Relationship between plasma ACE activity and the proliferative healing process in coronary vessel injury after coronary stenting (original) (raw)
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Effects of ACE polymorphisms and other risk factors on the severity of coronary artery disease
Genetics and Molecular Research, 2013
Coronary artery disease (CAD) is a multifactorial disease influenced by genetic and environmental factors. Major risk factors of CAD are hypertension, hyperlipidemia, smoking, family history and obesity. Also polymorphisms in the angiotensin-I converting enzyme (ACE) gene can associate with CAD. The relationship between ACE polymorphisms and other risk factors is not well understood in CAD, likely due to the complex interrelation of genetic and environmental risk factors. The aim of this study was to investigate the associations of CAD risk factors and ACE polymorphisms in patients with CAD. We enrolled 203 consecutive ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 12 (4): 6895-6906 (2013) A.I. Guney et al. patients and 140 healthy subjects in the study. The severity of CAD was evaluated according to the number of vessels with significant stenosis. ACE insertion (I)/deletion (D) genotype was determined by PCR. The frequency of the DD genotype was significantly higher in patients. D allele frequency was higher among CAD subjects when compared to the control group. The number of stenotic vessels were found to be statistically associated with a high frequency of DD polymorphism and D allele and a low frequency of I allele in patients, especially in male patients. The control group displayed II and ID genotypes more frequently than did the patients. The ACE I/D genotype was associated with hyperlipidemia and smoking history. We consider that the DD polymorphism and D allele may affect the severity of CAD, while I allele may have a protective effect. In conclusion, the ACE I/D genotype may interact with conventional risk criteria in determining the risk of CAD.
ACE insert/delete polymorphism and atherosclerosis
Atherosclerosis, 2005
We report on the results of a large autopsy study focusing upon the hypothesis that deletion of the Alu insert in the angiotensin converting enzyme (ACE) gene is associated with: (a) greater prevalence or extent of atherosclerosis in the aorta and coronary arteries; and (b) microscopic qualities of established atherosclerotic plaques in the coronary arteries. This study was conducted in young US black (n = 290) and white (n = 379) males using available materials and data from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study, a multicenter cooperative autopsy study organized in 1985 to explore the relationships of known cardiovascular risk factors to atherosclerosis in victims of accidents, homicides, or suicides in the age range of 15-34 years.
Experimental & Molecular Medicine, 2004
The angiotensin converting enzym e (ACE) is a strong candidate gene for m yocardial infarction (M I). Insertion-deletion dim orphism in intron 16 of this gene has been inconclusively found to be associated w ith it. Several new polym orphism s in the ACE gene have been identified and am ong these, a dim orphism in exon 17, ACE G2350A, has a significant effect on plasm a ACE concentrations. To assess the value of genotyping the ACE G2350A dim orphism in a genetically hom ogeneous population, we carried out a case-control study of dim orphism G 2350A for a putative association w ith M I am ong Pakistani nationals. W e investigated a sam ple population of 370 Pakistanis, com prising 163 controls, and 207 patients w ith clinical diagnosis of acute M I (AM I). ACE G 2350A alleles w ere visualized by assays based on polym erase chain reaction and restriction endonuclease analysis. Frequencies of G alleles were 0.68 am ong controls and 0.72 am ong AMI patients. The ACE G 2350A dim orphism show ed no significant association w ith M I (χ 2 = 0.90, 2 df, P = 0.64), plasm a levels of hom ocysteine (P = 0.52) or w ith serum levels of folate (P = 0.299). The results indicate that ACE G 2350A polym orphism is not associated w ith risk of m yocardial infarction in the Pakistani population investigated here.
Clinical Science, 2004
The ID (insertion/deletion) polymorphism of the ACE (angiotensin-converting enzyme) gene controls plasma ACE levels. Both have been correlated with ISR (in-stent restenosis) in preliminary analyses, but not confirmed in larger studies. In the present study, baseline and 6-month quantitative coronary analysis were performed in 897 patients who had stent implantation and the ID polymorphism genotyped. Plasma ACE levels were measured in 848 patients (95 %). Restenosis rates among genotypes were 31.2 % DD, 25.5 % ID and 28.8 % II (not significant). Plasma ACE levels were significantly higher in restenotic patients compared with patients without restenosis (30.7 + − 18.6 units/l compared with 22.8 + − 12.8 units/l; P = 0.0001) and a strong independent predictor of ISR [OR (odds ratio) = 3.70; 95 % CI (confidence interval), 2.40-5.71; P < 0.0001], except in diabetics. In the subgroup of diabetics and patients with AMI (acute myocardial infarction), the DD genotypes actually had a lower risk of ISR than the II genotypes (diabetics, OR = 0.16; 95 % CI, 0.04-0.69; P = 0.014; and patients with AMI, OR = 0.21; 95 % CI, 0.061-0.749; P = 0.016). After exclusion of diabetics and patients with AMI, ISR rates for genotypes in 632 patients were 31.7 % DD, 24.3 % ID and 17.6 % II (P = 0.02; DD compared with non-DD OR = 1.57; 95 % CI, 1.09-2.25). The association between the D allele and ISR observed in selected populations does not hold with a larger sample size. Other than sample size, clinical variables can modulate the association between ID polymorphism and ISR. Plasma ACE level is a risk factor for ISR, independently of the ID genotype.
Cardiovascular effects of I/D angiotensin-converting enzyme gene polymorphism in healthy subjects
Acta Cardiologica, 2005
Background -An increasing number of studies with conflicting results regarding the association between angiotensin-converting enzyme (ACE) gene deletion polymorphism and cardiovascular disease has recently been published. The present prospective long-term study was conducted to evaluate whether the DD genotype could also be associated with a higher prevalence of hypertension in healthy subjects over 6∞ ∞years of follow-up. We also investigated the effects of the ACE-I/D genotypes on diastolic function by echocardiography in healthy subjects without any risk factors and any events after 6∞ ∞years of follow-up. Methods -Population: 684 healthy volunteers (aged 25-55∞ ∞ years) normotensive and free of cardiovascular diseases, with acceptable echocardiographic window were enrolled. All subjects had to have a normal electrocardiogram (ECG) and echocardiogram (ECHO) at entry.All subjects have undergone a complete physical examination, 12-lead ECG and ECHO; DNA analysis and serum cholesterol have been performed on venous blood samples. All subjects underwent a clinical evaluation each year for the 6-year duration of the study. In addition, 275 subjects without any risk factors underwent an ECHO every year of the follow-up, to check the influence of genotypes on myocardial diastolic performances. Results -All 684 subjects completed 6∞ ∞ years of follow-up.We obtained 3 genetically distinct groups: 1) the ACE-DD group (n∞ ∞ =∞ ∞225, 80 F/145 M, mean age 43.4∞ ∞±∞ ∞ 7.6∞ ∞years) with 42 hypertensive subjects (18.3%), 5 heart failure (HF) subjects and 6 subjects with acute coronary syndromes (ACS). There was no association between family history, smoking habit, hypercholesterolaemia and events. 2) the ACE-ID group (n∞ ∞=∞ ∞ 335, 116 F/219 M, mean age 43.6∞ ∞±∞ ∞7∞ ∞years) with16 hypertensive subjects (4.7%) and 3 subjects with ACS. 3) the ACE-II group (n∞ ∞=∞ ∞ 124, 45 F/79 M, mean age 42.5∞ ∞±∞ ∞6.9∞ ∞ years) with 2 hypertensive subjects (1.6%) and 1 HF subject.The incidence of hypertension and cardiovascular events, was significantly higher in the ACE-DD (53 cases, 23%) than in the ACE-ID and ACE-II groups (20 and 3 cases, 5.9% and 2.4%, respectively), p∞ ∞=∞ ∞0.0001.The higher incidence of hypertension was observed in the older age groups (36-45 and 46-55∞ ∞ years) with ACE-DD and ACE-ID genotypes. Moreover,ACE-DD significantly and early affected myocardial diastolic properties in the total group examined, also when stratified for age. There was a reduction of E/A ratio and it was more evident in subjects aged 36-45 and 46-55∞ ∞ years, p∞ ∞=∞ ∞0.0001. Conclusion -Our data suggest that ACE-DD polymorphism is associated with a higher incidence of hypertension in baseline healthy subjects, irrespective of other risk factors, and appears to affect the diastolic function. These effects were apparent predominantly in the older age groups. (Acta Cardiol 2005; 60(4): 427-435)
Atherosclerosis, 1998
Background: Presence of the D allele or homozygosity for the deletion (D) allele of the ACE insertion/deletion (I/D) polymorphism has been discussed as potent risk factor for coronary artery disease (CAD) and myocardial infarction (MI). Methods and results: In 2267 male Caucasians the relation of the ACE I/D gene polymorphism to CAD and MI were investigated. An association of the D allele to CAD was detected in younger subjects (e.g. B 61.7 years, mean value), but not in older patients (e.g. ]61.7 years). Additional exclusion of individuals with other cardiovascular risk factors (e.g. high BMI) produced an even stronger association of the D allele to CAD. In contrast, a relation of this polymorphism to non-fatal MI was only observed in older subjects; additional limitation to individuals without cardiovascular risk factors (e.g. BMI and/or diabetes) yielded a further enhancement of this association to MI. In younger subjects (e.g. B61.7 years) the gene polymorphism was not related to non-fatal MI even after exclusion of additional risk factors. Conclusions: The present large case-control study strengthens the assumption of an association of the ACE D allele with the risk of ischemic heart disease.
Journal of the Renin-Angiotensin-Aldosterone System, 2011
Angiotensin II, a vasoconstrictor and the main effector molecule of the renin-angiotensin system, is known to influence inflammation, thrombosis, low-density lipoprotein oxidation and growth factors, all of which contribute to cardiovascular disease. The associations of polymorphisms in the angiotensin-converting enzyme 2 (ACE2) gene with cardiovascular risk have not been fully determined. Single nucleotide polymorphisms (SNPs) in ACE2 were genotyped in participants of the prospective MORGAM study (n = 5092) from five cohorts: ATBC, FINRISK, Northern Sweden, PRIME/Belfast and PRIME/France. Using a case-cohort design, associations were sought between SNPs and haplotypes with cardiovascular events during follow-up (Cox proportional hazards model). The comparison group were a subset of all MORGAM participants who were selected to ensure similar age and sex distributions among the cases and controls. The A allele of the rs2285666 SNP (HR = 0.3, p = 0.04) was significantly associated with the risk of cardiovascular death in female subjects. These findings complement those found in other studies of SNPs in the ACE2 gene in relation to cardiovascular disease risk. As females carry two copies of the ACE2 gene, and given its plausible biological role in cardiovascular disease risk, further studies of ACE2 should be prioritized.
2005
ABSTRACT The present prospective long-term study was conducted to evaluate whether the DD genotype could also be associated with a higher prevalence of hypertension in healthy subjects over 6 years of follow-up. We also investigated the effects of the ACE-I/D genotypes on diastolic function by echocardiographic method in healthy subjects without any risk factors and without any events after 6 years of follow-up. 684 healthy volunteers (aged 25–55 years) with acceptable echocardio-graphic window were enrolled. Physical examination,12-lead ECG, echocardiograms and venous blood samples for DNA analysis were performed. All subjects had a clinical evaluation each year for the 6 year. In addition,275 subjects without any risk factors underwent an ECHO every year of the follow-up, to check the influence of genotypes on myocardial diastolic performances. All 684 subjects completed 6 years of follow up. We obtained 3 genetically distinct groups. ACE-DD group,(n=225,80F/145M,mean age 43.4±7.6 years),had 42 hypertensive subjects (18.3%), 5 heart failure (HF) subjects and 6 subjects with acute coronary syndromes (ACS).There was not association between family history,smoking habit,hypercholesterolemia and events.ACE-ID group: (n=335, 116F/219M, mean age 43.6±7 years),had 16 hypertensive subjects (4.7%),and 3 subjects with ACS. ACE-II group:(n=124,45/79 F/M, mean age 42.5±6.9 years),had 2 hypertensive subjects (1.6%), and 1 HF subject. The incidence of hypertension and cardiovascular events, were significantly higher in ACE-DD (53 cases, 23%) than ACE-ID and ACE-II groups (20 and 3 cases,5.9% and 2.4%, respectively), p=0.0001. The higher incidence of hypertension was observed in the older age groups (36–45 and 46–55 years) with ACE-DD and ACE-ID genotypes. Moreover, ACE-DD significantly and early affected myocardial diastolic properties in the whole examined group, also when stratified for the age. There was a reduction of E/A ratio and it was more evident in subjects aged 36–45 and 46–55 years, p=0.0001.Our data suggest that ACE-DD polymorphism is associated to a higher incidence of hypertension and appears to affect the diastolic function.