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(Hypertension. 2008;51:1465.)
© 2008 American Heart Association, Inc.
Editorial Commentaries |
From the SUNY Downstate College of Medicine and St. Lukes – Roosevelt Medical Center, Columbia University College of Physicians and Surgeons, New York.
Correspondence to Michael A. Weber, MD, SUNY Downstate College of Medicine, 308 E 38th St, Ste 201, New York, NY 10016. E-mail michaelwebermd@cs.com
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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One of the chief attributes of the ACE inhibitors has been their overall tolerability. By far the most commonly encountered complaint with these agents is a dry, nonproductive cough. The cause of this cough has never been established, but bradykinin—which exists in increased concentrations as a direct result of the action of the ACE inhibitors—is the most commonly cited culprit. This cough is generally not of medical significance, but can sometimes lead to increased doctor visits and costs when the explanation for a newly evident cough is being sought. This symptom is sufficiently intrusive to cause discontinuation of ACE inhibitor therapy in up to 20% of patients.
Angioedema is potentially far more troubling. As with cough, bradykinin seems to be the cause of this event.3
Related Article:
Hypertension 2008 51: 1624-1630.
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