Angiotensin-converting enzyme gene polymorphism influences degree of left ventricular hypertrophy and its regression in patients undergoing operationfor aortic stenosis
G. Dellgren et al., Angiotensin-converting enzyme gene polymorphism influences degree of left ventricular hypertrophy and its regression in patients undergoing operationfor aortic stenosis, AM J CARD, 84(8), 1999, pp. 909-913
Citations number
31
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzym
e (ACE) gene has been associated with increased left ventricular hypertroph
y (LVH) in patients with cardiomyopathy and congestive heart failure. Patie
nts with aortic stenosis (AS) have varying degrees of LVH at a given valve
area, The aim of this study was to examine the relation between ACE gene po
lymorphism and the degree of LVH in patients undergoing operation for AS, E
ighty-two patients who underwent operation for AS with a stentless valve we
re followed prospectively with echocardiographic assessments of left ventri
cular mass index (LVMI), ACE gene polymorphism was determined by polymerase
chain reaction. The genotype (DD, ID, and II) frequency was the same as in
healthy controls, The pressure difference across the aortic valve did not
differ between genotypes, Patients with the DD genotype of the ACE gene had
a higher LVMI (197 +/- 47 g/m(2)) preoperatively than those with ID (175 /- 41 g/m(2)) or II (155 +/- 43 g/m(2)) genotypes (p = 0.01), LVMI decrease
d significantly in DD (p <0.001) and ID (p <0.001) genotypes but not in the
II genotype during follow-vp (mean 15 months). There was a significant dif
ference in regression of LVMI over time between genotypes (p = 0.0056), wit
h no significant difference between genotypes at follow-up, The DD genotype
of the ACE gene is associated with increased preoperative LVH in patients
treated surgically for AS. The DD genotype appears to be an important facto
r which increases hypertrophic myocardial reactivity to pressure overload.
(C) 1999 by Excerpta Medica, Inc.