Discontinuation/Dose Reduction of Angiotensin-Converting Enzyme Inhibitors/Angiotensin Receptor Blockers during Acute Decompensated Heart Failure in African-American Patients with Reduced Left-Ventricular Ejection Fraction

Abstract

Objectives: Patients with heart failure (HF) and reduced left-ventricular ejection fraction (LVEF) benefit from angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blocker (ARB) therapy. While dose reduction/discontinuation (r/d) of β-blockers (BB) and furosemide in acute decompensated HF (ADHF) worsen outcomes, data on ACEI/ARB are lacking. Methods: To determine the frequency and reasons for ACEI/ARB therapy r/d in ADHF patients, we studied 174 patients with LVEF <40% on ACEI/ARB and BB therapy upon admission over 1 year. Results: ACEI/ARB doses were r/d in 17.2% because of acute kidney injury (56.7%), hypotension (23.3%), and hyperkalemia (10%). Clinical characteristics were similar between patients with r/d and continued therapy. Admission and discharge creatinine (Cr) levels were higher in the r/d group. On multivariate analysis, admission Cr and admission systolic blood pressures were independent predictors of r/d. Among patients with renal dysfunction cited as the r/d reason, Cr did not significantly rise in 23.5%. The r/d group had a longer length of stay (LOS). Conclusions: ACEI/ARB dose is reduced and/or discontinued in nearly one-fifth of all ADHF admissions, and LOS is longer in the ACEI/ARB r/d group. While impaired renal function is the most frequently cited reason, nearly one-fourth of the patients had stable renal function. ACEI/ARB r/d therapy in the setting of ADHF merits further study.

Implications of renin‐angiotensin‐system blocker discontinuation in acute decompensated heart failure with systolic dysfunction

“…Importantly, there was a lack of association RASB therapy was reduced or discontinued in 17.2% of patients due to acute kidney injury (56.7%), hypotension (23.3%), and hyperkalemia (10%). 20 Admission creatinine and SBP were both associated with RASB discontinuation and nonuse. Although the rationale for RASB discontinuation or nonuse was unknown in our cohorts, the lack of an association between RASB prescription and systolic blood pressure suggests that hypotension may not be the primary impetus for RASB discontinuation.…”

“…Practice patterns underlying RASB discontinuation and nonuse vary without clear supporting evidence currently to justify reasoning, particularly in patients who remain hemodynamically stable. In a cohort of 174 patients admitted with ADHF, Kane et al showed that RASB therapy was reduced or discontinued in 17.2% of patients due to acute kidney injury (56.7%), hypotension (23.3%), and hyperkalemia (10%) . Admission creatinine and SBP were both associated with RASB discontinuation and nonuse.…”

<p>Interactive and potentially independent roles of renin-angiotensin-aldosterone system blockade and the development of cardiorenal syndrome, type 1 on in-hospital mortality among elderly patients admitted with acute decompensated congestive heart failure</p>

“…1,10 Therapeutic measures that can lead to WRF, such as the use of ACEIs/A2RBs, may not necessarily increase the mortality associated with CRS1, and under certain circumstances may even improve clinical outcome. 8,15,24,25 Therefore, teasing apart the interaction and independent roles of CRS1 and ACEI/A2RB usage in determining in-hospital mortality among patients admitted with ADCHF can be extremely challenging.…”

“…1,6 Management of ADCHF is complicated by the fact that CRS1 or concerns regarding its development often limit the use of common therapeutic strategies, such as inhibition of the renin-angiotensin-aldosterone system (RAAS) and/or escalation of diuretic therapy. 5,[7][8][9] Although WRF may be transient in ADCHF patients, RAAS inhibition and/or escalation of diuretic therapy may in themselves lead to WRF, further complicating the clinical picture. [10][11][12][13][14] An important question for patients hospitalized with ADCHF is at what level of WRF RAAS inhibitions lose its survival advantage.…”

“…[10][11][12][13][14] An important question for patients hospitalized with ADCHF is at what level of WRF RAAS inhibitions lose its survival advantage. 8,15 For example, in patients with chronic CHF, the benefits of RAAS inhibition are maintained for rises of serum creatinine (SCr) up to 30%-50%. 16,17 Unfortunately, similar data in the case of ADCHF remain scarce.…”