open access

Vol 13, No 6 (2009)
Prace oryginalne
Published online: 2010-02-26
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The association between 3020INSC mutation in NOD2 gene and arterial stiffness in hypertensives

Grażyna Szumczyk-Muszytowska, Jacek Manitius, Andrzej Tretyn, Joanna Jarkiewicz-Tretyn, Marek Muszytowski
Nadciśnienie tętnicze 2009;13(6):371-375.

open access

Vol 13, No 6 (2009)
Prace oryginalne
Published online: 2010-02-26

Abstract

Background The innate immune system elicits an inflammatory process which is believed to be involved in the development of vascular damage in hypertension. The NOD2 gene (CARD15) is involved in the control of the innate immune system. The aim of this study was to assess the occurrence of the 3020insC mutation in the NOD2 gene in relation to vascular damage in hypertensives. Materials and methods In 466 hypertensives, genotyping for 3020insC mutation, cholesterol, serum creatinine, and echocardiography were carried out. Systolic (SBP) and diastolic (DBP) blood pressure and pulse pressure (PP) were taken at 2-3 month intervals for one year and treated according to ESC/ESH guidelines. Results The 3020insC mutation was found in 7.08% of hypertensives and was associated with earlier onset of hypertension 48.2 ± 12.1 v. 42.8 ± 10.9, p < 0.01 (age of pts). After one year of treatment, patients with the mutation had significantly higher SBP (138.48 ± 18.35 v. 131.74 ± 14.97, p < 0.04) and PP (57.27 ± 14.04 v. 52.70 ± 12.96, p < 0.04) than patients without the mutation, whereas the number of drugs was the same in both groups.
Conclusions The results suggest that the 3020insC mutation is associated with earlier onset of hypertension and increased arterial stiffness.

Abstract

Background The innate immune system elicits an inflammatory process which is believed to be involved in the development of vascular damage in hypertension. The NOD2 gene (CARD15) is involved in the control of the innate immune system. The aim of this study was to assess the occurrence of the 3020insC mutation in the NOD2 gene in relation to vascular damage in hypertensives. Materials and methods In 466 hypertensives, genotyping for 3020insC mutation, cholesterol, serum creatinine, and echocardiography were carried out. Systolic (SBP) and diastolic (DBP) blood pressure and pulse pressure (PP) were taken at 2-3 month intervals for one year and treated according to ESC/ESH guidelines. Results The 3020insC mutation was found in 7.08% of hypertensives and was associated with earlier onset of hypertension 48.2 ± 12.1 v. 42.8 ± 10.9, p < 0.01 (age of pts). After one year of treatment, patients with the mutation had significantly higher SBP (138.48 ± 18.35 v. 131.74 ± 14.97, p < 0.04) and PP (57.27 ± 14.04 v. 52.70 ± 12.96, p < 0.04) than patients without the mutation, whereas the number of drugs was the same in both groups.
Conclusions The results suggest that the 3020insC mutation is associated with earlier onset of hypertension and increased arterial stiffness.
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Keywords

arterial stiffness; innate immunity; NOD2 mutation

About this article
Title

The association between 3020INSC mutation in NOD2 gene and arterial stiffness in hypertensives

Journal

Arterial Hypertension

Issue

Vol 13, No 6 (2009)

Pages

371-375

Published online

2010-02-26

Bibliographic record

Nadciśnienie tętnicze 2009;13(6):371-375.

Keywords

arterial stiffness
innate immunity
NOD2 mutation

Authors

Grażyna Szumczyk-Muszytowska
Jacek Manitius
Andrzej Tretyn
Joanna Jarkiewicz-Tretyn
Marek Muszytowski

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