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

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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.

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

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