Wong K, Summers K, Burstow D, West M
Renin angiotensin system genetic variants and pressure load in
cardiac hypertrophy
16th Scientific Meeting of the International Society of Hypertension
ISH Abstract Book
(Jun) 16: 1996
57 normals and 53 patients with mild aortic stenosis (gradient greater
than 50 mmHg) were studied. LV mass was increased in AoS. The ACE I/D
genotype, angiotensinogen T174M genotype and AT1-microsatellite
genotype were determined. They had no influence on ventricular wall
thickness (WT) in normotensives. In patients with aortic stenosis,
however, both angiotensinogen genotype (AGT-MM+MT vs TT) and ACE
genotype (DD vs ID + II) were associated with increased WT. Also, the
AT1 - B allele was associated with increased WT. The conclusion of the
study was, that genetic variants affecting the renin-angiotensin
system modify the ventricular response to AoS but have no effect in
normals.
Comment: Specifically, this study fits with published
data that polymorphisms in the renin-angiotensin system associated
with increased activity of this system and increased production of the
pressor and growth hormone Ang II cause ventricular hypertrophy. This
may only be evident when there is another stimulus to ventricular
hypertrophy eg HBP or AoS. However, this study is under-powered (less
than 100 subjects) even for a single polymorphism analysis. Multiple
comparisons make significance likely by chance and the authors have
grouped the genotypes (eg MM + MT). The groupings are inconsistent
(MM+MT in one, DI+II) in another. Manipulating the data to look for
significance in this way is probably justified and is necessary in
small exploratory studies like this - but the results will need to be
confirmed or repeated in further, larger studies. Therefore, although
tantalizing the data are inadequate to justify the conclusions
(Alan Jardine, M.D., Glasgow University, Scotland).
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16th Scientific Meeting of the International Society of Hypertension
H: Pathophysiology :
Genetics
H: Pathophysiology :
Heart in hypertension