Therapies for acute heart failure in patients with reduced kidney function: a community-based perspective.

BACKGROUND: Limited data exist describing the management of patients with decreased kidney function at the time of hospital presentation for acute heart failure (HF). STUDY DESIGN: Nonconcurrent prospective study. SETTING & PARTICIPANTS: Patients hospitalized with clinical findings of decompensated HF (n = 4,350) at all 11 greater Worcester, MA, medical centers in 1995 and 2000. Patients were categorized into varying levels of kidney function based on their estimated glomerular filtration rate (eGFR). PREDICTOR: GFR estimates from serum creatinine levels measured at the time of hospital admission. OUTCOMES: Hospital receipt of angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs), beta-blockers, digoxin, and diuretics. MEASUREMENTS: Hospital charts were reviewed for prescribing of disease-modifying cardiac therapies, as well as therapies designed to provide symptomatic relief from HF. RESULTS: Average eGFR in our study sample was 64.4 +/- 33.1 mL/min/1.73 m(2), and patients were categorized further into 3 eGFR levels of less than 30 (n = 569), 30 to 59 (n = 1,488), and 60 mL/min/1.73 m(2) or greater (n = 2,293) for comparative purposes. Patients with greater eGFRs (>or=60 mL/min/1.73 m(2)) were more likely to be treated with ACE inhibitors/ARBs (56% versus 39%) and digoxin (51% versus 46%) during hospitalization for HF than patients with lower eGFRs (<30 mL/min/1.73 m(2); P < 0.05). Patients with lower eGFRs (<30 mL/min/1.73 m(2)) were more likely to be prescribed beta-blockers than patients with greater eGFRs (>or=60 mL/min/1.73 m(2); 46% versus 39%; P < 0.01). Use of ACE inhibitors/ARBs increased between 1995 and 2000 in 2 of the 3 eGFR groups examined: eGFRs less than 30 mL/min/1.73 m(2) (33% in 1995; 42% in 2000) and eGFRs of 60 mL/min/1.73 m(2) or greater (51% in 1995; 59% in 2000). Use of beta-blockers increased appreciably in all 3 eGFR groups (<30 mL/min/1.73 m(2), 27% in 1995; 58% in 2000; >or=60 mL/min/1.73 m(2): 25% in 1995; 49% in 2000). However, less than one third of all patients were treated with both disease-modifying therapies in 2000. LIMITATIONS: We were unable to classify patients into those with systolic versus diastolic HF. CONCLUSIONS: Our results suggest that use of disease-modifying therapies for patients hospitalized with clinical findings of acute HF and decreased kidney function remains less than desirable. Educational programs are needed to enhance the management of patients with decreased kidney function who develop HF.