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Neurohormonal activation rapidly decreases after intravenous therapy withdiuretics and vasodilators for class IV heart failure

Wendy Johnson, MD^*, Torbjørn Omland, MD^*, Christian Hall, MD, Caroline Lucas, MD, Ole L. Myking, MD, Caroline Collins, RN^*, Marc Pfeffer, MD, FACC^*, Jean-Lucien Rouleau, MD, FACC^|| and Lynne W. Stevenson, MD, FACC^*,*

^* Brigham and Women’s Hospital, Cardiovascular Division, Harvard Medical School, Boston, Massachusetts, USA
Research Institute for Internal Medicine, University of Oslo, Oslo, Norway
Rijnland Hospital, Leiderdorp, Netherlands
University Hospital of Bergen, Department of Clinical Chemistry, Division of Endocrinology, Bergen, Norway
^|| Toronto General Hospital, University of Toronto, Cardiology Division, Toronto, Canada

View larger version (11K): [in a new window]   Figure 1 Effect of therapy on plasma aldosterone levels (left) and plasma renin activity (right) before intervention (A), after intravenous vasodilators and diuretics (B) and after transition to an oral regimen, including captopril (C). *p < 0.05 compared to A.

View larger version (16K): [in a new window]   Figure 2 Effect of therapy on plasma norepinephrine levels before intervention (A), after intravenous vasodilators and diuretics (B) and after transition to an oral regimen (C). *p < 0.05 compared to A.

View larger version (12K): [in a new window]   Figure 3 Effect of therapy on plasma endothelin levels before intervention (A), after intravenous vasodilators and diuretics (B) and after transition to an oral regimen (C). *p < 0.05 compared to A.

View larger version (16K): [in a new window]   Figure 4 Effect of therapy on plasma levels of atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP) (left), and N-terminal pro-ANP (N-ANP) (right) before intervention (A), after intravenous vasodilators and diuretics (B) and after transition to an oral regimen (C). *p < 0.05 compared to A.