Usefulness of the I/D angiotensin-converting enzyme genotype for detectingthe risk of left ventricular hypertrophy in pharmacologically treated hypertensive men

Citation
J. Lopez-contreras et al., Usefulness of the I/D angiotensin-converting enzyme genotype for detectingthe risk of left ventricular hypertrophy in pharmacologically treated hypertensive men, J HUM HYPER, 14(5), 2000, pp. 327-331
Citations number
29
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF HUMAN HYPERTENSION
ISSN journal
09509240 → ACNP
Volume
14
Issue
5
Year of publication
2000
Pages
327 - 331
Database
ISI
SICI code
0950-9240(200005)14:5<327:UOTIAE>2.0.ZU;2-6
Abstract
The insertion/deletion polymorphism (I/D) of the angiotensin-converting enz yme (ACE) gene has been associated in some studies with a higher prevalence of left ventricular hypertrophy (LVH), but few of them were performed on p harmacologically treated hypertensive patients. The present study was under taken to determine whether ACE genotype determination could help in the ide ntification of pharmacologically treated hypertensive patients at a higher risk of LVH. Ninety-six consecutive men with essential hypertension were se lected for the study. Left ventricular mass (LVM) was assessed by echocardi ography and indexed by body surface area and 82 patients were considered su itable for the study. Three groups of patients were defined on the basis of their IID ACE genotype: DD (n = 39), ID (n = 33) and II (n = 10). There we re no statistically significant differences between the three groups regard ing to the severity of hypertension at diagnosis, degree of control of bloo d pressure or type of antihypertensive drug therapy used. No statistically significant differences were found between the three groups regarding to LV M index (total 124 +/- 31, DD 121 +/- 29, ID 127 +/- 35 and II 122 +/- 18 g /m(2)), relative wail thickness (total 0.5 +/- 0.2, DD 0.5 +/- 0.3, ID 0.48 +/- 0.07 and II 0.47 +/- 0.04) or prevalence of LVH (total 34%, DD 31%, ID 39% and II 30% by Cornell criteria and total 39%, DD 33%, ID 45% and II 40 % by Framingham criteria). Furthermore, the I and D allele frequency distri bution was similar in the whole group of patients, in patients with LVH, an d in a control group of healthy volunteers. Our data do not support that th e IID ACE genotype determination helps in identifying treated hypertensive patients at higher risk of LVH.