The benefit of angiotensin converting enzyme (ACE) inhibition in chronic heart failure (HF) is partially due to its effects on pulmonary function and particularly on lung diffusion, the latter being counteracted by acetylsalicylic acid (ASA). Tissue ACE activity is largely determined by an insertion/deletion (I/D) polymorphism resulting in three possible genotypes (DD, ID and II). It is not clear if ACE inhibitor therapy could exert different effects in these genotypes.

The aim of this new study was to understand whether I/D polymorphism interferes with ACE inhibitor's protection of the lungs in HF during acute fluid overload. The Authors found that ACE DD genotype is associated with higher vulnerability of the alveolar-capillary membrane to acute fluid overload in HF patients treated with ACE inhibitors.

Reference

Contini M, Compagnino E, Cattadori G, Magrì D, Camera M, Apostolo A, Farina S, Palermo P, Gertow K, Tremoli E, Fiorentini C, Agostoni P. ACE-Inhibition Benefit on Lung Function in Heart Failure is Modulated by ACE Insertion/Deletion Polymorphism. Cardiovasc Drugs Ther. 2016 Feb 4. [Epub ahead of print]. Go to PubMed abstract