the rise in pulmonary artery pressure and fall in systemic venous oxygen saturation in all six patients studied with rebound pulmonary hypertension after withdrawal of inhaled nitric oxide.
Conclusion: We conclude that dipyridamole therapy acutely attenuates the adverse hemodynamic effects of rapid withdrawal of inhaled nitric oxide therapy. Children with higher pulmonary artery pressure and who are treated with inhaled nitric oxide for a longer duration may be at increased risk for adverse hemodynamic effects of inhaled nitric oxide therapy withdrawal. We speculate that dipyridamole therapy may sustain elevations of smooth muscle cyclic guanosine monophosphate induced by inhaled nitric oxide and that phosphodiesterase activity contributes to acute pulmonary hypertension after inhaled nitric oxide withdrawal. (J Thorac Cardiovasc Surg 1998;115:875-82)
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