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Polymorphisms in the angiotensinogen and angiotensin II type 1 receptor gene are related to change in left ventricular mass during antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial
Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
Division of Internal Medicine, Karolinska Institutet Danderyd Hospital, Stockholm, Sweden.
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2002 (Engelska)Ingår i: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 20, nr 4, s. 657-663Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

BACKGROUND: Our aim was to determine if gene polymorphisms in the renin-angiotensin-aldosterone system (RAAS) were related to the degree of change in left ventricular hypertrophy (LVH) during antihypertensive treatment.

METHODS AND RESULTS: Patients with essential hypertension and echocardiographically diagnosed LVH were included in a double-blind study to receive treatment with either the angiotensin II type 1 receptor (AT1-receptor) antagonist irbesartan (n = 41), or the beta-1 adrenergic receptor blocker atenolol (n = 43) as monotherapy for 3 months. The angiotensinogen T174M and M235T, the angiotensin-converting enzyme I/D, the AT1-receptor A1166C and the aldosterone synthase (CYP11B2) -344 C/T polymorphisms were analysed and related to the change in left ventricular mass (LVM). Patients with the angiotensinogen 174 TM genotype treated with irbesartan responded with the greatest reduction in LVM (-23 +/- 31SD g/m2 for TM and +0.5 +/- 18 g/m2 for TT, P = 0.005), independent of blood pressure reduction. Both the angiotensinogen 235 T-allele (P = 0.02) and the AT1-receptor 1166 AC genotype responded with the greatest reduction in LVM when treated with irbesartan (-0.1 +/- 19 g/m2 for AA and -18 +/- 30 g/m2 for AC, P = 0.02), independent of blood pressure reduction. These polymorphisms were not associated with the change in LVM during treatment with atenolol.

DISCUSSION: The angiotensinogen T174M and M235T and the AT1-receptor A1166C polymorphisms were related to the change in LVH during antihypertensive treatment with an AT1-receptor antagonist; of these angiotensinogen T174M was the most powerful. This highlights the role of the RAAS for left ventricular hypertrophy and the potential of pharmacogenetics as a tool for guidance of antihypertensive therapy.

Ort, förlag, år, upplaga, sidor
Lippincott Williams & Wilkins, 2002. Vol. 20, nr 4, s. 657-663
Nyckelord [en]
hypertension, left ventricular hypertrophy, renin-angiotensin system, gene polymorphisms, treatment
Nationell ämneskategori
Kardiologi Farmakologi och toxikologi Medicinsk genetik
Identifikatorer
URN: urn:nbn:se:oru:diva-69400DOI: 10.1097/00004872-200204000-00023ISI: 000174960500023PubMedID: 11910301OAI: oai:DiVA.org:oru-69400DiVA, id: diva2:1254518
Tillgänglig från: 2018-10-09 Skapad: 2018-10-09 Senast uppdaterad: 2018-10-10Bibliografiskt granskad

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KardiologiFarmakologi och toxikologiMedicinsk genetik

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