Pneumonia and ACE inhibitors—and cough
BMJ 2012; 345 doi: https://doi.org/10.1136/bmj.e4566 (Published 11 July 2012) Cite this as: BMJ 2012;345:e4566- Rosemary A Barnes, professor and honorary consultant
- 1Department of Medical Microbiology and Infectious Diseases, Institute of Infection and Immunity, School of Medicine, Cardiff University, Cardiff CF14 4XN, UK
- barnesra{at}cf.ac.uk
Angiotensin converting enzyme (ACE) inhibitors are widely used to treat heart failure and hypertension. They act through blocking the conversion of angiotensin I to angiotensin II; this inhibits the breakdown of bradykinin, which in turn lowers arteriole resistance and increases venous return. Many patients taking ACE inhibitors experience a persistent dry cough, which is thought to be caused by increased concentrations of bradykinin; the cough is triggered by the endothelial effects of bradykinin and other peptides. Refractory cough is the most common reason for switching from ACE inhibitors to angiotensin II receptor blockers (ARBs), which do not inhibit the breakdown of kinins and are less likely to cause troublesome coughing. In the linked study (doi:10.1136/bmj.e4260), Caldeira and colleagues examined the risk of pneumonia with both classes of drug, hypothesising that the cough associated with ACE inhibitors might protective against pneumonia.1
Coughing is one of the most common reasons that patients consult a primary care doctor, and it has a substantial effect on quality of life. It also …
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