Low cardiac output stimulates vasopressin release in patients with stage D heart failure – Its relevance to poor prognosis and reversal by surgical treatment –

Teruhiko Imamura, Masaru Hatano, Takeo Fujino, Toshiro Inaba, Hisataka Maki, Issei Komuro, Koichiro Kinugawa, Shunei Kyo, Osamu Kinoshita, Kan Nawata, Minoru Ono

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Abstract

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.

Original languageEnglish
Pages (from-to)2259-2267
Number of pages9
JournalCirculation Journal
Volume78
Issue number9
DOIs
Publication statusPublished - Sep 1 2014

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Low Cardiac Output
Vasopressins
Heart Failure
Arginine Vasopressin
Therapeutics
Sodium
Serum
Heart-Assist Devices
Hyponatremia
Heart Transplantation
Cardiac Output
Osmolar Concentration
Hemodynamics
Guidelines
Survival

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Low cardiac output stimulates vasopressin release in patients with stage D heart failure – Its relevance to poor prognosis and reversal by surgical treatment –. / Imamura, Teruhiko; Hatano, Masaru; Fujino, Takeo; Inaba, Toshiro; Maki, Hisataka; Komuro, Issei; Kinugawa, Koichiro; Kyo, Shunei; Kinoshita, Osamu; Nawata, Kan; Ono, Minoru.

In: Circulation Journal, Vol. 78, No. 9, 01.09.2014, p. 2259-2267.

Research output: Contribution to journalArticle

Imamura, T, Hatano, M, Fujino, T, Inaba, T, Maki, H, Komuro, I, Kinugawa, K, Kyo, S, Kinoshita, O, Nawata, K & Ono, M 2014, 'Low cardiac output stimulates vasopressin release in patients with stage D heart failure – Its relevance to poor prognosis and reversal by surgical treatment –', Circulation Journal, vol. 78, no. 9, pp. 2259-2267. https://doi.org/10.1253/circj.CJ-14-0368
Imamura, Teruhiko ; Hatano, Masaru ; Fujino, Takeo ; Inaba, Toshiro ; Maki, Hisataka ; Komuro, Issei ; Kinugawa, Koichiro ; Kyo, Shunei ; Kinoshita, Osamu ; Nawata, Kan ; Ono, Minoru. / Low cardiac output stimulates vasopressin release in patients with stage D heart failure – Its relevance to poor prognosis and reversal by surgical treatment –. In: Circulation Journal. 2014 ; Vol. 78, No. 9. pp. 2259-2267.
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abstract = "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.",
author = "Teruhiko Imamura and Masaru Hatano and Takeo Fujino and Toshiro Inaba and Hisataka Maki and Issei Komuro and Koichiro Kinugawa and Shunei Kyo and Osamu Kinoshita and Kan Nawata and Minoru Ono",
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AU - Imamura, Teruhiko

AU - Hatano, Masaru

AU - Fujino, Takeo

AU - Inaba, Toshiro

AU - Maki, Hisataka

AU - Komuro, Issei

AU - Kinugawa, Koichiro

AU - Kyo, Shunei

AU - Kinoshita, Osamu

AU - Nawata, Kan

AU - Ono, Minoru

PY - 2014/9/1

Y1 - 2014/9/1

N2 - 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.

AB - 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.

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