Captopril‐Associated Cough Is Not due to Increased Airway Responsiveness

• Published in: Canadian respiratory journal 1994-01, Vol.1 (4), p.235-240
• Main Authors: Blackie, SP, Hilliam, C, Porter, R, Rangno, R, Paré, PD
• Format: Article
• Language: English
• ISSN: 1198-2241; 1916-7245
• DOI: 10.1155/1994/519168

BACKGROUND: Angiotensin‐converting enzyme (ACE) inhibitors commonly cause cough. There is controversy as to whether preexisting airway hyperresponsivencss predisposes patients to ACE inhibitor‐induced cough and whether ACE inhibitor therapy can cause airway hypcrresponsiveness. OBJECTIVES: To lest the predictive value of baseline airway responsiveness fur the development of cough induced by ACE inhibitors, and whether patients who developed cough during ACE inhibitor therapy showed an increase in airway responsiveness. METHODS: Baseline spiromctry and airway responsiveness to methacholinc (expressed as the concentrat ion of mcthacholine required to cause a 10% fall in forced expired volume in 1 s [ FEV 1 or PC 10 ) were measured in 23 hypertensive patients before and after 10 to l 2 weeks of treatment with captopril at an initial daily dose of 50 mg. RESULTS: During caplopril therapy seven (30%) patients developed new cough, which resolved after discontinuation of captopril. The base line PC 10 was the same in coughers and noncoughers and did not predict the development of cough. During caplopril therapy there was a nonsignificant decrease in the geometric mean PC 10 for all patients from 15 mg/mL (range 0.8 to 62) to 13 mg/ml (range 0.7 to 62) (P=0.08). These changes were not different in cougher, and noncoughers. FEV 1 , forced vital capacity and total lung capacity did not change during the study. CONCLUSIONS: Cough caused by captopril is not predicted by baseline airway responsiveness and is not associated with increased airway res ponsiveness