Angiotensin-Converting Enzyme Insertion/Deletion Polymorphism and Cerebrovascular Disease

Catto, Andrew J.; Carter, Angela M.; Barrett, Jennifer H.; Stickland, M. H.; Bamford, John; Davies, J. A.; Grant, Peter J.

doi:10.1161/01.str.27.3.435

Cited by 110 publications

(90 citation statements)

References 22 publications

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“…118 In clinical-genetic studies, the ACE I/D genotype has been associated with ischemic stroke in hypertensives, 119 the DD genotype with lacunar stroke, 120 and low ACE activity at stroke presentation and the D allele with increased risk of early death from acute cerebral infarction. 121 There has been inconsistent results for angiotensinogen mutations M235T and T174M for ischemic stroke, 122 and there is an association with the B haplotype of the angiotensinogen promotor gene in absence of the wild-type A haplotype as a susceptibility factor for microangiopathy-related cerebral damage. 123 Angiotensin-Converting Enzyme Inhibitors ACE-I were introduced for the treatment of high blood pressure in the United States in the1970s.…”

Section: Renin-angiotensin System and Strokementioning

confidence: 99%

Stroke Prevention Therapy Beyond Antithrombotics: Unifying Mechanisms in Ischemic Stroke Pathogenesis and Implications for Therapy

Gorelick

2002

Stroke

196

115

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Background — It is estimated that about half of cardiovascular disease risk is explained by conventional risk factors. The realization that atherosclerosis is an inflammatory disease has led to a search for new stroke and cardiovascular disease risk factors and treatments. As such, the vulnerable atherosclerotic plaque has become the main focus for new medical strategies for plaque stabilization and stroke prevention. Summary of Review — In this invited review, I discuss inflammation as a possible risk factor for stroke, unifying mechanisms in ischemic stroke pathogenesis, and new avenues for stroke prevention—statin agents, angiotensin-converting enzyme inhibitors, and vitamins. These new stroke prevention therapies may help to reduce inflammation, serve to stabilize the atherosclerotic plaque, or act by other protective mechanisms. Conclusion — Beyond the traditional antithrombotic agents, statin agents, angiotensin-converting enzyme inhibitors, and vitamins may prove to be important additions to our armamentarium for stroke prevention.

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Section: Renin-angiotensin System and Strokementioning

confidence: 99%

Stroke Prevention Therapy Beyond Antithrombotics: Unifying Mechanisms in Ischemic Stroke Pathogenesis and Implications for Therapy

Gorelick

2002

Stroke

196

115

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“…A strong association between the DD genotype and the D allele with ischemic stroke (IS) was revealed in a number of studies, [7][8][9][10] while others showed no such association. [11][12][13][14] Siera et al [15] investigated a possible association between 3 different genetic polymorphisms of RAS and the presence of cerebral white matter lesions (WML) in 60 never-treated essential hypertensive patients (36 men, 24 women), aged 50 to 60 years, without clinical evidence of target organ damage.…”

Section: Discussionmentioning

confidence: 99%

The ACE Gene Insertion/Deletion Polymorphism and Cerebrovascular Diseases in Uzbek Patients with Arterial Hypertension

Makhkamova¹,

Khamidullaeva²

2016

Int J Biomed

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The aim of the present study was to investigate the association between the ACE gene I/D polymorphism and the development of hypertensive encephalopathy (HE) in Uzbek patients with hypertension (HT).Materials and methods: The study included 91 male patients aged from 32 to 74 years (mean age 52.5±9.2) with HT Grade 1, 2 and 3 (ESH/ESC, 2013) and presence of HE. All patients were checked on office BP using Korotkov's method and ambulatory blood pressure monitoring (ABPM). Intima-media thickness (IMT) of the carotid artery was measured by a 7.5 MHz high-resolution ultrasound. Genomic DNA was isolated from peripheral blood using the Diatom TM DNA Prep 200 Kit according to the manufacturer's protocol. ACE gene I/D polymorphism genotypes were determined by PCR.Results: Among HT patients with HE, we have identified a statistically significant predominance of ID genotype carriers (65.9%) against carriers of the II genotype (18.7%) and DD genotype (15.4%) (P=0.000); the frequency of I and D alleles was 51.6% and 48.4%, respectively (P>0.05). Comparative analysis showed a possible association between the ID genotype/D allele and HE development in HT patients, according to the general model (OR=6.36; 95%CI: 3.04 -13.31; P=0.000) and multiplicative model (OR=2.02; 95%CI: 1.25-3.27; P=0.004) of inheritance. High grades of HT were predominant in carriers of the DD genotype. IMT was significantly higher in carriers of the DD genotype than in carriers of the II and ID genotypes. The carriage of D allele was associated with the highest levels of TC, TG, and VLDL-C. Carriers of the DD genotype were characterized by higher values of daytime SBP, nighttime SBP variability and nighttime SBP load. (Int J Biomed. 2016;6(3):174-178.).

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“…[7][8][9][10][11] The previously established difference in levels of plasma ACE activity between BN and LE rats 12 offers the opportunity to study a possible predictive role for the genetically determined basal plasma ACE activity in ICV pathology in the rat. This was investigated in 2 consecutive series of BC(F1XBN) rats.…”

Section: Discussionmentioning

confidence: 99%

“…4 An association between ACE polymorphism and various cardiovascular disorders has been investigated, 5,6 and conflicting results were obtained for the association between ACE gene polymorphism and stroke in humans. [7][8][9][10][11] Different levels of plasma ACE activity have also been demonstrated in various strains of rats and shown to be primarily genetically determined. 12 Indeed, plasma ACE activity levels are higher in the BN rat, which is also prone to intracerebral vascular lesions, than in the LE rat.…”

Section: See Editorial Comment Page 2684mentioning

confidence: 99%

Heritability of Intracerebral Hemorrhagic Lesions and Cerebral Aneurysms in the Rat

Coutard

Wei

Osborne-Pellegrin

2000

Stroke

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Background and Purpose-Under certain conditions, the Brown Norway (BN) rat is susceptible to intracerebral hemorrhagic vascular (ICV) lesions within the cerebral cortex, whereas the Long-Evans (LE) rat is prone to develop aneurysms in the circle of Willis. The incidence of these 2 pathological phenotypes was studied in progeny of different BNXLE crosses to determine their heritability in these new rat models. In addition, a possible link between ICV lesion occurrence and either the susceptibility to spontaneous rupture of the arterial internal elastic lamina (IEL) or basal plasma angiotensin-converting enzyme (ACE) activity was also studied in back-cross (BC) F1XBN rats, the only second-generation group with a high incidence of ICV lesions. Methods-To induce cerebrovascular lesions, rats were submitted to experimental hypertension associated with ligation of 1 carotid artery. After death, the brain was examined for cerebral lesions. Numbers of arterial IEL ruptures were determined microscopically with the use of en face preparations. Plasma ACE activity was determined before the induction of hypertension. Results-In general, groups that developed ICV lesions presented a low incidence of aneurysms. ICV lesion incidence was similar in F1 hybrids and BC(F1XBN) and greatly decreased in F2 and BC(F1XLE) rats compared with BN rats. No cerebral aneurysms developed in F1 rats. Aneurysmal incidence was 24% (20% ruptured) in LE, 42% (59% ruptured) in F2, and 50% (75% ruptured) in BC(F1XLE) rats. In BC(F1XBN) rats, neither the incidence of IEL rupture nor the plasma ACE activity was higher in the rats with ICV lesions. However, the mean blood pressure level was higher in these rats, and peak blood pressure was higher in rats with the most severe grades of ICV lesions. Conclusions-These data suggest a polygenic and dominant mode of inheritance of ICV pathology. The formation of aneurysms in the circle of Willis tended to be favored, and their rupture was clearly increased by the presence of BN rat alleles within the LE rat genome. These data may provide the basis for future studies to determine, in new rat models, which genes are involved in these pathologies. (Stroke. 2000;31:2678-2684.)

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Angiotensin-Converting Enzyme Insertion/Deletion Polymorphism and Cerebrovascular Disease

Abstract: Low ACE activity at sroke presentation and possession of the D allele may be associated with increased risk of early death from acute cerebral infarction.

Cited by 110 publications

References 22 publications

Stroke Prevention Therapy Beyond Antithrombotics: Unifying Mechanisms in Ischemic Stroke Pathogenesis and Implications for Therapy

Stroke Prevention Therapy Beyond Antithrombotics: Unifying Mechanisms in Ischemic Stroke Pathogenesis and Implications for Therapy

The ACE Gene Insertion/Deletion Polymorphism and Cerebrovascular Diseases in Uzbek Patients with Arterial Hypertension

Heritability of Intracerebral Hemorrhagic Lesions and Cerebral Aneurysms in the Rat

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