Author + information
- Received February 21, 1996
- Revision received June 17, 1996
- Accepted July 10, 1996
- Published online November 15, 1996.
- Jean-Luc Dubois-Randé, MD, PhD∗,
- Olivier Montagne, MD∗,b,
- Miriam Alvarez-Guerra, PhD∗,
- Corinne Nazaret∗,
- Bertrand Crozatier, MD, PhD∗,
- Pascal Gueret, MD∗,
- Alain Castaigne, MD∗ and
- Ricardo P. Garay, MD, PhD∗,1
- ↵1Address for correspondence: Dr. Ricardo P. Garay, INSERM U400, Faculté de Médecine de Créteil, 8 rue du Général Sarrail, 94010 Créteil Cédex, France.
Objectives. This study sought to evaluate the relation, if any, between fluid overload in congestive heart failure (CHF) and a newly discovered endogenous natriuretic factor acting like loop diuretic drugs: contransport inhibitory factor (CIF).
Background. The humoral mechanisms regulating volume overload in CHF are not fully understood. Therefore, we investigated whether there is a role for CIF in this pathologic condition.
Methods. Plasma and urinary CIF levels were investigated in 23 patients with chronic CHF and compared with changes in plasma atrial natriuretic peptide (ANP). Twelve patients without CHF served as control subjects.
Results. CHF was associated with a highly significant threefold increase in both plasma CIF levels (mean ± SD 7.10 ± 3.01 vs. 2.28 ± 0.92 U/ml, p < 0.0001) and urinary CIF excretion (7,849 ± 3,600 vs. 2,351 ± 1,297 U/day, p < 0.0001) with respect to patients without CHF. CIF increased as a function of impairment in left ventricular ejection fraction (r = −0.703, p < 0.0001) and the severity of clinical status. Plasma ANP was also increased in patients with CHF, although to a lesser extent (68%, p = 0.0501) than plasma CIF, and was also significantly correlated with left ventricular ejection fraction (r = −0.552, p = 0.0004).
Conclusions. Plasma and urinary CIF activities were strongly and very significantly increased in chronic CHF. In addition to ANP, this long-term natriuretic agent may be of potential importance in reducing fluid overload in CHF.
☆ This study was supported in part by a grant from the Fédération Française de Cardiologie, Paris, France.
- Received February 21, 1996.
- Revision received June 17, 1996.
- Accepted July 10, 1996.