The 212A Variant of the APJ Receptor Gene for the Endogenous Inotrope Apelin is Associated With Slower Heart Failure Progression in Idiopathic Dilated Cardiomyopathy

Riccardo Sarzani, Cinzia Forleo, Francesca Pietrucci, Alessandro Capestro, Elli Soura, Pietro Guida, Sandro Sorrentino, Massimo Iacoviello, Roberta Romito, Paolo Dessì-Fulgheri, Mariavittoria Pitzalis, Alessandro Rappelli

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Background: Idiopathic dilated cardiomyopathy (IDC) has multiple genetic and acquired causes. Apelin is an endogenous peptide that increases cardiac inotropism through his APJ receptor. No data are available concerning the APJ gene mutations responsible for IDC or on the role of APJ receptor gene variants in predicting heart failure (HF) progression. Methods and Results: We prospectively evaluated 202 consecutive patients with IDC and 202 matched controls: 90 were screened for APJ gene mutations and all 202 were genotyped for G212A and A445C APJ receptor polymorphisms. No mutations were found within the coding or untranslated regions of the APJ receptor, and no differences in allelic or genotype frequencies were observed comparing patients with a healthy control population. The correlations between APJ receptor polymorphisms and HF progression were assessed. During a median follow-up of 37 months, 35 patients experienced HF progression. Univariate analysis showed that patients carrying at least 1 copy of 212A had a significantly lower risk for HF-related events than those who were homozygous for the G212 variant, and multivariate analysis confirmed that it was significantly related to a more favorable prognosis. Conclusions: APJ is unlikely to be a gene causing IDC, but the independent correlation between the 212A allele and a better prognosis suggests that it might act as a modifier gene.

Original languageEnglish
Pages (from-to)521-529
Number of pages9
JournalJournal of Cardiac Failure
Volume13
Issue number7
DOIs
Publication statusPublished - Sep 2007

Fingerprint

Dilated Cardiomyopathy
Heart Failure
Mutation
Genes
Modifier Genes
Untranslated Regions
Myocardial Contraction
Multivariate Analysis
Alleles
Genotype
Peptides
Population

Keywords

  • apelin
  • APJ
  • cardiomyopathy

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

The 212A Variant of the APJ Receptor Gene for the Endogenous Inotrope Apelin is Associated With Slower Heart Failure Progression in Idiopathic Dilated Cardiomyopathy. / Sarzani, Riccardo; Forleo, Cinzia; Pietrucci, Francesca; Capestro, Alessandro; Soura, Elli; Guida, Pietro; Sorrentino, Sandro; Iacoviello, Massimo; Romito, Roberta; Dessì-Fulgheri, Paolo; Pitzalis, Mariavittoria; Rappelli, Alessandro.

In: Journal of Cardiac Failure, Vol. 13, No. 7, 09.2007, p. 521-529.

Research output: Contribution to journalArticle

Sarzani, R, Forleo, C, Pietrucci, F, Capestro, A, Soura, E, Guida, P, Sorrentino, S, Iacoviello, M, Romito, R, Dessì-Fulgheri, P, Pitzalis, M & Rappelli, A 2007, 'The 212A Variant of the APJ Receptor Gene for the Endogenous Inotrope Apelin is Associated With Slower Heart Failure Progression in Idiopathic Dilated Cardiomyopathy', Journal of Cardiac Failure, vol. 13, no. 7, pp. 521-529. https://doi.org/10.1016/j.cardfail.2007.04.002
Sarzani, Riccardo ; Forleo, Cinzia ; Pietrucci, Francesca ; Capestro, Alessandro ; Soura, Elli ; Guida, Pietro ; Sorrentino, Sandro ; Iacoviello, Massimo ; Romito, Roberta ; Dessì-Fulgheri, Paolo ; Pitzalis, Mariavittoria ; Rappelli, Alessandro. / The 212A Variant of the APJ Receptor Gene for the Endogenous Inotrope Apelin is Associated With Slower Heart Failure Progression in Idiopathic Dilated Cardiomyopathy. In: Journal of Cardiac Failure. 2007 ; Vol. 13, No. 7. pp. 521-529.
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abstract = "Background: Idiopathic dilated cardiomyopathy (IDC) has multiple genetic and acquired causes. Apelin is an endogenous peptide that increases cardiac inotropism through his APJ receptor. No data are available concerning the APJ gene mutations responsible for IDC or on the role of APJ receptor gene variants in predicting heart failure (HF) progression. Methods and Results: We prospectively evaluated 202 consecutive patients with IDC and 202 matched controls: 90 were screened for APJ gene mutations and all 202 were genotyped for G212A and A445C APJ receptor polymorphisms. No mutations were found within the coding or untranslated regions of the APJ receptor, and no differences in allelic or genotype frequencies were observed comparing patients with a healthy control population. The correlations between APJ receptor polymorphisms and HF progression were assessed. During a median follow-up of 37 months, 35 patients experienced HF progression. Univariate analysis showed that patients carrying at least 1 copy of 212A had a significantly lower risk for HF-related events than those who were homozygous for the G212 variant, and multivariate analysis confirmed that it was significantly related to a more favorable prognosis. Conclusions: APJ is unlikely to be a gene causing IDC, but the independent correlation between the 212A allele and a better prognosis suggests that it might act as a modifier gene.",
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AU - Sarzani, Riccardo

AU - Forleo, Cinzia

AU - Pietrucci, Francesca

AU - Capestro, Alessandro

AU - Soura, Elli

AU - Guida, Pietro

AU - Sorrentino, Sandro

AU - Iacoviello, Massimo

AU - Romito, Roberta

AU - Dessì-Fulgheri, Paolo

AU - Pitzalis, Mariavittoria

AU - Rappelli, Alessandro

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N2 - Background: Idiopathic dilated cardiomyopathy (IDC) has multiple genetic and acquired causes. Apelin is an endogenous peptide that increases cardiac inotropism through his APJ receptor. No data are available concerning the APJ gene mutations responsible for IDC or on the role of APJ receptor gene variants in predicting heart failure (HF) progression. Methods and Results: We prospectively evaluated 202 consecutive patients with IDC and 202 matched controls: 90 were screened for APJ gene mutations and all 202 were genotyped for G212A and A445C APJ receptor polymorphisms. No mutations were found within the coding or untranslated regions of the APJ receptor, and no differences in allelic or genotype frequencies were observed comparing patients with a healthy control population. The correlations between APJ receptor polymorphisms and HF progression were assessed. During a median follow-up of 37 months, 35 patients experienced HF progression. Univariate analysis showed that patients carrying at least 1 copy of 212A had a significantly lower risk for HF-related events than those who were homozygous for the G212 variant, and multivariate analysis confirmed that it was significantly related to a more favorable prognosis. Conclusions: APJ is unlikely to be a gene causing IDC, but the independent correlation between the 212A allele and a better prognosis suggests that it might act as a modifier gene.

AB - Background: Idiopathic dilated cardiomyopathy (IDC) has multiple genetic and acquired causes. Apelin is an endogenous peptide that increases cardiac inotropism through his APJ receptor. No data are available concerning the APJ gene mutations responsible for IDC or on the role of APJ receptor gene variants in predicting heart failure (HF) progression. Methods and Results: We prospectively evaluated 202 consecutive patients with IDC and 202 matched controls: 90 were screened for APJ gene mutations and all 202 were genotyped for G212A and A445C APJ receptor polymorphisms. No mutations were found within the coding or untranslated regions of the APJ receptor, and no differences in allelic or genotype frequencies were observed comparing patients with a healthy control population. The correlations between APJ receptor polymorphisms and HF progression were assessed. During a median follow-up of 37 months, 35 patients experienced HF progression. Univariate analysis showed that patients carrying at least 1 copy of 212A had a significantly lower risk for HF-related events than those who were homozygous for the G212 variant, and multivariate analysis confirmed that it was significantly related to a more favorable prognosis. Conclusions: APJ is unlikely to be a gene causing IDC, but the independent correlation between the 212A allele and a better prognosis suggests that it might act as a modifier gene.

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