Literature DB >> 19270454

Disrupted serotonergic and sympathoadrenal systems in patients with chronic heart failure may serve as new therapeutic targets and novel biomarkers to assess severity, progression and response to treatment.

Razina R Nigmatullina1, Venera V Kirillova, Roen K Jourjikiya, Marat A Mukhamedyarov, Vladimir S Kudrin, Petr M Klodt, András Palotás.   

Abstract

BACKGROUND: It is well established that the serotonergic system (SS) plays important roles in the pathogenesis of cardiovascular diseases. However, the impact of serotonin and its inter-relation with the sympathoadrenal system (SAS) in chronic heart failure (CHF) is poorly understood.
METHODS: Utilizing high-performance liquid chromatography with electrochemical detection, we determined blood plasma levels of serotonin (5-hydroxy-triptamine, [5-HT](p)), 5- hydroxy-indole-acetic acid ([5-HIAA](p)), epinephrine ([E](p)), norepinephrine ([NE](p)), 3,4-dihydroxy-L-phenyl-alanine ([DOPA](p)), dopamine ([DA](p)) and the platelet concentration of serotonin ([5-HT](pt)) in CHF patients with different morphofunctional alterations of myocardium. The morphofunctional alterations included diastolic dysfunction (DD), diastolic dysfunction with left ventricular hypertrophy (DD&LVH), and diastolic and systolic dysfunction (D&SD).
RESULTS: All CHF groups showed significant rises of [5-HT](p) and [5-HT](pt). DD&LVH and D&SD individuals also had increased [5-HIAA](p). Levels of SAS blood biomarkers were also significantly changed. The correlation between SS and SAS was increased in CHF and corresponded with disease severity.
CONCLUSIONS: These results clearly demonstrate that in CHF patients significant changes in SS and SAS occur, which are thought to relate to the morphofunctional alterations of myocardium. The observed changes in the levels of these biomarkers may serve as potential surrogates to monitor severity of disease, to evaluate response to drug treatment, and as a rational basis for new therapeutic approaches. Copyright 2009 S. Karger AG, Basel.

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Year:  2009        PMID: 19270454     DOI: 10.1159/000205962

Source DB:  PubMed          Journal:  Cardiology        ISSN: 0008-6312            Impact factor:   1.869


  12 in total

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Authors:  Christelle Villeneuve; Céline Guilbeau-Frugier; Pierre Sicard; Olivier Lairez; Catherine Ordener; Thibaut Duparc; Damien De Paulis; Bettina Couderc; Odile Spreux-Varoquaux; Florence Tortosa; Anne Garnier; Claude Knauf; Philippe Valet; Elisabetta Borchi; Chiara Nediani; Abdallah Gharib; Michel Ovize; Marie-Bernadette Delisle; Angelo Parini; Jeanne Mialet-Perez
Journal:  Antioxid Redox Signal       Date:  2012-08-10       Impact factor: 8.401

Review 3.  Monoamine oxidases as sources of oxidants in the heart.

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4.  Role of serotonin 5-HT2A receptors in the development of cardiac hypertrophy in response to aortic constriction in mice.

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5.  Effect of cardiac resynchronization therapy on broad neurohormone biomarkers in heart failure.

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6.  A xanthine-derivative K(+)-channel opener protects against serotonin-induced cardiomyocyte hypertrophy via the modulation of protein kinases.

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8.  Monoamine Oxidase Is Overactivated in Left and Right Ventricles from Ischemic Hearts: An Intriguing Therapeutic Target.

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Review 9.  Monoamine Oxidases, Oxidative Stress, and Altered Mitochondrial Dynamics in Cardiac Ageing.

Authors:  Damien Maggiorani; Nicola Manzella; Dale E Edmondson; Andrea Mattevi; Angelo Parini; Claudia Binda; Jeanne Mialet-Perez
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10.  Direct evidences for sympathetic hyperactivity and baroreflex impairment in Tako Tsubo cardiopathy.

Authors:  Angelica Vaccaro; Fabien Despas; Clement Delmas; Olivier Lairez; Elisabeth Lambert; Gavin Lambert; Marc Labrunee; Thibaut Guiraud; Murray Esler; Michel Galinier; Jean Michel Senard; Atul Pathak
Journal:  PLoS One       Date:  2014-03-25       Impact factor: 3.240

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