Author + information
- Received November 9, 1982
- Revision received January 11, 1983
- Accepted January 14, 1983
- Published online June 1, 1983.
- Steven R. Goldsmith, MD, FACC*,*,
- Gary S. Francis, MD, FACC,
- Allen W. Cowley Jr, PhD,
- T. Barry Levine, MD and
- Jay N. Cohn, MD, FACC
- ↵*Address for reprints: Steven R. Goldsmith, MD, Hennepin County Medical Center. Cardiology Section, 701 Park Avenue South, Minne-apolis, Minnesota 55415.
The antidiuretic hormone arginine vasopressin could contribute to both the vasoconstriction and impaired water handling frequently found in patients with congestive heart failure. In order to determine basal levels for vasopressin in this condition, plasma vasopressin was measured by radioimmunoassay in a group of 31 patients with advanced congestive heart failure. At the same time, plasma norepinephrine, plasma renin activity and numerous hemodynamic variables were also measured. In a subgroup of patients, the response of vasopressin to hemodynamic changes induced by nitroprusside infusion and to inhibition of the renin-angiotensin system with captopril was studied. The basal vasopressin levels in the patients were compared with those obtained from 51 comparably aged normal subjects. The mean vasopressin level (± standard error of the mean) in the patients was 9.5 ± 0.89 pg/ml as compared with 4.7 ± 0.66 (probability [p] < 0.001) in the normal subjects. Serum sodium was 137 ± 0.56 mEq/liter. The vasopressin level did not correlate with any hemodynamic variable and was increased to the same degree in patients with both low and normal cardiac index. The vasopressin level failed to correlate with serum sodium, and was similarly increased in patients with low and normal serum sodium. There was no correlation of vasopressin and plasma norepinephrine, but vasopressin did correlate modestly with plasma renin activity (r = 0.53, p < 0.02). Acute hemodynamic changes induced by nitroprusside did not influente vasopressin levels, nor did comparable changes aceompanied by inhibition of the renin-angiotensin system with captopril.
Thus, vasopressin levels measured under steady state conditions are usuallv increased in patients with congestive heart failure. The increase is not dependent on reduced cardiac index. There appears to be an abnormality in the relation between vasopressin and serum sodium in some persons and vasopressin does not respond to acute hemodynamic changes with or without the inhibition of the renin-angiotensin system. The mechanisms causing increased vasopressin levels and their biologic importance in congestive heart failure remain to be defined.
↵* Dr. Goldsmith is the recipient of a Clinical Investigator Award from the National Heart, Lung, and Blood Institute
This research was supported in part by Training Grant HL07184-06 and Research Grant HL22977-03 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, and by a Research Grant from the Veterans Administration, Washington D.C.
- Received November 9, 1982.
- Revision received January 11, 1983.
- Accepted January 14, 1983.
- American College of Cardiology Foundation