Relaxin: Review of Biology and Potential Role in Treating Heart Failure

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Abstract

Relaxin is a naturally occurring human peptide initially identified as a reproductive hormone. More recently, relaxin has been shown to play a key role in the maternal hemodynamic and renal adjustments that accommodate pregnancy. An understanding of these physiologic effects has led to the evaluation of relaxin as a pharmacologic agent for the treatment of patients with acute heart failure. Preliminary results have been encouraging. In addition, the other known biologic properties of relaxin, including anti-inflammatory effects, extracellular matrix remodeling effects, and angiogenic and anti-ischemic effects, all may play a role in potential benefits of relaxin therapy. Ongoing, large-scale clinical testing will provide additional insights into the potential role of relaxin in the treatment of heart failure.

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Cardiac troponin and outcome in acute heart failure.

F S Apple, , Deborah B Diercks … (2008)

Cardiac troponin provides diagnostic and prognostic information in acute coronary syndromes, but its role in acute decompensated heart failure is unclear. The purpose of our study was to describe the association between elevated cardiac troponin levels and adverse events in hospitalized patients with acute decompensated heart failure. We analyzed hospitalizations for acute decompensated heart failure between October 2001 and January 2004 that were recorded in the Acute Decompensated Heart Failure National Registry (ADHERE). Entry criteria included a troponin level that was obtained at the time of hospitalization in patients with a serum creatinine level of less than 2.0 mg per deciliter (177 micromol per liter). A positive troponin test was defined as a cardiac troponin I level of 1.0 microg per liter or higher or a cardiac troponin T level of 0.1 microg per liter or higher. Troponin was measured at the time of admission in 84,872 of 105,388 patients (80.5%) who were hospitalized for acute decompensated heart failure. Of these patients, 67,924 had a creatinine level of less than 2.0 mg per deciliter. Cardiac troponin I was measured in 61,379 patients, and cardiac troponin T in 7880 patients (both proteins were measured in 1335 patients). Overall, 4240 patients (6.2%) were positive for troponin. Patients who were positive for troponin had lower systolic blood pressure on admission, a lower ejection fraction, and higher in-hospital mortality (8.0% vs. 2.7%, P<0.001) than those who were negative for troponin. The adjusted odds ratio for death in the group of patients with a positive troponin test was 2.55 (95% confidence interval, 2.24 to 2.89; P<0.001 by the Wald test). In patients with acute decompensated heart failure, a positive cardiac troponin test is associated with higher in-hospital mortality, independently of other predictive variables. (ClinicalTrials.gov number, NCT00366639 [ClinicalTrials.gov].). Copyright 2008 Massachusetts Medical Society.

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Activation of orphan receptors by the hormone relaxin.

Sheau Yu Teddy Hsu, Koji Nakabayashi, Shinya Nishi … (2002)

Relaxin is a hormone important for the growth and remodeling of reproductive and other tissues during pregnancy. Although binding sites for relaxin are widely distributed, the nature of its receptor has been elusive. Here, we demonstrate that two orphan heterotrimeric guanine nucleotide binding protein (G protein)-coupled receptors, LGR7 and LGR8, are capable of mediating the action of relaxin through an adenosine 3',5'-monophosphate (cAMP)-dependent pathway distinct from that of the structurally related insulin and insulin-like growth factor family ligand. Treatment of antepartum mice with the soluble ligand-binding region of LGR7 caused parturition delay. The wide and divergent distribution of the two relaxin receptors implicates their roles in reproductive, brain, renal, cardiovascular, and other functions.

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Fluid overload in acute heart failure--re-distribution and other mechanisms beyond fluid accumulation.

Gad Cotter, Mihai Gheorghiade, Howard Dittrich … (2008)

Although fluid overload is one of the most prominent features of acute heart failure (AHF), its mechanism remains challenging, due to the lack of consistent data from prospective studies. Traditionally, fluid overload was thought to be mainly the result of either increased intake of fluid and salt or non-adherence with diuretic therapy. However, recent data showed little weight change before or during an AHF event suggesting that in many cases fluid overload is caused by other mechanisms such as fluid redistribution and neurohormonal or inflammatory activation. Redistribution may be the result of a combined vascular and cardiac process reducing capacitance in the venous system (and hence increasing preload) and increasing arterial stiffness and resistance (and hence afterload). When these vascular processes occur acutely and are superimposed on reduced cardiac function; fluid is redistributed to the lungs instigating pulmonary congestion. In this paper we elaborate on this possible pathophysiological mechanism and review its potential causes and amplifiers.

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Author and article information

Contributors

: steichman@corthera.com

: eunemori@corthera.com

: john.teerlink@ucsf.edu

: GadCotter@momentum-research.com

: metramarco@libero.it

Journal

Journal ID (nlm-ta): Curr Heart Fail Rep

Title: Current Heart Failure Reports

Publisher: Current Science Inc. (New York )

ISSN (Print): 1546-9530

ISSN (Electronic): 1546-9549

Publication date (Electronic): 28 April 2010

Publication date PMC-release: 28 April 2010

Publication date (Print): June 2010

Volume: 7

Issue: 2

Pages: 75-82

Affiliations

[1 ]Corthera, Inc, a subsidiary of Novartis Pharmaceuticals Corp., 1660 South Amphlett Boulevard, Suite 200, San Mateo, CA 94402 USA

[2 ]Section of Cardiology, Veterans Affairs Medical Center, University of California, San Francisco VA Medical Center, Cardiology-111C, Building 203, Room 2A-49, 4150 Clement Street, San Francisco, CA 94121-1545 USA

[3 ]Momentum Research, Inc, 3100 Tower Boulevard, Suite 802, Durham, NC 27707 USA

[4 ]Section of Cardiovascular Diseases, Department of Experimental and Applied Medicine, University of Brescia, Cardiology, University and Civil Hospital, Piazza Spedali Civili 1, 25123 Brescia, Italy

Article

Publisher ID: 10

DOI: 10.1007/s11897-010-0010-z

PMC ID: 2875472

PubMed ID: 20424993

SO-VID: 308bc633-e725-4557-b9fa-4cdf59f50946

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ScienceOpen disciplines: Cardiovascular Medicine

Keywords: congestive heart failure,relaxin,pharmacologic therapy,vasodilation,acute heart failure,dyspnea

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ScienceOpen disciplines: Cardiovascular Medicine

Keywords: congestive heart failure, relaxin, pharmacologic therapy, vasodilation, acute heart failure, dyspnea

Relaxin: Review of Biology and Potential Role in Treating Heart Failure

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Cardiovascular Innovations and Applications

Most cited references 50

Cardiac troponin and outcome in acute heart failure.

Activation of orphan receptors by the hormone relaxin.

Fluid overload in acute heart failure--re-distribution and other mechanisms beyond fluid accumulation.

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