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Vol. 70. Issue 6.
Pages 516-517 (June 2017)
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Vol. 70. Issue 6.
Pages 516-517 (June 2017)
Letter to the Editor
DOI: 10.1016/j.rec.2017.02.034
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Relaxin Concentrations in Acute Heart Failure Patients. Response
Concentración de relaxina en pacientes con insuficiencia cardiaca aguda. Respuesta
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Jesus Sánchez-Mása, M. Carmen Asensio-Lópezb, Ángela Soriano-Filiuc, Domingo Pascual-Figalb,c,
Corresponding author
dpascual@um.es

Corresponding author:
a Departamento de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad CEU Cardenal Herrera, Moncada, Valencia, Spain
b Departamento de Medicina Interna, Facultad de Medicina, Universidad de Murcia, Murcia, Spain
c Servicio de Cardiología, Grupo ICTC, Hospital Clínico Universitario Virgen de la Arrixaca, IMIB-Arrixaca, El Palmar, Murcia, Spain
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Rev Esp Cardiol. 2017;70:51610.1016/j.rec.2016.12.027
Dennis R. Stewart
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To the Editor,

We would like to thank Dr. Stewart for his constructive contribution to the discussion of our study findings with the suggestion that failure to find a clinical determinant for of circulating relaxin concentrations in patients with acute cardiac failure could be due to the commercial assay used (Inmunodiagnostik; Bensheim, Germany).1 Several points, however, suggest that this assay is appropriate. First, this is the most sensitive assay on the market and the most widely used in clinical trials.1,2 Our study had quality levels (quartile 1, 19.12; quartile 2, 108.2) within those given in the technical specifications (maximum values: quartile 1, 20.7; quartile 2, 108.5). Second, as a quality control measure, relaxin was measured in 2 women in week 12 of pregnancy, and elevated concentrations were found (351 and 402 pg/mL), that is, much higher concentrations than those found in patients with acute cardiac failure (median, 14.3 pg/mL). This is also in agreement with other studies in pregnant women (586 [295] pg/mL).3 Finally, the assay suggested by Dr. Stewart (R&D Systems; Minneapolis, United States) has not been used in publications for measuring endogenous hormone levels; the references are pharmacodynamic studies that measure the concentration of recombinant serelaxin after intravenous infusion, reaching concentrations of the order of ng/mL, that is, higher than endogenous concentrations of the order of pg/mL. When we were designing our study, we performed tests on some samples with the proposed alternative assay, without detection of endogenous relaxin concentrations. We attributed this observation to the lower sensitivity of the alternative assay. Therefore, although we support the immunoanalysis used in our study, we cannot rule out the hypothesis put forward by Dr. Stewart that other molecules may interfere in the measurement of endogenous relaxin. These scientific letters should therefore serve to highlight the need for further studies to clarify these questions, as well as the role of endogenous relaxin in heart failure, as also indicated in our original article.

CONFLICTS OF INTEREST

D. Pascual-Figal has received speaker's fees and a research grant from Novartis, unrelated to the present study.

References
[1]
J. Martínez Solano, J.J. Santos Mateo, J. Sánchez-Más, et al.
Relaxin concentrations in acute heart failure patients: kinetics and clinical determinants.
Rev Esp Cardiol., 69 (2016), pp. 1230-1232
[2]
C. Fisher, C. Berry, L. Blue, et al.
N-terminal pro B type natriuretic peptide, but not the new putative cardiac hormone relaxin, predicts prognosis in patients with chronic heart failure.
Heart., 89 (2003), pp. 879-881
[3]
S. Lurie, Z. Matas, A. Fux, et al.
Association of serum relaxin with striae gravidarum in pregnant women.
Arch Gynecol Obstet., 283 (2011), pp. 219-222
Copyright © 2017. Sociedad Española de Cardiología
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