Neurohumoral overactivation in severe chronic heart failure is a key determinant of sodium and water excretion abnormalities and predicts a less favorable clinical course.
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Neurohumoral overactivation may inform HF risk stratification; leaves open whether renin-angiotensin modulation alters sodium excretion or prognosis.
The renal hemodynamic and neurohumoral determinants of sodium and water excretion abnormalities were studied in 66 patients with severe chronic congestive heart failure. Abnormalities were not closely related to any one variable but were the result of the convergence of a number of determinants. The most important determinants for sodium excretion were activation of the renin-angiotensin system and ventricular function; and the most important for water excretion were plasma vasopressin, plasma norepinephrine, and renal and ventricular functions. In a subgroup of patients, neurohumoral overactivation led to severe sodium and water excretion abnormalities and to increased furosemide requirements. A 17-month follow-up of all 66 patients showed a less favorable clinical course for this subgroup even when compared with hemodynamically matched patients.
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Bertrand Mettauer (1986) studied this question.
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