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J. Heart Lung Transplant. · Jun 2005
Randomized Controlled Trial Comparative Study Clinical TrialNitric oxide versus prostaglandin E1 for reduction of pulmonary hypertension in heart transplant candidates.
- Branislav Radovancevic, Bojan Vrtovec, Cynthia D Thomas, Mihai Croitoru, Timothy J Myers, Rajko Radovancevic, Tehreen Khan, Edward K Massin, and O H Frazier.
- Department of Cardiology, Texas Heart Institute at St. Luke's Episcopal Hospital, Houston, Texas 77225, USA. bradovancevic@heart.thi.tmc.edu
- J. Heart Lung Transplant. 2005 Jun 1; 24 (6): 690-5.
BackgroundWe sought to directly compare the effects of prostaglandin E1 (PGE1) and nitric oxide (NO) in testing for pulmonary hypertension reversibility in heart transplant candidates.MethodsWe included 19 heart transplant candidates who fulfilled at least 1 of 3 criteria: pulmonary vascular resistance (PVR) of >4 Wood units; transpulmonary gradient (TPG) of >12 mmHg; or systolic pulmonary artery pressure (PAP) of >60 mmHg. Patients randomly received either PGE1 (0.05, 0.2 and 0.5 microg/kg/min) or NO (40, 60 and 80 ppm) and were crossed-over to the second medication after receiving the maximal dose of the first.ResultsWith PGE1, TPG decreased by 21% (baseline 20.3 +/- 6.8 mmHg; final 16.0 +/- 7.0 mmHg) compared to a 34% decrease with NO (baseline 20.8 +/- 6.2 mmHg; final 13.8 +/- 5.4 mmHg) (p = 0.13). PVR decreased by 42% with PGE1 (baseline 6.2 +/- 4.0 Wood units; final 3.6 +/- 1.8 Wood units) and by 47% with NO (baseline 6.0 +/- 3.9 Wood units; final 3.2 +/- 1.6 Wood units) (p = 0.87). Mean systemic pressure decreased with PGE1 (baseline 76.1 +/- 10.5 mmHg; final 69.4 +/- 12.2 mmHg; -9%) but not with NO administration (baseline 70.2 +/- 14.7 mmHg; final 71.6 +/- 10.9 mmHg; +2%) (p = 0.01). TPG was lowered to <12 mmHg in 14 patients. Of these, 6 (46%) responded to both PGE1 and NO, 4 (27%) responded only to PGE1, and 4 (27%) responded only to NO.ConclusionsThe effects of PGE1 and NO on pulmonary hypertension are comparable, with PGE1 having more systemic hypotensive effects. Due to variability of patient responses, we recommend multiple rather than single-agent pharmacologic testing for the reversibility of pulmonary hypertension.
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