The association of chronic kidney disease with the use of renin-angiotensin system inhibitors after acute myocardial infarction

Abstract

Renin-angiotensin system (RAS) inhibitor use after acute myocardial infarction (AMI) is a quality indicator, but there may also be reasons not to use this therapy. We sought to determine how chronic kidney disease (CKD) and acute kidney injury (AKI) affected RAS inhibitor prescription after AMI in patients with and without decreased ejection fraction (EF). Participants from the TRIUMPH registry were categorized by admission estimated glomerular filtration rate (eGFR in mL/min per 1.73 m(2); severe [<30], moderate [30-59], mild [60-89], and no [≥90] CKD) and occurrence of AKI (an increase in creatinine ≥0.3 mg/dL or ≥50%). Renin-angiotensin system inhibitor prescriptions at discharge were compared across categories of CKD, AKI, and decreased EF (<40% vs ≥40%) using a hierarchical modified Poisson model. Among 4,223 AMI patients (mean age 59.0 years, 67.0% male, 67.3% white), RAS inhibitor use decreased significantly with lower eGFR (P < .001), but there was no effect of decreased EF on this relationship (interaction P = .40). Without AKI, severe and moderate CKD were associated with significantly less RAS inhibitor use: relative risks (RRs) 0.67 (95% CIs, 0.58-0.78) and 0.94 (0.90-0.99), respectively. When AKI occurred, CKD was associated with less RAS inhibitor use: RRs 0.84 (0.76-0.93) for mild CKD, 0.78 (0.68-0.88) for moderate CKD, and 0.50 (0.42-0.61) for severe CKD. Ejection fraction <40% was associated with use (RR 1.11, 1.03-1.18), independent of renal function. Chronic kidney disease and AKI are associated with fewer RAS inhibitor prescriptions at discharge, but in both AKI and non-AKI patients, eGFR was more strongly associated with use than EF.