ACEI-induced cough: A review of current evidence and its practical implications for optimal CV risk reduction

Abstract

Cough is one of the common adverse effects in patients receiving angiotensin-converting enzyme inhibitors (ACEIs). This review presents the current evidence on incidence and mechanisms of cough associated with ACEIs use, and proposes a practical approach for managing the same for optimal cardiovascular (CV) risk reduction. The incidence of dry cough in patients receiving ACEIs vary among individual ACEIs, and is the lowest with perindopril. Cough is thought to originate from multiple mechanisms, bradykinin theory is the most commonly appealed hypothesis. The strategies for optimal management could be temporarily discontinuation of ACEI upon a reported incidence of cough and reintroduction after its remission. However, studies have reported disappearance of cough despite continuing treatment. Another important approach could be adding calcium channel blockers to ACEIs. Switching to alternative drugs such as angiotensin receptor blockers should be suggested in case intolerable symptoms recur and after exclusion of all other possible causes of cough.

Keywords: Angiotensin-converting enzyme inhibitors; Cardiovascular risk reduction; Cough; Current evidence.

Fig. 1

Role of ACEI in maintaining overall homeostasis in the body. ACE: Angiotensinconvertingenzyme; ICAM-1: Intercellularadhesionmolecule1; VCAM-1: Vascular cell adhesion protein 1; PAI-1: Plasminogen activator inhibitor-1-; t-Pa: Tissueplasminogenactivator.

Fig. 2

Algorithm for management of ACEI-induced cough. ACEI: Angiotensin converting enzyme inhibitor; ARB: Angiotensin II receptor blocker; ARNI:Angiotensin receptor neprilysin inhibitor.