Author + information
- Received November 18, 1985
- Revision received April 21, 1986
- Accepted May 1, 1986
- Published online October 1, 1986.
- Steven R. Goldsmith, MD, FACC*,1,**,
- Gary S. Francis, MD, FACC†,
- Allen W. Cowley Jr., PHD‡,
- Irvin F. Goldenberg, MD§ and
- Jay N. Cohn, MD, FACC§
- ↵**Address for reprints: Steven R. Goldsmith, MD, Hennepin County Medical Center, Cardiology Section. 701 Park Avenue South, Minneapolis, Minnesota 55415.
The hemodynamic effects of exogenously administered arginine vasopressin were assessed in 11 patients with chronic congestive heart failure. Infusion rates of 0.1 to 0.8 pmol/kg per min increased plasma arginine vasopressin from 6.5 ± 2.7 (SD) pg/ml at control to 63 ± 39 pg/ml at the highest infusion rate. There were progressive decreases in cardiac output and stroke volume, with increases in systemic vascular resistance and pulmonary capillary wedge pressure, but only minimal changes in heart rate and blood pressure. Changes in cardiac output, stroke volume and systemic resistance were evident from the first infusion rate, which increased plasma arginine vasopressin from 6.5 ± 2.7 to 9.9 ± 4.6 pg/ml. A paired analysis of baseline hemodynamic data with those measured during infusions producing an arginine vasopressin level averaging 15 ± 2.6 pg/ml yielded the following changes: cardiac output decreased from 4.6 ± 1.2 to 4.2 ± 0.96 liters/min (p < 0.01), stroke volume decreased from 60 ± 19 to 54 ± 16 ml (p < 0.005) and systemic vascular resistance increased from 1,329 ± 396 to 1,443 ± 395 dynes·s·cm−5(p = 0.01).
Thus, small increases in circulating arginine vasopressin cause modest but significant adverse circulatory effects in patients with congestive heart failure. A fall in cardiac output, probably as a result of increased after load, is seen at levels of arginine vasopressin within the basal range found in congestive heart failure. These data demonstrate that circulating arginine vasopressin in physiologic concentrations is capable of influencing hemodynamics in patients with congestive heart failure and suggest that therapy for this condition directed at inhibition of the vascular effect of arginine vasopressin may be potentially useful.
- Received November 18, 1985.
- Revision received April 21, 1986.
- Accepted May 1, 1986.
- American College of Cardiology Foundation