Low Cardiac Output Stimulates Vasopressin Release in Patients With Stage D Heart Failure - Its Relevance to Poor Prognosis and Reversal by Surgical Treatment

Background: Depressed hemodynamics stimulates arginine vasopressin (AVP) release, but the relationship between plasma AVP levels (P-AVP) and cardiac parameters, especially in patients with stage D heart failure (HF) receiving guideline-directed medical therapy, has not examined. Methods and Results: Data including P-AVP were obtained from 162 in-hospital patients with stage D HF and from 80 patients receiving ventricular assist device (VAD, n=46) or heart transplantation (HTx, n=34) at 3 months after surgery. In the HF group, considerably high P-AVP (5.9 +/- 6.1 pg/ml) negatively correlated with serum sodium concentration (S-Na, 135.3 +/- 5.8 mEq/L, r=-0.548 [P<0.01]) and cardiac index (CI, 2.2 +/- 0.5 L min(-1).m(-2), r=-0.458 [P< 0.01]). After VAD/HTx treatment, improvement in the CI (2.7 +/- 0.5 L min(-1).m(-2) [P<0.01] vs. HF) was accompanied by normalization of serum sodium concentration (S-Na; 138.2 +/- 2.0 mEq/L [P<0.01] vs. HF) and suppressed release of AVP (1.7 +/- 3.4 pg/ml [P<0.01] vs. HF). P-AVP positively correlated with only S-Na (r=0.454 [P<0.01]), whereas no correlation was observed with CI after VAD/HTx treatment. P-AVP >= 5.3 pg/ml well predicted poor 2-year survival in HF group (60% [P<0.01] vs. 90%). Conclusions: Low cardiac output stimulates AVP release via a non-osmotic process that results in hyponatremia and poor prognosis in patients with stage D HF. After sufficient recovery of cardiac output by cardiac replacement therapy, AVP release is suppressed and is mainly regulated by serum osmolality.