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Sildenafil for primary and secondary pulmonary hypertension
Author(s) -
Watanabe Hiroshi,
Ohashi Kyoichi,
Takeuchi Kazuhiko,
Yamashita Kazuhiro,
Yokoyama Taku,
Tran QuangKim,
Satoh Hiroshi,
Terada Hajime,
Ohashi Hiroyuki,
Hayashi Hideharu
Publication year - 2002
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1067/mcp.2002.123554
Subject(s) - sildenafil , medicine , pulmonary hypertension , pulmonary artery , cyclic guanosine monophosphate , hemodynamics , vascular resistance , cardiac catheterization , cgmp specific phosphodiesterase type 5 , cardiology , cardiac index , erectile dysfunction , treprostinil , heart disease , anesthesia , cardiac output , nitric oxide
Background Sildenafil is a selective inhibitor of cyclic guanosine monophosphate‐specific phosphodiesterase type 5, an enzyme that is abundant in both lung and penile tissues. Sildenafil is widely used to dilatepenile arteries, suggesting that it may also dilate pulmonary arteries in patients with pulmonary hypertension. However, the long‐term hemodynamic effects and safety of the drug in pulmonary hypertension are not known. Methods One patient with primary pulmonary hypertension and another with secondary pulmonary hypertension caused by collagen disease were given 50 mg oral sildenafil during cardiac catheterization for assessment of the acute hemodynamic effects of the drug. The patients were then given maintenance treatment with 25 mg oral sildenafil twice a day. Long‐term hemodynamic effects were evaluated by repeated cardiac catheterization after 3 months, with the last oral dose given 15 hours before the procedure. The acute hemodynamic effects of sildenafil after the long‐term treatment were studied during the same cardiac catheterization. Results Sildenafil did not affect aortic pressure, but it significantly decreased pulmonary artery pressure and increased cardiac index, thereby reducing pulmonary vascular resistance. Long‐term maintenance therapy with 25 mg oral sildenafil twice a day remarkably improved the clinical condition of the patients, without causing any adverse effects; New York Heart Association functional classification returned to class II (from class III). The acute efficacy of sildenafil was well preserved after the long‐term treatment; there was no tolerance. Conclusions The data strongly suggest that sildenafil can be used as a valuable pulmonary vasodilator inpatients with pulmonary hypertension, with good long‐term hemodynamic effects and safety. The results necessitate larger trials to confirm these observations in a larger cohort of patients. Clinical Pharmacology & Therapeutics (2002) 71 , 398–402; doi: 10.1067/mcp.2002.123554