Neurohormonal effects of furosemide withdrawal in elderly heart failure patients with normal systolic function

Autor: van Kraaij, Dave J.W., Jansen, René W.M.M., Sweep, Fred C.G.J., Hoefnagels, Willibrord H.L., Jansen, René W M M
Předmět:
Zdroj: European Journal of Heart Failure; Jan2003, Vol. 5 Issue 1, p47-53, 7p
Abstrakt: Background: In heart failure patients, diuretics cause renin–angiotensin–aldosterone system (RAS) activation, which may lead to increased morbidity and mortality despite short-term symptomatic improvement. Aim: To determine changes in RAS activation and clinical correlates following furosemide withdrawal in elderly heart failure patients without left ventricular systolic dysfunction. Methods and results: We performed clinical assessments and laboratory determinations of aldosterone, plasma renin activity (PRA), atrial natriuretic peptide (ANP), norepinephrine, and endothelin in 29 heart failure patients [aged 75.1±0.7 (mean±S.E.M.) years], before, 1 and 3 months after placebo-controlled furosemide withdrawal. Recurrent congestion occurred in 2 of 19 patients withdrawn, and in 1 of 10 patients continuing on furosemide. Three months after withdrawal, PRA had decreased −1.61±0.71 nmol/l/h (P<0.05). Decreases in aldosterone levels did not reach significance (−0.17±0.38 nmol/l). The decreases in PRA after withdrawal correlated with decreases in systolic (rs=0.61, P=0.020) and diastolic blood pressure (rs=0.80, P=0.01). Successful withdrawal was associated with increases in norepinephrine (+0.58±0.22 nmol/l) and ANP (+3.5±1.3 pmol/l) (P<0.05) after 1 month, but these changes did not persist after 3 months. Endothelin levels did not change in both groups. Conclusion: Successful furosemide withdrawal in elderly heart failure patients causes persistent decreases in RAS activation. [Copyright &y& Elsevier]
Databáze: Complementary Index