Angiotensin-converting enzyme gene deletion polymorphism modulation of onset of symptoms and survival rate of patients with heart failure.
BACKGROUND
Angiotensin-converting enzyme is involved in the pathophysiology of heart failure. We hypothesized that clinical characteristics as well as survival rate in patients with heart failure of different etiologies may be modulated by functional variants DD, ID and II of the angiotensin-converting enzyme gene.


METHODS
We studied 333 patients with heart failure, aged 43.3 +/- 10.5 years, 262 (78.7%) men and 71 (21.3%) women. Heart failure was ascribed to idiopathic dilated cardiomyopathy in 125 patients. Heart failure was caused by ischemic heart disease in 63 patients, Chagas' disease in 58, hypertensive heart disease in 41, alcoholic cardiomyopathy in 24, and was due to other etiologies in 22 patients. Statistical analysis was performed with the chi(2) test, Student's t-test, analysis of variance, Kaplan-Meier and Cox proportional hazards methods.


RESULTS
The DD genotype was associated with increased systolic left ventricular diameter (p = 0.031). Earlier onset of symptoms was observed in patients with alcoholic cardiomyopathy and DD genotype (p = 0.033, codominant D) and in patients with hypertensive cardiomyopathy and DD genotype (p = 0.048, codominant D; p = 0.024, recessive D). Mortality was higher in patients older than 50 years with DD genotype (p = 0.007, codominant D; p = 0.002, recessive D). Variables independently associated with higher mortality in patients older than 50 years were age, diabetes mellitus, Chagas' disease etiology and DD genotype.


CONCLUSIONS
These results add evidence for an association of the DD genotype of the angiotensin-converting enzyme gene with earlier onset of symptoms and decreased survival rate of selected patients with heart failure.
Cuoco
Marco Antonio Romeo
MA
Heart Institute (InCor), Clinical Division, General Out Patient Clinics, University of São Paulo Medical School, Av. Dr. Eneas de Carvalho Aguiar, 44, São Paulo 05403-000, Brazil. cuocomar@incor.usp.br
Pereira
Alexandre Costa
AC
de Freitas
Humberto Felício Gonçalves
HF
de Fátima Alves da Mota
Glória
G
Fukushima
Júlia Tizue
JT
Krieger
José Eduardo
JE
Mansur
Alfredo José
AJ
D000293:Adolescent; D000328:Adult; D000368:Aged; D005260:Female; D017353:Gene Deletion; D006333:Heart Failure / Q000175:diagnosis / Q000235:genetics* / Q000401:mortality; D006801:Humans; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D015996:Survival Rate
D007703:Peptidyl-Dipeptidase A