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Transforming growth factor beta1 genotype and change in left ventricular mass during antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA)
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. (Osteoporos)
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper. (Osteoporos)
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. (Orthopaedics)
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2004 (Engelska)Ingår i: Clinical Cardiology, ISSN 0160-9289, E-ISSN 1932-8737, Vol. 27, nr 3, s. 169-73Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

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 beta1 (TGF-beta1); AT1-receptor antagonists reverse these changes. The TGF-beta1 G + 915C polymorphism is associated with interindividual variation in TGF-beta1 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-beta1 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-beta1 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-beta1, 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-beta1 G + 915C polymorphism is related to the change in LVMI in response to antihypertensive treatment with the AT1-receptor antagonist irbesartan.

Ort, förlag, år, upplaga, sidor
2004. Vol. 27, nr 3, s. 169-73
Nyckelord [en]
Antihypertensive Agents/*therapeutic use, Atenolol/therapeutic use, Biphenyl Compounds/*therapeutic use, Double-Blind Method, Female, Genotype, Humans, Hypertension/complications/*drug therapy, Hypertrophy; Left Ventricular/complications/*drug therapy/physiopathology, Linear Models, Male, Polymorphism; Genetic, Research Support; Non-U.S. Gov't, Sweden, Tetrazoles/*therapeutic use, Transforming
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
URN: urn:nbn:se:uu:diva-65946DOI: 10.1002/clc.4960270315PubMedID: 15049387OAI: oai:DiVA.org:uu-65946DiVA, id: diva2:93857
Tillgänglig från: 2005-08-16 Skapad: 2005-08-16 Senast uppdaterad: 2018-11-30

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Hallberg, PärMichaëlsson, KarlLiljedahl, UlrikaMelhus, Håkan

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