Does the Angiotensin-Converting Enzyme (ACE) Gene Polymorphism Affect Rate of Abdominal Aortic Aneurysm Expansion?

Yeung, J.M.C.; Heeley, Mary E.; Gray, Stuart R.; Lingam, M K; Manning, George W.; Nash, J.R.; Donnelly, Richard

doi:10.1053/ejvs.2002.1693

Cited by 20 publications

(21 citation statements)

References 16 publications

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“…The presence of the insertion leads to decreased ACE activity in plasma. ACE I/D genotype failed to associate with the incidence and rate of AAA expansion in Japanese and British studies, respectively [36,37]. When the subject pool was restricted to normotensive individuals, the DD genotype was found to be more common in AAA patients compared with controls [38].…”

Section: Evidence Linking Angiotensin Peptides To Human Abdominal Aormentioning

confidence: 91%

Angiotensin II and abdominal aortic aneurysms

Daugherty

Cassis

2004

Current Science Inc

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Abdominal aortic aneurysms (AAAs) have devastating effects on the morbidity and mortality of a large portion of the elderly population. Current therapeutic options for AAAs are limited to surgical approaches, because there are no proven pharmacologic treatments. Recently, there is evolving evidence that angiotensin II (Ang II) participates in the initiation and propagation of AAAs. Animal studies have consistently demonstrated the ability of Ang II to promote the formation of AAAs, although the mechanisms of this effect have not been defined. Further definition of the role of the renin-angiotensin system in AAA formation and progression will identify potential therapeutic strategies for treatment of this disease.

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Section: Evidence Linking Angiotensin Peptides To Human Abdominal Aormentioning

confidence: 91%

Angiotensin II and abdominal aortic aneurysms

Daugherty

Cassis

2004

Current Science Inc

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“…Because the D allele of the ACE gene is associated with increased serum levels of circulating ACE, investigators suggested that ACE gene polymorphism may be useful as a marker or predictor of human AAA formation [40]. However, another study failed to find any relationship between ACE I/D polymorphism and AAAs [41]. The controversy between these two ACE polymorphism studies may be partially attributable to different populations and a small number of patients.…”

Section: Ras and Human Aaasmentioning

confidence: 99%

The role of the renin-angiotensin system in aortic aneurysmal diseases

Lü¹,

Rateri²,

Cassis³

et al. 2008

Current Science Inc

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The renin-angiotensin system has been invoked in the development of both abdominal and thoracic aortic aneurysms. This has been demonstrated experimentally by the chronic subcutaneous infusion of angiotensin II, which consistently leads to development of abdominal aortic aneurysms (AAAs) in mice. Angiotensin II-induced AAAs have highly heterogenous cellular and extracellular matrix characteristics throughout the aorta that change markedly with infusion duration. The mechanistic basis for the reproducible location of AAA development has not been elucidated, but many insights have been provided, especially regarding receptor and inflammatory mechanisms. A recent clinical study provided limited evidence for extrapolating these results to mechanisms of human AAAs. Experimental evidence has also demonstrated that antagonism of angiotensin II type 1 (AT1) receptors prevents ascending aortic aneurysms in a murine model of Marfan's syndrome. A clinical study is currently ongoing to demonstrate the efficacy of AT1 receptor antagonism in humans.

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“…Two studies have found that ACE polymorphisms resulting in elevated levels of ACE are associated with a predisposition for developing AAAs in normotensive [177] and hypertensive patients [86]. However, Hamano et al found no differences in the distribution of ACE genotypes in patients affected by AAA [178] and Yeung et al found no difference in ACE polymorphism and AAA expansion rate [179]. When comparing genetic studies of this nature, it must be remembered that the conflicting results may be due to variance of polymorphism, and it's subsequent impact, in populations with differing genetic backgrounds…”

Section: Consequences Of Ace Polymorphismmentioning

confidence: 99%

Pharmacotherapy of Abdominal Aortic Aneurysms

Dawson¹,

Choke²,

Sayed³

et al. 2006

CVP

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Aortic aneurysms account for 10,000 deaths annually in the UK, due to rupture. At present the only effective therapeutic strategy to treat abdominal aortic aneurysms is to surgically repair them; this carries an elective mortality of up to 10%. Recent advances in vascular biology have led to a greater understanding of the pathophysiological process that causes aortic aneurysms to expand and rupture. Key pathological processes include widespread aortic inflammation, proteolytic degradation of the extracellular matrix, neovascularisation and generation of reactive oxygen species. Identification of these processes has lead to pharmacological strategies to prevent aneurysm expansion and rupture. Many of these strategies have undergone proof of concept in animal models and some have now entered clinical trials. This review outlines current thinking regarding the molecular events leading to aneurysm expansion and explains how these processes may be inhibited. Experimental data on agents retarding aneurysm expansion in animal models are discussed. A significant proportion of the review details pharmacological agents that have undergone or are undergoing clinical trials. Pharmacological treatment for abdominal aneurysms is urgently required given the number of small aneurysms being diagnosed by screening programmes. This is a rapidly evolving field and one in which translation from experimental research to clinical practice is anticipated within 5 years.

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Does the Angiotensin-Converting Enzyme (ACE) Gene Polymorphism Affect Rate of Abdominal Aortic Aneurysm Expansion?

Cited by 20 publications

References 16 publications

Angiotensin II and abdominal aortic aneurysms

Angiotensin II and abdominal aortic aneurysms

The role of the renin-angiotensin system in aortic aneurysmal diseases

Pharmacotherapy of Abdominal Aortic Aneurysms

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