IJCS | Volume 32, Nº1, January/ February 2019

58 Silva et al. ACE polymorphism and echocardiographic data in HF Int J Cardiovasc Sci. 2019;32(1)55-60 Original Article significant difference was found in the distribution of genotypes between men and women, with a predominance of men with DI genotype (59.3%). Functional class varied from II to IV; most patients were in NYHA functional class IV. Analysis of repeated measures for categorical data showed that there was no significant variation in functional class andD/I genotype (p = 0.472). No difference was found in mean values of echocardiographic variables or genotypes. Patients with the DI genotype showed higher LVDD (60.3) as compared with the other genotypes. Significant correlations were found for the variables sex, age, smoking, heart rate and dyslipidemia; male sex was associated with increased risk of HF (p = 0.023). Smoking was considered a risk factor for HF. Most patients didnot consume alcohol, and thereby alcohol consumptionwas considered a protective factor (p= 0.008). Dyslipidemia was associated with a five times higher risk for HF. DD, DI and II genotypes were not considered a risk factor or HF. Discussion Many researches involving ACE polymorphisms have been conducted to study the pathophysiology of HF and, so far, it is still controversial whether ACE polymorphism is associatedwith HF. Although ACE polymorphismhas been associated with several pathophysiological events and with morbidity and mortality of cardiovascular diseases, in this study, we aimed to determine a relationship of this polymorphism with HF caused exclusively by Chagas disease. Most of our patients were men (63%), similarly to other studies. 4,17,18 HF is an increasing epidemic that affects mostly older men, and its increasing incidence has been associatedwith higher survival. 4 No statistically significant difference in genotype distributionwas found between men and women, which is in agreement with a previous study conducted in 2014. 19 To evaluate an association of ACE polymorphism with HF severity, we investigated a possible association of D/I genotype with echocardiographic parameters, but no association was found. In contrast, a previous national study 20 reported an association of DD and ID genotype with worse and better echocardiographic profile, respectively. 20 We also did not find differences in EF values between the two genotypes (p = 0.664). HF is a common clinical conditionwith highmorbidity and mortality, affecting 1.5% - 2.0% of the general population. Its prevalence increases with age and affects approximately 10% of individuals older than 65 years. 21 Our findings corroborate this finding, since we found a statistically significant association of age with HF in the study population. We did not find any difference in the frequency of genotypes after adjustment for gender, which agrees with the results of a study conducted in a Chinese population. 22 A national study performed in 2005 23 reported augmented LVSD in patients with DD genotype, which was associated with higher morbidity and mortality in patients with different causes of HF. Our results differ from these findings, since we did not find any relationship between D/I genotypes and LVSD. Similar occurrence of D/I genotypes was found in the study population, contradicting the hypothesis that D/I genotype is a risk factor for HF. 4,24 We did not find any association of D/I genotypes with HF severity, differently from previous studies 25,26 reporting an association of the D allele with HF progression and higher mortality as compared with the I allele. Our study corroborates another Brazilian, clinical comparative study on 193 patients, that did not find any difference in the frequency of D/I genotype in patients with HF caused by Chagas disease without systolic dysfunction. 27 Hospitalization for HF is an important public health problem. 28 Clinical treatment of this patients involves multidisciplinary approach, since they have many comorbidities that may have an impact on the clinical course of the disease. There is evidence that the risk for HF in the general population depends on a genetic predisposition characterized by a very complex genetic architecture. Predisposition to individual conditions and genetic variations modulate the pathophysiological responses. 29 Possible limitations of this study include a small number of patients; however, there are available in the literature studies involving larger number of patients, 10,23 but also others with smaller samples. 27,30 Due to the lack of patients’ follow-up in the study, we could not evaluate the natural course of the disease. Socioeconomical aspects can interact with genetic factors and influence HF outcomes. Our study included only patients attending public clinics and therefore our findings may not be reproduced to other populations.