Imamura Teruhiko, Kinugawa Koichiro, Hatano Masaru, Fujino Takeo, Inaba Toshiro, Maki Hisataka, Kinoshita Osamu, Nawata Kan, Kyo Shunei, Ono Minoru, Komuro Issei
Department of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo.
Circ J. 2014;78(9):2259-67. doi: 10.1253/circj.cj-14-0368. Epub 2014 Jul 10.
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%).
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.
血流动力学抑制会刺激精氨酸加压素（AVP）释放，但血浆AVP水平（P-AVP）与心脏参数之间的关系，尤其是在接受指南指导药物治疗的D期心力衰竭（HF）患者中，尚未得到研究。方法与结果：收集了162例住院D期HF患者以及80例在术后3个月接受心室辅助装置（VAD，n = 46）或心脏移植（HTx，n = 34）患者的包括P-AVP在内的数据。在HF组中，相当高的P-AVP（5.9±6.1 pg/ml）与血清钠浓度（S-Na，135.3±5.8 mEq/L，r = -0.548 [P<0.01]）和心脏指数（CI，2.2±0.5 L·min⁻¹·m⁻²，r = -0.458 [P<0.01]）呈负相关。在VAD/HTx治疗后，CI改善（2.7±0.5 L·min⁻¹·m⁻²[P<0.01] vs. HF）伴随着血清钠浓度正常化（S-Na；138.2±2.0 mEq/L [P<0.01] vs. HF）以及AVP释放受抑制（1.7±3.4 pg/ml [P<0.01] vs. HF）。VAD/HTx治疗后，P-AVP仅与S-Na呈正相关（r = 0.454 [P<0.01]），而与CI无相关性。P-AVP≥5.3 pg/ml能很好地预测HF组2年生存率较低（60% [P<0.01] vs. 90%）。结论：低心输出量通过非渗透过程刺激AVP释放，这导致D期HF患者出现低钠血症和不良预后。通过心脏替代治疗使心输出量充分恢复后，AVP释放受到抑制，且主要受血清渗透压调节。
