(Chest. 2001;120:305-306.)
© 2001
American College of Chest Physicians
Does Sildenafil Also Improve Breathing?*
Nirmal B. Charan, MD, FCCP
*
From the Section of Pulmonary and Critical Care Medicine, Veterans Affairs Medical Center, Boise, ID.
Correspondence to: Nirmal B. Charan, MD, FCCP, Section of Pulmonary/Critical Care Medicine (111), VA Medical Center, 500 W Fort St, Boise, ID 83702-4598; e-mail: Nirmal.Charan{at}med.va.gov
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Abstract
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Sildenafil is being used by a number of patients with erectile
dysfunction. Some of these patients also may have concomitant COPD. The
effect of sildenafil on lung function is not known. Two patients with
severe COPD and erectile dysfunction reported that their dyspnea
improved when they took oral sildenafil for erectile dysfunction.
Spirometry performed in these patients revealed an improvement in
FEV1 by 24% and 12%. This suggests that, in COPD
patients, oral sildenafil does not have any deleterious effect on
pulmonary function, and in some patients it may produce a modest
improvement in FEV1.
Key Words: COPD erectile, dysfunction sildenafil
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Introduction
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Oral sildenafil
citrate (Viagra; Pfizer; New York, NY) has been shown to improve
erectile dysfunction.1
However, the use of this drug in
patients with COPD and erectile dysfunction has not been described.
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Case Reports
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Case 1
A 64-year-old male patient, an ex-smoker, who had severe but
stable COPD and erectile dysfunction, obtained a prescription for
sildenafil (100 mg) from his urologist. After using this drug for a few
days, he reported that sildenafil not only helped his erectile
dysfunction but also improved the postcoital respiratory distress.
Because this improvement in dyspnea could merely be due to a placebo
effect, he was asked to measure his peak expiratory flow rates (PEFRs)
at home, before and after taking sildenafil. The patient agreed and
intermittently returned to report his PEFR measurements. He measured
PEFR, immediately before and approximately 2 to 4 h after taking
sildenafil, on 15 separate occasions in a 10-week period. For accuracy
and consistency, he repeated the test five times to obtain pretreatment
and posttreatment PEFR values. His mean (± SD) baseline PEFR was
295 ± 37 L/min and, after taking sildenafil, it improved to
372 ± 31 L/min (p < 0.001). Although there was variability in
response, he did have some improvement in PEFR (12 to 44%) every time
he took sildenafil. The patient reported again that sildenafil not only
improved his erectile dysfunction but also improved his breathing and
that the beneficial effects lasted until the next day.
To confirm this interesting observation, the patient underwent
spirometry testing in the pulmonary function laboratory before and
1 h after receiving oral sildenafil, 100 mg. His FVC improved from
2.71 L to 3.73 L (38% increase), and his FEV1 improved
from 0.96 L to 1.19 L (24% increase).
Case 2
A 78-year-old man, an ex-smoker, with severe but stable COPD and
erectile dysfunction was also taking oral sildenafil. After
questioning, he also mentioned that his breathing may have been better
after taking this drug. The patient refused to perform PEFR
measurements at home. However, he agreed to come to the pulmonary
function laboratory for further testing. He underwent spirometry
testing before and 1 h after receiving sildenafil, 50 mg (his
usual dose). His FVC changed from 2.86 to 2.98 L (4% increase), and
his FEV1 changed from 0.67 to 0.75 L (12% increase).
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Discussion
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It has been estimated that about 12 million Americans have
COPD.2
It is also recognized that erectile dysfunction is
common in this patient population.3
Many COPD patients are
reluctant to engage in sexual activity because of the respiratory
distress associated with this activity. This case report suggests that
sildenafil does not have any deleterious effects on pulmonary function
and, therefore, can be used in patients with COPD. Although both
patients in this report experienced some improvement in
FEV1, it is difficult to draw any conclusions from this
because of the following limitations: (1) the observation was made in
only two patients; (2) a placebo was not used; (3) one patient had only
a borderline increase in FEV1; and (4) the improvement in
FEV1 observed in these patients could have been due just to
natural variability in pulmonary function.
Although improvement in airway function with sildenafil has not been
reported previously, this association may have some scientific basis.
Sildenafil is a selective inhibitor of cyclic guanosine
3',5'-monophosphate-specific phosphodiesterase (PDE) type 5, which is
the predominant enzyme that metabolizes cyclic guanosine
3',5'-monophosphate.4
Isoenzyme-selective PDE inhibitors
that have been known to cause bronchodilation are usually related to
PDE type 3 and PDE type 4 types, but recently PDE type 5 inhibition
also has been implicated in reversing
bronchoconstriction.5
Therefore, it is possible that oral
sildenafil therapy may improve airway functions by causing airway
smooth muscle relaxation. However, a systematic and placebo-controlled
study will be required to confirm this hypothesis.
In conclusion, it appears that sildenafil does not have any deleterious
effect on pulmonary functions in patients with COPD. In fact, in
certain patients with COPD who also experience erectile dysfunction,
sildenafil may improve not only the erectile dysfunction but may also
have a beneficial effect on postcoital respiratory distress, a unique
but perhaps an important additive benefit of the drug in this patient
population.
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Footnotes
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Abbreviations: PDE = phosphodiesterase; PEFR = peak
expiratory flow rate
Received for publication March 7, 2000.
Accepted for publication January 17, 2001.
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References
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Goldstein, I, Lue, TF, Padma-Nathan, H, et al (1998) Oral sildenafil in the treatment of erectile dysfunction. N Engl J Med 338,1397-1404[Abstract/Free Full Text]
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Feinleib, M, Rosenberg, HM, Collins, JG, et al (1989) Trends in COPD morbidity and mortality in the United States. Am Rev Respir Dis 140,S9-S18[ISI][Medline]
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Fletcher, EC, Martin, RJ (1982) Sexual dysfunction and erectile impotence in chronic obstructive pulmonary disease. Chest 81,413-421[Abstract/Free Full Text]
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Utiger, RD (1998) A pill for impotence. N Engl J Med 338,1458-1459[Free Full Text]
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Torphy, TJ (1998) Phosphodiesterase isozymes: molecular targets for novel antiasthma agents. Am J Respir Crit Care Med 157,351-370[Free Full Text]