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. 2006 Dec 5;27(3):169–173. doi: 10.1002/clc.4960270315

Transforming growth factor β1 genotype and change in left ventricular mass during antihypertensive treatment–results from the swedish irbesartan left ventricular hypertrophy investigation versus atenolol (Silvhia)

Pär Hallberg 1,✉, Lars Lind 1,2,†, Katarina Billberger 1, Karl Michaelsson 3, Julia Karlsson 1, Lisa Kurland 1, Thomas Kahan 4, Karin Malmqvist 4, K Peter Öhman 2,5, Fredrik Nyström 5,6, Ulrika Liljedahl 1, Ann‐Christine Syvänen 1, Håkan Melhus 1
PMCID: PMC6654118  PMID: 15049387

Abstract

Background: Angiotensin II, via the angiotensin II type 1 (AT1) receptor, may mediate myocardial fibrosis and myocyte hypertrophy seen in hypertensive left ventricular (LV) hypertrophy through production of transforming growth factor β1(TGF‐β1); AT1‐receptor antagonists reverse these changes. The TGF‐(β1 G + 915C polymorphism is associated with in‐terindividual variation in TGF‐ β1 production. No study has yet determined the impact of this polymorphism on the response to antihypertensive treatment.

Hypothesis: We aimed to determine whether the TGF‐ β1 G + 915C polymorphism was related to change in LV mass during antihypertensive treatment with either an AT1 ‐receptor antagonists or a beta1 ‐adrenoceptor blocker. The polymorphism was hypothesized to have an impact mainly on the irbesartan group.

Methods: We determined the association between the TGF‐β1 genotype and regression of LV mass in 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, randomized in a double‐blind study to receive treatment for 48 weeks with either the AT1 ‐receptor antagonist irbesartan or the beta1 ‐adrenoceptor blocker atenolol.

Results: Irbesartan‐treated patients who were carriers of the C‐allele, which is associated with low expression of TGF‐β1, responded with a markedly greater decrease in LV mass index (LVMI) than subjects with the G/G genotype (adjusted mean change in LVMI –44.7 g/m2 vs. –22.2 g/m2, p = 0.007), independent of blood pressure reduction. No association between genotype and change in LVMI was observed in the atenolol group.

Conclusions: The TGF‐ β1 G + 915C polymorphism is related to the change in LVMI in response to antihypertensive treatment with the AT1 ‐receptor antagonist irbesartan.

Keywords: transforming growth factor, angiotensin, hypertension, polymorphism, left ventricular hypertrophy, irbesartan

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