Lack of association between angiotensin-converting enzyme gene polymorphism and type I aortic dissection

The relationship between angiotensin-converting enzyme (ACE) gene polymorphism and type I aortic dissection was examined in 205 unrelated hypertensives. A total of 94 patients underwent emergency repair due to type I aortic dissection, confirmed by computed tomography, and the remaining 111 were controls. Polymerase chain reaction was used to confirm that ACE gene polymorphism was due to insertion (I) or deletion (D) of a 287 base pair (bp) DNA sequence within intron 16. The genotype distribution and allele frequency of ACE I/D polymorphism between patients and controls were not statistically significant. When the frequency of at least one D allele carrier (DD or ID genotype) was compared with the II homozygous genotype, there was also no significant difference between the study groups. The findings revealed no association between ACE I/D polymorphism and aortic dissection. We conclude that I/D mutation of the ACE gene does not seem to be a risk factor for aortic dissection.     

Increased deformability of red blood cells is associated with a deletion polymorphism of the angiotensin-converting enzyme gene

Angiotensin-converting enzyme (ACE) plays important roles in the renin-angiotensin system. ACE converts angiotensin I to angiotensin II and also inactivates bradykinin, thereby modulating the vascular tone. A polymorphism of the ACE gene, located on chromosome 17, has been found in intron 16, and is characterized by the presence (insertion [I]) or absence (deletion [D]) of a 287-base-pair Alu repeat. Individuals with the D allele of the ACE gene have higher ACE levels and are at higher risk of cardiovascular events. We aimed to investigate the possible relationship between the I/D polymorphism of the ACE gene and hemorheological parameters, including red blood cell (RBC) deformability. The study was performed on 28 healthy young volunteers (13 women and 15 men, mean age 24 +/- 2). The prevalence of the I and D alleles was 30.4% and 69.6%, respectively. The I/I genotype (II) was found in 21.4%, I/D genotype (ID) in 17.9%, and D/D genotype (DD) in 60.7% of the subjects tested. No significant relationship between ACE I/D polymorphism and RBC aggregation or whole blood and plasma viscosity was observed. In contrast, RBC deformability was significantly increased in the subjects with the DD genotype compared with the II (p < 0.05) or the ID (p < 0.01) genotype, and in the subjects with the D allele compared with the I allele (p < 0.01). We suggest that RBC deformability of individuals with the D allele, who have higher risk for cardiovascular pathologies, may have been increased by a compensatory mechanism.     

Polymorphisms of the angiotensin-converting-enzyme gene in subjects who die from coronary heart disease

It has been shown that myocardial infarction sur vivors aremore likely to carry an insertion/deletion polymorphism (I/D)of the angiotensin-converting enzyme (ACE) gene than age-matchedpopulation controls. To test whether the association with coronary risk had been under-estimated, the frequency of the ACElID was studied in 213 fatal cases of definite and possiblemyocardial infarction which came to autopsy in the Belfast MONICAProject area. In comparison to controls from the same population,the autopsy cases had an increased frequency of the ACE D allele(p<0.02). The overall odds ratios were 2.2 for DD vs. II,and 1.8 for ID vs II (test for trend p=0.01). The findings bearout the hypothesis that the ACE l/D polymorphism is a risk factorfor fatal myocardial infarction and sudden cardiac death.     

晚发性抑郁症与血管紧张素转化酶基因多态性关系研究

目的探讨晚发性抑郁症(LOD)与血管紧张素转换酶(ACE)基因第16内含子中Alu重复序列的插入/缺失(In-sertion/Deletion,I/D)多态性的关系。方法入组183例60~85岁老年人,晚发性抑郁症组(93例,下称LOD组)和正常对照组(90例,下称对照组),用聚合酶链式反应(PCR)法进行ACE基因I/D多态性分型。结果LOD组和对照组间基因型频率及等位基因频率分布差异无显著(χ2=0.241,P=0.886;χ2=0.127,P=0.722),各基因型亚型患者在年龄、性别、发病次数、病程、HAMD评分、有无精神病性症状、有无自杀企图间差异无显著(P均>0.05)。结论ACE基因I/D多态性与晚发性抑郁症无显著相关性。     

Angiotensin-converting enzyme insertion/deletion polymorphism is associated with severe hypoxemia in pediatric ARDS

Purpose  

The D allele of the insertion/deletion (I/D) polymorphism of a 287-bp sequence in the angiotensin-converting enzyme (ACE) gene has been associated with an increased activity of this enzyme. Its role in susceptibility to acute respiratory distress syndrome (ARDS) has not been well defined. We hypothesized that ACE I/D genotype in pediatrics is associated with ARDS and plasma levels of angiotensin II.     

Angiotensin I-converting enzyme gene polymorphism and drug response.

An insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene has been described in chromosome 17q23 of the human genome. Subjects with the genotype DD have markedly higher plasma ACE levels than those with genotype II; although ACE concentration in plasma is not rate-limiting for the production of angiotensin II, it has been suggested that the renin-angiotensin system may have an enhanced role in cardiovascular homeostasis in subjects with DD genotype or D allele. Meta-analysis confirmed the association of the D allele with an increased risk of myocardial infarction and stroke, but these relations are still uncertain with longevity and renal deterioration. Otherwise, I allele seems to be related with an improved response to physical training. The I/D polymorphism of the ACE gene is not a marker for any form of hypertension, though some conflicting results have been described. Nevertheless this polymorphism may have an influence on the antihypertensive response, particularly when using ACE inhibitors (ACEI). For example, blood pressure normalization with captopril in patients suffering from cardiac failure would be more effective in II genotype; conversely, both regression in left ventricular hypertrophy and improvement in diastolic filling would be greater after long-term treatment with enalapril in patients with essential hypertension and DD genotype. Conflicting results were also described using ACEI as a renoprotective therapy. This review therefore supports the justification for further evaluation in appropriately powered studies.     

ACE I/D polymorphism study in a Cuban hypertensive population

BACKGROUND: The angiotensin converting enzyme (ACE) is a key protein of the renin angiotensin system, whose main function is the conversion of angiotensin I to II. ACE is involved in the physiological control of blood pressure and it is a candidate gene for essential hypertension in humans. We tested the relevance of the ACE insertion/deletion (I/D) polymorphism in our population. METHODS: We recruited 243 hypertensive and 407 normotensive subjects in the city of Havana, matched according to age, sex and ethnic group. The ACE (I/D) polymorphism was determined by the polymerase chain reaction (PCR) technique. The fit of genotype frequencies to Hardy-Weinberg proportions was evaluated in all groups analyzed. The possible association between the ACE I/D polymorphism and hypertension status was tested by chi2 and odds ratio tests. RESULTS: All groups but black female cases were in Hardy-Weinberg equilibrium. The frequencies of the D allele in hypertensive/normotensive subjects were 0.61/0.59 in white males, 0.58/0.58 in white females, 0.47/0.59 in black males and 0.58/0.54 in black females. The distribution of ACE genotypes differed significantly between cases and controls only in black women according to the additive model (chi2p=0.04) but the adjusted OR did not show significant association (OR 1.14 95% CI 0.62 to 2.10). CONCLUSION: The ACE I/D polymorphism was not associated with hypertension in our multiethnic sample. While the chi2 test for additive model in black women suggested a marginal significance, the adjusted OR did not show any significant association.     

The relationship between ACE insertion/deletion polymorphism and coronary artery disease with or without myocardial infarction

OBJECTIVES: Presence of the D allele or homozygosity for the deletion (D) allele of the angiotensicen-converting enzyme (ACE) insertion/deletion (I/D) polymorphism has been discussed as potent risk factor for coronary artery disease (CAD) and myocardial infarction (MI). The D allele is associated with higher levels of circulating ACE and therefore may predispose one to cardiovascular damage. DESIGN AND METHODS: The study presented here was performed to investigate the association between the ACE genotype and ACE levels. The study group was comprised of 118 angiographically verified CAD patients. 65 patients were MI (+) and 53 patients were MI (-) in this group. A total of 70 healthy individuals were taken as controls. Genomic DNA of 188 subjects was extracted from whole blood. The polymerase chain reaction was used for ACE genotyping, and ACE levels were measured by ELISA. RESULTS: The D allele was found to be significantly more frequent in patients with MI (+) compared with controls (P = 0.024). ACE levels were significantly higher in both MI (-) and MI (+) groups with CAD patients than in controls (P < 0.005). Plasma ACE level was higher in all three groups in the DD genotype compared to II genotype. In groups I and III, this was statistically significant (P < 0.0001, P < 0.01). CONCLUSIONS: It was shown that the I/D polymorphism in the gene for ACE is a genetic risk factor for CAD patients who have a history of MI. ACE insertion/deletion gene polymorphism is also associated with plasma ACE levels in CAD patients with a history of MI.     

血管紧张素转化酶基因多态性与老年高血压及合并糖尿病的相关性研究

目的 探讨血管紧张素转化酶(ACE)基因插入/缺失(I/D)多态性与老年人原发性高血压及合并糖尿病患者的关系.方法 应用聚合酶链反应(PCR)技术对60名正常对照组,105例老年高血压患者,38例老年高血压合并糖尿病患者进行ACE基因I/D多态性检测.结果 老年高血压患者中的DD基因型频率(0.352)和等位基因频率(0.543),老年高血压合并糖尿病患者的DD基因型频率(0.421)和等位基因频率(0.579)均明显高于正常对照组的0.133和0.250,而老年高血压组与老年高血压合并糖尿病组患者的DD基因型频率和D等位基因频率之间的差别无显著性.结论 ACE基因缺失型是老年高血压的危险因素,但ACE基因缺失不是糖尿病的危险因素之一.     

The D allele of angiotensin I-converting enzyme gene insertion/deletion polymorphism is associated with the severity of atherosclerosis

BACKGROUND: Angiotensin II is produced primarily by angiotensin I-converting enzyme (ACE) within atherosclerotic lesions and ACE level in plaques correlates with the severity of vessel wall damage. Therefore, we investigated the possible association of ACE gene insertion/deletion (I/D) polymorphism and the severity of atherosclerosis, estimated on the basis of the number of coronary stenoses and critical arterial occlusions observed during coronary angiography. METHODS: The study cohort included 172 patients with angiographically confirmed premature coronary artery disease. The ACE gene I/D polymorphism was genotyped using a PCR method. RESULTS: The frequencies of DD genotype, D allele carrier-state (DD+ID genotypes) and the D allele increased with the number of stenoses in coronary vessels. D allele carriers (DD+ID genotypes) were more frequent in the subgroup of patients with stenoses in at least four coronary vessels than in other patients including subjects with one-, two- and three-vessel disease (97.4% vs. 74.4%, OR=13.05, 95% CI: 1.81-100.00, chi2=9.84, p=0.0017). Furthermore, the D allele was significantly more frequent in patients with critical arterial occlusions (>90%) than in subjects without critical stenoses (61.1% vs. 49.3%, chi2=9.84, p=0.023). CONCLUSIONS: The ACE I/D polymorphism influences individual differences in severity of coronary artery disease and the D allele promotes generation of numerous and critical atherosclerotic lesions.     

东莞市T2DM患者与健康人ACE基因多态性研究

目的研究血管紧张素转换酶基因插入（I）／缺失（D）多态性在东莞市T2DM患者与健康人中的分布。方法采用限制性片段长度多形态多聚酶链式反应（PCR—RFLP）技术对东莞市200例T2DM患者和93例健康者进行ACE基因内含子16插入／缺失（I／D）多态性检测。结果东莞市T2DM患者ACEDD、Ⅱ、ID基因型分布频率分别为8．5％、46．0％和45,5％．等位基因频率分别为I：68,8％、D：31．2％。健康对照组的频率分别为19．4％、35．5％和45,2％．等位基因频率分别为1：58,1％、D：41．9％。T2DM患者与健康对照组比较,I等位基因频率显著增高,而D等位基因频率显著降低（P％0,05）。结论ACE基因多态性是致T2DM的遗传危险因素之一。     

ACE 基因 I/D 多态性与动脉血栓性脑梗死的关联性研究

目的研究血管紧张素转换酶（ACE）基因I/D多态位点与动脉血栓性脑梗死的关联性及相关机制。方法选取动脉血栓性脑梗死患者112例和年龄、性别匹配的对照组180例,采用PCR-AFLP技术对ACE基因I/D位点进行分型。 结果单因素分析提示病例组收缩压水平（138.1±19.7 mmHg）显著高于对照组（126.6±20.6 mmHg）（t=4.716,P<0.001）;病例组舒张压水平（88.9±10.1 mmHg）显著高于对照组（79.9±10.0 mmHg）（t=7.450,P<0.001）。病例组中ACE基因I/D位点D等位基因频率和DD基因型频率分布均显著高于对照组（等位基因:χ2=4.953,P=0.026; 基因型:χ2=6.303,P=0.043）。病例组和对照组中ACE基因I/D位点基因型DD携带者收缩压及舒张压水平显著高于基因型ID及II携带者。 结论ACE基因I/D位点等位基因D可能是汉族人群动脉血栓性脑梗死遗传易感基因。等位基因D可能通过升高个体血压的机制导致动脉血栓性脑梗死发生。       

Frequency of angiotensin-converting enzyme gene polymorphism in Turkish hypertensive patients

Hypertension is a multifactorial disease, in which genetic factors play an important role. This study was carried out to determine angiotensin-converting enzyme levels and angiotensin-converting enzyme gene polymorphism in Turkish hypertensive patients, and to establish whether there is an association of angiotensin-converting enzyme gene polymorphism with clinical and echocardiographic parameters. We have investigated the association among the allelic distribution of the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme gene identified by polymerase chain reaction, angiotensin-converting enzyme activity determined spectrophotometrically, cardiac morphology and function assessed by means of echocardiography. Distribution of angiotensin-converting enzyme gene I/D polymorphism and allele frequencies in hypertensive patients was not significantly different from controls. D allele frequency was 51.7% in hypertensives vs. 51.9% in controls and I allele 48.3 vs. 48.1%, respectively. The level of angiotensin-converting enzyme activity was significantly higher in the patients homozygotes for D allele (DD = 59.93 U/l) than in heterozygotes (ID = 39.49) and in homozygotes for I allele (II = 40.28 U/l). In addition to these, the level of angiotensin-converting enzyme activity was significantly lower in the ID and especially II patients receiving ACE inhibitors than the others. Also, it was determined that left atrium diameter was larger in the patients homozygotes for I allele than the others.     

汉族人群血管紧张素转换酶基因插入/缺失(I/D)的遗传多态性

背景:血管紧张素转换酶是肾素-血管紧张素-醛固酮系统的重要组成部分,血管紧张素转换酶基因第16内含子内存在一个287bp的Alu序列的插入/缺失(I/D)多态性,与心血管疾病、IgA肾病等疾病的发生具有一定的相关性。目的:分析汉族人群血管紧张素转换酶基因插入/缺失(I/D)多态性的分布,并与已知的其他种族人群进行比较。设计:以健康汉族人为观察对象的观察性实验。单位:江苏省临床免疫学重点实验室,苏州大学附属第一医院检验科,江苏大学医学技术学院检验系。对象:受检者为2005-12/2006-01苏州大学附属第一医院门诊健康体检者241名,男152名,女89名,平均年龄(27±8)岁,均为无血缘关系的苏州地区汉族人,经临床及实验室检查确认排除肝、肾、内分泌、心脑血管疾病。方法:应用聚合酶链反应检测了241名汉族健康体检者血管紧张素转换酶基因I/D多态性等位基因的基因型,并采用荧光标记末端终止法对基因型为D/D、I/I的PCR纯化产物进行DNA测序确认。主要观察指标:血管紧张素转换酶基因I/D基因型,等位基因频率以及与其他种族人群的比较。结果:241名受检者全部进入结果分析。①血管紧张素转换酶的基因型表现为缺失纯合子(DD)、插入纯合子(II)以及缺失和插入杂合子(DI),等位基因D较等位基因Ⅰ缺失一段287bp的核苷酸,即Alu序列。②II,ID,DD基因型频率分别为46.1%,41.5%,12.4%;等位基因I,D频率分别为66.8%,33.2%。③日本人与汉族人群血管紧张素转换酶基因型分布相似,均以II型最常见,DD型最少;欧美人群以ID居多,II型较少。汉族人群与日本人及欧美人群血管紧张素转换酶基因型频率的分布具有种族差异性。与其他各民族人群比较,汉族人群等位基因I显著高于上述各民族(χ2=105.55,P<0.01),等位基因D明显较低(χ2=87.54,P<0.01)。结论:血管紧张素转换酶基因多态性具有种族差异性。了解不同种族人群间血管紧张素转换酶基因多态性的遗传特点,是研究血管紧张素转换酶基因I/D多态性与疾病相关性的基础和前提。     

No association found between the insertion/deletion of a 287-bp alu repeat sequence within intron 16 of the angiotensin-I-converting enzyme (ACE) gene in Mexican patients and binary restenosis after coronary stenting

BACKGROUND: It has been suggested that the incidence of coronary restenosis after a percutaneous coronary intervention is much higher in patients with a 287-bp alu repeat sequence within intron 16 of the angiotensin-I-converting enzyme (ACE) gene (deletion allele) than in others, but published studies are conflicting. METHODS: The presence (insertion) or absence (deletion) of a 287-bp alu repeat sequence within intron 16 of the ACE gene (I/D polymorphism) was analyzed by polymerase chain reaction in a group of 168 patients with coronary artery disease who underwent coronary artery stenting. Basal and procedure coronary angiographies were analyzed searching for angiographic predictors of restenosis and follow-up angiography was analyzed looking for binary restenosis. RESULTS: Distribution of angiotensin converting enzyme I/D polymorphisms was similar in patients with and without restenosis. Similar results were observed when the analysis was made considering the type of stent implanted. On the other hand, the whole group of coronary artery disease patients showed increased frequencies of the D allele (p=0.00001, OR=2.17, 95% CI=1.49-3.16) and ID genotype (p=0.0002, OR=2.58, 95%CI=1.49-4.47) when compared to healthy controls. CONCLUSIONS: Genetic variations of the ACE gene could be a genetic factor related to coronary artery disease in the Mexican mixed racial ancestry individuals, but do not support its role as a risk factor for developing restenosis after coronary stenting.     

Angiotensin-converting enzyme insertion/deletion polymorphism and polyneuropathy in type 2 diabetes without macroalbuminuria

Angiotensin-converting enzyme (ACE) gene polymorphism is thought to be a potent risk factor for nephropathy and retinopathy in diabetes. We investigated the association between polyneuropathy and gene polymorphisms of both the ACE insertion/deletion (I/D) and angiotensinogen (AGT) M235T genes in 84 type 2 diabetic patients without macroalbuminuria (21 with polyneuropathy and 63 without). ACE genotype distribution did not differ significantly between patients with and without polyneuropathy, but the frequency of the I allele was significantly higher in those with polyneuropathy than in those without. In contrast, neither the genotype distribution nor the allele frequencies of the AGT gene differed between the two groups. In logistic regression analysis using a D-additive model, the D allele had a protective effect on polyneuropathy (odds ratio [OR], 0.34; 95% confidence interval [CI], 0.13-0.88). A D-dominant model hypothesis also gave a significant OR (0.28; 95% CI, 0.09-0.90). ACE I/D polymorphism, but not AGT M235T polymorphism, may affect polyneuropathy development in type 2 diabetes without macroalbuminuria.     

蒙古族人群血管紧张素转换酶基因多态性与高血压的关系

背景有关血管紧张素转换酶基因多态性与高血压关系的研究已有报道,但在蒙古族人群中尚不十分清楚.蒙古族是高血压患病率较高的民族,因此有必要探讨蒙古族人群中血管紧张素转换酶基因多态性与高血压的关系.目的探讨蒙古族人群血管紧张素转换酶基因多态性与高血压的关系.设计采用现况调查的方法.地点和对象选择内蒙古自治区通辽市科左后旗朝鲁吐苏木作为本研究现场,所有研究对象均为在此长期居住的蒙古族居民.共获得有高血压家族史的高血压者51例、血压正常者32例和没有高血压家族史的高血压者64例、血压正常者85例.干预应用聚合酶链式反应检测血管紧张素转换酶基因的插入/缺失多态性.主要观察指标血管紧张素转换酶多态性基因型频率和I、D等位基因频率.结果血管紧张素转换酶基因的三种基因型(II,ID,DD)在4组人群间的分布差异无显著性意义(P＞0.1).在4组人群中均表现出ID基因型频率最高,其次为Ⅱ基因型,DD基因型频率最低.I,D等位基因在4组人群间的分布也差异无显著性意义(P＞0.1).在4组人群中I等位基因频率均高于D等位基因频率.结论血管紧张素转换酶基因I/D多态性与蒙古族高血压的发生无关联.     

血管紧张素转化酶及血管紧张素Ⅱ-1型受体基因多态性与高血压相关性

目的 探讨血管紧张素转化酶(ACE)基因插入/缺失(I/D)多态性、血管紧张素Ⅱ-1型受体(AT1R)基因A1166C多态性与原发性高血压(EH)的相关性,以及多种危险因素与EH的关系.方法 选取125例健康者(对照组)和148例EH患者(EH组)作为研究对象作问卷调查、医学体检和血液生化项目检测,应用聚合酶链反应(PCR)技术检测研究对象ACE基因的I/D多态性;应用PCR、限制性内切酶酶切的方法检测AT1R基因A1166C多态性,并用Logistic回归筛选高血压的危险因素.结果 EH组和对照组的DD基因型频率和D等位基因频率差异均不显著.EH组的AC基因型频率23.0%,C等位基因频率11.5%,均显著高于对照组的12.8%和6.4%.EH组ACE基因DD型+AT1R基因AC型联合基因型频率7.4%,显著高于对照组的1.6%.多因素Logistic回归结果表明,EH的危险因素主要有BMI、EH家族史和DD+AC联合基因型.结论 ACE基因D等位基因可能与EH发病无关联;AT1R基因A1166C多态性可能是EH的重要遗传因素;DD+AC联合基因型对EH的发病有显著的联合促进作用.     

The link between angiotensin-converting enzyme genotype and pulmonary artery pressure in patients with COPD

OBJECTIVE: The insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been associated with an increased risk of cardiovascular diseases. In patients with primary pulmonary hypertension, the homozygous ACE DD genotype is more prevalent than the non-DD genotype. However, the relationship of ACE gene polymorphism to secondary pulmonary hypertension remains unclear, and ethnicity may be one of the factors that can modulate the effects of ACE genotypes reported in different studies. We hypothesized that in patients with chronic obstructive pulmonary disease (COPD) the presence of the D allele in the ACE gene polymorphism is associated with increased pulmonary artery pressure (Ppa). PATIENTS AND METHODS: Bodyplethysmography was used to assess lung function in 66 consecutive patients with COPD; pulmonary artery pressures were determined using echocardiography. ACE gene I/D polymorphism was identified with the polymerase chain reaction. 118 healthy persons served as the control group. All patients and controls were Caucasian. Genotype II was identified in 15 patients with COPD, genotype ID in 31 and genotype DD in 20. In the control group, genotype II was identified in 19 persons, genotype ID in 68 and genotype DD in 31. The distribution of ACE gene polymorphism did not differ between patients and the control group. RESULTS: In patients with COPD, no differences were seen between the three genotype groups in mean age, smoking history, hemoglobin concentrations or ventilometric or blood gas variables. Both systolic and mean Ppa differed significantly between the II, ID and DD groups (Systolic Ppa: 24.4 +/- 2.2 versus 31.3 +/- 2.5 and 36.7 +/- 3.9 mm Hg, respectively, ANOVA, p < 0.05; Mean Ppa: 13.0 +/- 1.5 versus 17.5 +/- 1.4 and 21.2 +/- 2.8 mm Hg, respectively, ANOVA, p < 0.05). In multiple linear regression analysis, the I/D ACE gene polymorphism (p < 0.05), SaO2 (p < 0.05) and the duration of COPD (p < 0.02) were independent predictors of systolic and mean Ppa. CONCLUSION: The results of the study suggest that I/D ACE gene polymorphism is linked to pulmonary artery pressure in Caucasian patients with COPD.     

肾素-血管紧张素系统基因多态性与冠状动脉血栓疾病

为了观察中国人群中肾素-血管紧张素系统基因多态性的分布特征，并分析这些基因多态性与冠状动脉血栓(CATD)疾病的相关性以及该基因多态性间的相互作用，采用直接聚合酶链式反应(PCR)和PCR-限制性片段长度多态性(PCR—RFLP)方法对192例冠状动脉血栓疾病患者和110例对照组个体进行血管紧张素转换酶(ACE)、血管紧张素原(AGT)和血管紧张素II I型受体(AT1R)基因的基因多态性进行检测。结果表明：①在中国人群中，ACE基因各基因型分布分别为DD12．2％、ID43．9％和II43．9％；AGT基因各基因型分布为MM8．2％，MT36．7％和TT55．1％；AT1R基因各基因型分布分别为AA91．8％和AC8．2％。②冠状动脉血栓疾病组与对照组相比，上述3种基因多态性的分布均无明显差异。③同时携带AT1R—AC和AGT—TT基因型的个体，与AT1R—AA和AGT—TT基因型个体相比，罹患CATD的相对危险度达到3．517(95％C10．988—12．527)；与AC基因型和非TT基因型个体相比，罹患CATD的危险性可增加至15．000(95％CI 1．940—115．963)；在AT1R—AC基因型个体，等位基因D在CATD组和对照组的分布亦存在有明显的差异(P=0．017)。结论：我国人群ACE基因I／D多态性、AGT基因M235T多态性和ATlR基因A1166C多态性各基因型和等位基因的分布明显不同于西方人群；上述3种基因多态性不是我国人群冠状动脉血栓疾病或心肌梗塞的独立的危险因素。但AT1R基因AC基因型与AGT基因TT基因型、AT1R基因AC基因型和ACE基因等位基因D在罹患冠状动脉血栓疾病的危险性上有显著的协同作用。