Year: 2011
Type: editorial
Abstract: A number of studies have demonstrated a linkage between renal dysfunction and adverse clinical outcomes in both acute and chronic heart failure.[1][2][3] Heart failure treatments can affect renal function in a variety of ways, with decreased glomerular filtration rate (GFR) during treatment often denoting a poorer prognosis.4 -6 Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) reduce GFR through intrarenal mechanisms yet convey reduced rates of morbidity and mortality, presenting the hypothesis that the association between change in GFR and clinical outcomes depends on the factors that drive that change more than on GFR itself.In this issue of Circulation: Heart Failure, Testani et al 7 present evidence that supports this hypothesis, showing that within the SOLVD (Studies of Left Ventricular Dysfunction) study, early reduction in GFR was associated with increased mortality within the placebo group but not in the enalapril group.It is reasonable to conclude that inhibiting the renin-angiotensin system (RAS) reduces GFR through a mechanism that does not convey an adverse prognosis.In evaluating new therapies, focus should be placed on clarifying the pathways through which agents influence renal function.
Source: Circulation Heart Failure
Author: Marvin A. Konstam
Institutions: Tufts University, Tufts Medical Center
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2153760817