Alpha-adducin Gly460Trp polymorphism, left ventricular mass and plasma renin activity

Mikolaj Winnicki, Virend Somers, Valentina Accurso, Michal Hoffmann, Ryszard Pawlowski, Gianfranco Frigo, Pieralberto Visentin, Paolo Palatini

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Objective: Left ventricular hypertrophy (LVH) is associated with an increased risk for cardiovascular morbidity and mortality. Epidemiological studies suggest that LVH may be influenced by genetic factors. However, the evidence associating individual genes with left ventricular (LV) mass is inconsistent and contradictory. Methods: We investigated the association between angiotensin-converting enzyme insertion/deletion, angiotensinogen M235T and α-adducin Gly460Trp polymorphisms with LV mass and plasma renin activity (PRA) in 162 men with mild, never-treated hypertension who were recruited for the Hypertension and Ambulatory Recording Venetia Study. The effect of each polymorphism on LV mass and PRA was tested in one-way analysis of covariance using LV mass index or PRA as the dependent variable after adjusting for covariates. Results: The α-adducin polymorphism was the only individual polymorphism independently associated with LV mass index (F = 7.78, P = 0.006). Patients homozygous for the Trp allele of that polymorphism had a LV mass index (123.4 ± 10.5 g/m2) significantly higher compared with heterozygotes (90.8 ± 2.5 g/m2, P < 0.01) or Gly homozygotes (94.7 ± 1.7 g/m2, P < 0.05). These subjects also have significantly lower PRA (F = 4.2, P = 0.017). Albeit uncommon, 40% of Trp homozygotes of the α-adducin polymorphism had LVH (odds ratio, 15.1;95% confidence interval, 3.0-82.1). Conclusions: The homozygotic state of the Trp allele of α-adducin Gly460Trp polymorphism is independently associated with increased LV mass and low PRA. These data suggest that genetic considerations may contribute importantly to risk stratification, and perhaps therapeutic interventions targeted at LVH and the renin-angiotensin system in hypertensive patients.

Original languageEnglish (US)
Pages (from-to)1771-1777
Number of pages7
JournalJournal of Hypertension
Volume20
Issue number9
DOIs
StatePublished - Sep 2002
Externally publishedYes

Fingerprint

Renin
Left Ventricular Hypertrophy
Homozygote
Alleles
Hypertension
Angiotensinogen
Peptidyl-Dipeptidase A
Heterozygote
Renin-Angiotensin System
Epidemiologic Studies
Odds Ratio
adducin
Confidence Intervals
Morbidity
Mortality
Genes
Therapeutics

Keywords

  • α-adducin
  • Angiotensin-converting enzyme
  • Angiotensinogen
  • Gene polymorphisms
  • Left ventricular mass
  • Plasma renin activity

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology

Cite this

Winnicki, M., Somers, V., Accurso, V., Hoffmann, M., Pawlowski, R., Frigo, G., ... Palatini, P. (2002). Alpha-adducin Gly460Trp polymorphism, left ventricular mass and plasma renin activity. Journal of Hypertension, 20(9), 1771-1777. https://doi.org/10.1097/00004872-200209000-00021

Alpha-adducin Gly460Trp polymorphism, left ventricular mass and plasma renin activity. / Winnicki, Mikolaj; Somers, Virend; Accurso, Valentina; Hoffmann, Michal; Pawlowski, Ryszard; Frigo, Gianfranco; Visentin, Pieralberto; Palatini, Paolo.

In: Journal of Hypertension, Vol. 20, No. 9, 09.2002, p. 1771-1777.

Research output: Contribution to journalArticle

Winnicki, M, Somers, V, Accurso, V, Hoffmann, M, Pawlowski, R, Frigo, G, Visentin, P & Palatini, P 2002, 'Alpha-adducin Gly460Trp polymorphism, left ventricular mass and plasma renin activity', Journal of Hypertension, vol. 20, no. 9, pp. 1771-1777. https://doi.org/10.1097/00004872-200209000-00021
Winnicki, Mikolaj ; Somers, Virend ; Accurso, Valentina ; Hoffmann, Michal ; Pawlowski, Ryszard ; Frigo, Gianfranco ; Visentin, Pieralberto ; Palatini, Paolo. / Alpha-adducin Gly460Trp polymorphism, left ventricular mass and plasma renin activity. In: Journal of Hypertension. 2002 ; Vol. 20, No. 9. pp. 1771-1777.
@article{a258f3838e4343f89deb89ccaf3751b6,
title = "Alpha-adducin Gly460Trp polymorphism, left ventricular mass and plasma renin activity",
abstract = "Objective: Left ventricular hypertrophy (LVH) is associated with an increased risk for cardiovascular morbidity and mortality. Epidemiological studies suggest that LVH may be influenced by genetic factors. However, the evidence associating individual genes with left ventricular (LV) mass is inconsistent and contradictory. Methods: We investigated the association between angiotensin-converting enzyme insertion/deletion, angiotensinogen M235T and α-adducin Gly460Trp polymorphisms with LV mass and plasma renin activity (PRA) in 162 men with mild, never-treated hypertension who were recruited for the Hypertension and Ambulatory Recording Venetia Study. The effect of each polymorphism on LV mass and PRA was tested in one-way analysis of covariance using LV mass index or PRA as the dependent variable after adjusting for covariates. Results: The α-adducin polymorphism was the only individual polymorphism independently associated with LV mass index (F = 7.78, P = 0.006). Patients homozygous for the Trp allele of that polymorphism had a LV mass index (123.4 ± 10.5 g/m2) significantly higher compared with heterozygotes (90.8 ± 2.5 g/m2, P < 0.01) or Gly homozygotes (94.7 ± 1.7 g/m2, P < 0.05). These subjects also have significantly lower PRA (F = 4.2, P = 0.017). Albeit uncommon, 40{\%} of Trp homozygotes of the α-adducin polymorphism had LVH (odds ratio, 15.1;95{\%} confidence interval, 3.0-82.1). Conclusions: The homozygotic state of the Trp allele of α-adducin Gly460Trp polymorphism is independently associated with increased LV mass and low PRA. These data suggest that genetic considerations may contribute importantly to risk stratification, and perhaps therapeutic interventions targeted at LVH and the renin-angiotensin system in hypertensive patients.",
keywords = "α-adducin, Angiotensin-converting enzyme, Angiotensinogen, Gene polymorphisms, Left ventricular mass, Plasma renin activity",
author = "Mikolaj Winnicki and Virend Somers and Valentina Accurso and Michal Hoffmann and Ryszard Pawlowski and Gianfranco Frigo and Pieralberto Visentin and Paolo Palatini",
year = "2002",
month = "9",
doi = "10.1097/00004872-200209000-00021",
language = "English (US)",
volume = "20",
pages = "1771--1777",
journal = "Journal of Hypertension",
issn = "0263-6352",
publisher = "Lippincott Williams and Wilkins",
number = "9",

}

TY - JOUR

T1 - Alpha-adducin Gly460Trp polymorphism, left ventricular mass and plasma renin activity

AU - Winnicki, Mikolaj

AU - Somers, Virend

AU - Accurso, Valentina

AU - Hoffmann, Michal

AU - Pawlowski, Ryszard

AU - Frigo, Gianfranco

AU - Visentin, Pieralberto

AU - Palatini, Paolo

PY - 2002/9

Y1 - 2002/9

N2 - Objective: Left ventricular hypertrophy (LVH) is associated with an increased risk for cardiovascular morbidity and mortality. Epidemiological studies suggest that LVH may be influenced by genetic factors. However, the evidence associating individual genes with left ventricular (LV) mass is inconsistent and contradictory. Methods: We investigated the association between angiotensin-converting enzyme insertion/deletion, angiotensinogen M235T and α-adducin Gly460Trp polymorphisms with LV mass and plasma renin activity (PRA) in 162 men with mild, never-treated hypertension who were recruited for the Hypertension and Ambulatory Recording Venetia Study. The effect of each polymorphism on LV mass and PRA was tested in one-way analysis of covariance using LV mass index or PRA as the dependent variable after adjusting for covariates. Results: The α-adducin polymorphism was the only individual polymorphism independently associated with LV mass index (F = 7.78, P = 0.006). Patients homozygous for the Trp allele of that polymorphism had a LV mass index (123.4 ± 10.5 g/m2) significantly higher compared with heterozygotes (90.8 ± 2.5 g/m2, P < 0.01) or Gly homozygotes (94.7 ± 1.7 g/m2, P < 0.05). These subjects also have significantly lower PRA (F = 4.2, P = 0.017). Albeit uncommon, 40% of Trp homozygotes of the α-adducin polymorphism had LVH (odds ratio, 15.1;95% confidence interval, 3.0-82.1). Conclusions: The homozygotic state of the Trp allele of α-adducin Gly460Trp polymorphism is independently associated with increased LV mass and low PRA. These data suggest that genetic considerations may contribute importantly to risk stratification, and perhaps therapeutic interventions targeted at LVH and the renin-angiotensin system in hypertensive patients.

AB - Objective: Left ventricular hypertrophy (LVH) is associated with an increased risk for cardiovascular morbidity and mortality. Epidemiological studies suggest that LVH may be influenced by genetic factors. However, the evidence associating individual genes with left ventricular (LV) mass is inconsistent and contradictory. Methods: We investigated the association between angiotensin-converting enzyme insertion/deletion, angiotensinogen M235T and α-adducin Gly460Trp polymorphisms with LV mass and plasma renin activity (PRA) in 162 men with mild, never-treated hypertension who were recruited for the Hypertension and Ambulatory Recording Venetia Study. The effect of each polymorphism on LV mass and PRA was tested in one-way analysis of covariance using LV mass index or PRA as the dependent variable after adjusting for covariates. Results: The α-adducin polymorphism was the only individual polymorphism independently associated with LV mass index (F = 7.78, P = 0.006). Patients homozygous for the Trp allele of that polymorphism had a LV mass index (123.4 ± 10.5 g/m2) significantly higher compared with heterozygotes (90.8 ± 2.5 g/m2, P < 0.01) or Gly homozygotes (94.7 ± 1.7 g/m2, P < 0.05). These subjects also have significantly lower PRA (F = 4.2, P = 0.017). Albeit uncommon, 40% of Trp homozygotes of the α-adducin polymorphism had LVH (odds ratio, 15.1;95% confidence interval, 3.0-82.1). Conclusions: The homozygotic state of the Trp allele of α-adducin Gly460Trp polymorphism is independently associated with increased LV mass and low PRA. These data suggest that genetic considerations may contribute importantly to risk stratification, and perhaps therapeutic interventions targeted at LVH and the renin-angiotensin system in hypertensive patients.

KW - α-adducin

KW - Angiotensin-converting enzyme

KW - Angiotensinogen

KW - Gene polymorphisms

KW - Left ventricular mass

KW - Plasma renin activity

UR - http://www.scopus.com/inward/record.url?scp=0036735724&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036735724&partnerID=8YFLogxK

U2 - 10.1097/00004872-200209000-00021

DO - 10.1097/00004872-200209000-00021

M3 - Article

C2 - 12195118

AN - SCOPUS:0036735724

VL - 20

SP - 1771

EP - 1777

JO - Journal of Hypertension

JF - Journal of Hypertension

SN - 0263-6352

IS - 9

ER -