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Transforming Growth Factor 1 Genotype and Change in Left Ventricular Mass during Antihypertensive Treatment — Results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol
| Content Provider | Semantic Scholar |
|---|---|
| Author | Lind, Lars Billberger, Katarina Karlsson, Julia Malmqvist, Karin |
| Copyright Year | 2006 |
| 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 1 (TGF1); AT1-receptor antagonists reverse these changes. The TGF1 G + 915C polymorphism is associated with interindividual variation in TGF1 production. No study has yet determined the impact of this polymorphism on the response to antihypertensive treatment. Hypothesis: We aimed to determine whether the TGF1 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 TGF1 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 TGF1, 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 TGF1 G + 915C polymorphism is related to the change in LVMI in response to antihypertensive treatment with the AT1-receptor antagonist irbesartan. |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://www.medsci.uu.se/digitalAssets/633/c_633362-l_1-k_hallberg_clincardiol_2004.pdf |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
