Pharmacotherapy in congestive heart failure: Effect of the insertion/deletion polymorphism of the ACE gene on response to ACE inhibitors in patients with heart failure.

The renin angiotensin aldosterone (RAA) axis is a common target for pharmacologic intervention in the treatment of hypertension, renal disease, and/or congestive heart failure (CHF). ACE inhibitors have increasingly been used in an effort to disable this neurohumoral system. Despite the almost elegant logic of this therapeutic approach it has not always proven uniformly successful. The fairly diverse response to ACE inhibitor therapy in CHF has been ascribed to a number of pharmacokinetic and pharmacodynamic considerations and most recently to a genetic polymorphism for ACE. The presence of a DD insertion/deletion pattern for ACE seems to predict an increased level of ACE, possibly increased angiotensin II concentrations, and a relative resistance to the hemodynamic effects of ACE inhibitors. The frequency of the particular insertion/deletion pattern in CHF is not known. Whether the particular insertion/deletion pattern of a patient will determine whether a patient receives angiotensin receptor antagonist therapy rather than ACE inhibitor treatment remains to be determined. (c)1999 by CHF, Inc.