Clinical analyses of angiotensin-converting enzyme inhibitor users presenting with cough to a chest diseases outpatient clinic: A single-center retrospective study

Objective Angiotensin-converting enzyme inhibitors are widely prescribed for cardiovascular disease and are a well-recognized cause of cough. However, cough in patients treated with angiotensin-converting enzyme inhibitor may also reflect underlying pulmonary disease. This study compared the clinical, laboratory, and medication-related characteristics of angiotensin-converting enzyme inhibitor users presenting with pulmonary and non-pulmonary cough. Methods This retrospective single-center study included 199 angiotensin-converting enzyme inhibitor–treated patients who presented with cough to the Chest Diseases Outpatient Clinic of Giresun Training and Research Hospital between October 2021 and January 2025. Patients were classified as having cough with pulmonary or non-pulmonary causes according to available clinical, laboratory, and radiological findings. Non-pulmonary cough was not considered synonymous with confirmed angiotensin-converting enzyme inhibitor–induced cough; however, it indicated the absence of identifiable pulmonary pathology based on retrospective data. Demographic, clinical, laboratory, and angiotensin-converting enzyme inhibitor subtype characteristics were compared. Results Among 199 patients, 153 (76.9%) had pulmonary cough and 46 (23.1%) had non-pulmonary cough. Cough duration was longer (p = 0.044) and dyspnea was more frequent (54.2% vs. 13.0%, p < 0.001) in the pulmonary group. Perindopril use was more common in the non-pulmonary group, whereas ramipril use was more common among patients with pulmonary cough ( p = 0.015). In a post hoc analysis limited to patients with documented angiotensin-converting enzyme inhibitor discontinuation and evaluable follow-up notes (n = 78), the overall distribution of cough-response categories differed between the groups (Fisher–Freeman–Halton exact p = 0.039), with complete resolution observed in 33.3% of the patients in the non-pulmonary group and 7.9% patients in the pulmonary group. C-reactive protein levels were higher in the pulmonary group (10.87 vs. 5.67 mg/L, p = 0.010), whereas other hematological parameters did not differ significantly. Conclusions In the angiotensin-converting enzyme inhibitor–treated patients presenting with cough, shorter symptom duration, absence of dyspnea, and lower C-reactive protein levels may be more compatible with non-pulmonary or presumed angiotensin-converting enzyme inhibitor–related cough, whereas prolonged cough, dyspnea, and elevated C-reactive protein levels may support the consideration of a pulmonary pathology. These findings are hypothesis-generating and require prospective validation.