Angiotensin converting enzyme gene deletion allele is independently and strongly associated with coronary atherosclerosis and myocardial infarction.

Arbustini, Eloisa; Grasso, Maurizia; Fasani, Roberta; Klersy, Catherine; Diegoli, Marta; Porcu, Emanuele; Banchieri, Nadia; Fortina, Paolo; Danesino, Cesare; Specchia, Giuśeppe

doi:10.1136/hrt.74.6.584

Cited by 84 publications

(49 citation statements)

References 33 publications

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“…Recently, the interest in the ACE gene has increased after the reports that the homozygosity for the short allele (DD) is significantly more frequent in patients with coronary artery disease, 16 left ventricular hypertrophy, 24,25 hyperglycemia, 17 and dilated cardiomyopathy.…”

Section: Ace Gene Polymorphism and Cardiovascular Diseasesmentioning

confidence: 99%

Angiotensin-Converting Enzyme Gene Polymorphism Is Associated With Endothelium-Dependent Vasodilation in Never Treated Hypertensive Patients

et al. 1998

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Abstract-The response of the forearm vasculature to acetylcholine (7.5, 15, and 30 g/min, each for 5 minutes) and sodium nitroprusside (0.8, 1.6, and 3.2 g/min, each for 5 minutes) was evaluated in 32 never-treated hypertensive outpatients (17 men and 15 women, aged 43Ϯ7 years) and in 24 normotensive control subjects (14 men and 10 women, aged 42Ϯ6 years). Drugs were infused into the brachial artery, and forearm blood flow was measured by strain-gauge plethysmography. In both hypertensive and normotensive groups, a deletion (D)/insertion (I) polymorphism in intron 16 of the angiotensin-converting enzyme (ACE) gene was determined by polymerase chain reaction. The response to acetylcholine was significantly reduced in hypertensive patients versus control subjects: at the highest dose (30 g/min), forearm blood flow was 13.9Ϯ6.3 mL ⅐ 100 mL tissue Ϫ1 ⅐ min Ϫ1 in hypertensives versus 27.1Ϯ9.7 mL ⅐ 100 mL tissue Ϫ1 ⅐ min Ϫ1 in the controls (PϽ.001); similarly, vascular resistance was 10.6Ϯ5.6 U in hypertensive patients and 4.9Ϯ1.9 U in normotensive subjects. In the hypertensive group, the patients with DD genotype showed significantly less endothelium-dependent vasodilation compared with IDϩII genotypes (at the highest dose of acetylcholine, forearm blood flow was 12.1Ϯ4.2 versus 17.0Ϯ4.1 mL ⅐ 100 mL tissue Ϫ1 ⅐ min Ϫ1 ) (PϽ.005). The vasodilator effect of sodium nitroprusside infusions was not statistically different in DD and IDϩII hypertensive patients. In conclusion, our data suggest that ACE polymorphism affects endothelium-dependent vasodilation in hypertensive patients and confirm that hypertensive patients had a blunted response to the endothelium-dependent agent acetylcholine. (Hypertension. 1998;31:900-905.) Key Words: angiotensin-converting enzyme Ⅲ polymorphism Ⅲ endothelium Ⅲ hypertension, essential T he normal endothelium plays a key role in modulating vascular tone, preventing thrombosis, and influencing smooth muscle growth.1 The EDRF identified as nitric oxide [2][3][4][5] induces vasodilation by stimulating the activity of soluble guanylate cyclase within the vascular smooth muscle, thereby elevating tissue levels of cyclic GMP. 4 On the other hand, SNP induces endothelium-independent vasodilation through the same effector pathway by providing an inorganic source of nitric oxide. 6 Recent studies in humans have confirmed these experimental findings and have demonstrated that this regulatory action of the endothelium is exerted on resistance vessels also. However, this endothelial function is impaired in different cardiovascular diseases 8 -17 ; in particular, ACh vasodilation is reduced in hypertensive patients compared with normotensive control subjects.In addition, the RAS seems to be involved in the pathophysiology of hypertension by regulating BP, as well as fluid and electrolyte balance. For these reasons, genes coding for components of this system are attractive candidates for the investigation of the genetic basis of essential hypertension. The cloning of the ACE gene has made it possible t...

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Section: Ace Gene Polymorphism and Cardiovascular Diseasesmentioning

confidence: 99%

Angiotensin-Converting Enzyme Gene Polymorphism Is Associated With Endothelium-Dependent Vasodilation in Never Treated Hypertensive Patients

et al. 1998

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“…The same allele is known to be associated with risk of myocardial infarction at a young age, ischemic heart dis ease, etc. [10,23]. It can be suggested that the D/D geno type in placentae results in an increase of placental infarc tions and partial detachment of the placenta, and thus it could contribute to abnormalities of blood circulation in the placenta and to development of PI.…”

Section: Discussionmentioning

confidence: 99%

“…The I allele is associated with decreased ACE production compared to the D allele. An association of the D allele of with cardiovascular disease, in particular, with hypertension [22,23] and with some kinds of preeclampsia [24], has been reported. Since ACE is responsible for processes of vasoconstriction and vaso dilatation in placental tissue, it is logical to assume an association between its allelic variants and development of PI.…”

Section: Discussionmentioning

confidence: 99%

The Angiotensin-Converting Enzyme Gene Polymorphism is Associated with Pregnancy Miscarriage and Placental Insufficiency

Bespalova¹,

Иващенко²,

Тарасенко³

et al. 2007

Balkan Journal of Medical Genetics

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Research of past decades has shown that pregnancy miscarriage (PM) and placental insufficiency (PI) underlie severe obstetric pathologies that result in complications of fetal development. The occurrence of PI developed during previous PMs varied from 47.6 to 77.3%. Pregnancy mis carriage can be considered to be the clinical manifestation of PI, which is a common complication in women with a previous history of PM. Endothelial dysfunction in the mother and in the fetoplacental complex are basic causes of PI. The angiotensin-converting enzyme (ACE) plays a key role in maintenance of proper balance between vaso constriction and vasodilatation of blood vessels, and thus, in blood pressure regulation. DNA samples were geno typed for insertion/deletion (I/D) polymorphism of the ACE gene by polymerase chain reaction (PCR) assay. This study shows that the frequency of allele I of the ACE gene in DNA samples from placentae of the women with PM and PI (group 4) is twice as high than in the placentae of women with a PM history but without PI in the current pregnancy (group 3) (64.6 and 30.4%, respectively, p <0.001). Odds ratio (OR) analyses showed that the D/D genotype in placentae increases by 3-fold the risk of PI in women negative for PM history.

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“…An insertion/deletion (I/D) polymorphism in intron 16 of the ACE gene on chromosome 17q23 has been identified resulting in three genotypes: homozygous DD, II and heterozygous ID [12]. A previous study of Tiret et al [13] found, that I/D polymorphism of the ACE gene is associated with ACE level, and that subjects who carry the I allele have a lower ACE level than subjects bearing the D allele.…”

Section: Introductionmentioning

confidence: 99%

ACE I/D polymorphism in Alzheimer’s disease

et al. 2008

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Angiotensin-converting enzyme (ACE) has been reported to show altered activity in patients with neurological diseases. The recent studies found that a 287 bp insertion/deletion (I/D) polymorphism of the ACE gene may be associated with susceptibility to Alzheimer's disease (AD) but the results have been heterogenous between studies in Europe. In the present study we examined for the first time the association of ACE I/D polymorphism along with APOE genotype in 70 sporadic AD and 126 control subjects in Slovak Caucasians (Central Europe). An increased risk for AD was observed in subjects with at least one APOE*E4 allele (OR=3.99, 95% CI=1.97-8.08). No significant differences for the genotype distribution or the allele frequency were revealed comparing controls and patients for ACE gene. Gene-gene interaction analysis showed increase of the risk to develop AD in subjects carrying both the ACE DD genotype and the APOE*E4 allele (OR=10.32, 95% C.I. 2.67-39.81).

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Angiotensin converting enzyme gene deletion allele is independently and strongly associated with coronary atherosclerosis and myocardial infarction.

Abstract: ACE deletion polymorphism is strongly and independently associated with coronary atherosclerosis and, to a lesser extent, with myocardial infarction. As such, the results are analogous to what has already been reported in French white, Japanese, and Welsh coronary patients.

Cited by 84 publications

References 33 publications

Angiotensin-Converting Enzyme Gene Polymorphism Is Associated With Endothelium-Dependent Vasodilation in Never Treated Hypertensive Patients

Angiotensin-Converting Enzyme Gene Polymorphism Is Associated With Endothelium-Dependent Vasodilation in Never Treated Hypertensive Patients

The Angiotensin-Converting Enzyme Gene Polymorphism is Associated with Pregnancy Miscarriage and Placental Insufficiency

ACE I/D polymorphism in Alzheimer’s disease

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