Angiotensin-Converting Enzyme Gene Polymorphism Is Associated With Carotid Arterial Wall Thickness in Non–Insulin-Dependent Diabetic Patients

Hosoi, Masayuki; Nishizawà, Yoshiki; Kogawa, Kyoko; Kawagishi, Takahiko; Konishi, Toshiaki; Maekawa, Kiyoshi; Emoto, Masanori; Fukumoto, Shinya; Shioi, Atsushi; Shoji, Tetsuo; Inaba, Masaaki; Okuno, Yasuhisa; Morii, Hirotoshi

doi:10.1161/01.cir.94.4.704

Cited by 94 publications

(51 citation statements)

References 18 publications

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“…A lack of association between ACE gene polymorphism and carotid IMT has also been demonstrated in a low-risk population (Dessi-Fulgheri et al 1995). On the other hand, an association of polymorphisms of the ACE gene and IMT was reported in specific populations, such as noninsulin-dependent diabetes mellitus (NIDDM) patients (Hosoi et al 1996), hemodialysis patients (Nergizoglu et al 1999), and hypertensive patients (Jeng 2000). These findings suggest risk factor-genotype interactions of the ACE gene.…”

Section: Discussionmentioning

confidence: 99%

Risk factor–gene interaction in carotid atherosclerosis: effect of gene polymorphisms of renin-angiotensin system

et al. 2001

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The risk factor-gene interaction in carotid atherosclerosis was investigated in 205 community-dwelling healthy subjects aged 50 years or more in Japan. The intima-media thickness (IMT) of the common carotid artery was evaluated by ultrasonography with a 7.5-MHz probe. Gene polymorphisms were determined for each subject with angiotensin-converting enzyme (ACE) insertion/deletion (I/D), angiotensinogen (AGT) M235T, angiotensin II type 1 receptor (AT1R) A1166C, and apolipoprotein E (apoE) genotypes. There was no genotype-specific difference in carotid IMT among any genes examined. Combinations of genotypes did not increase carotid IMT compared with subjects without these genotypes. In the total population, multiple regression analysis showed that age, systolic blood pressure (SBP), sex, and body mass index (BMI) were significantly associated with carotid IMT. However, the association between risk factors and IMT was genotype-specific. Age was significantly associated with IMT in ACE D carriers, but not in subjects with the ACE II genotype. Analysis of covariance adjusted with other risk factors showed that the age-dependent change in IMT was significantly different between subjects with the ACE II genotype and the ACE D carriers (F[1.196] ϭ 4.97; P ϭ 0.027). Similarly, the regression of IMT on SBP was significantly different between AGT TT and AGT MT ϩ MM (F[1.196] ϭ 7.20; P ϭ 0.0079). The regression of IMT on BMI was also significantly different between apo E4 carriers and noncarriers (F[1.196] ϭ 6.78; P ϭ 0.0099). Furthermore, general linear model analysis with risk factors, genotype, and risk factor-genotype interactions revealed that the age*ACE genotype interaction, the SBP*AGT genotype interaction, and the BMI*apoE genotype interaction were significantly associated with IMT. These findings further support the role of risk factor-gene interaction in carotid atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Risk factor–gene interaction in carotid atherosclerosis: effect of gene polymorphisms of renin-angiotensin system

et al. 2001

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“…2 The same limitations appear to apply to the small number of studies that have examined the association of ACE I/D polymorphism with carotid IMT, and reported similarly heterogeneous findings (summarized in Table 5). [11][12][13][14][15][16] Four of these studies found a positive association, 11,14 -16 although this was only after a quarter of subjects on drug treatment were excluded from analysis in 1 small study 11 and only among nonsmokers in another study 16 ; 2 other studies 12,13 showed no association of the D allele with carotid wall thickening or disease despite that it conferred an increased risk of lacunar stroke in 1 study. 13 None of the studies were able to demonstrate a relationship between the D allele and carotid plaque or stenosis.…”

Section: Discussionmentioning

confidence: 99%

“…[11][12][13][14][15][16] We therefore decided to test for the association of carotid IMT and ACE I/D polymorphism in the Perth Carotid Ultrasound Disease Assessment Study (CUDAS). The latter consisted of 1111 male and female subjects, aged 27 to 77 years, randomly selected from the Perth community population, all of whom had high-resolution bilateral B-mode carotid ultrasound examination and ACE I/D gene polymorphism determined as part of a detailed risk factor assessment.…”

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Angiotensin-Converting Enzyme Gene Polymorphism and Carotid Wall Thickening in a Community Population

Hung

McQuillan

Nidorf

et al. 1999

ATVB

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Abstract-The insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been associated with an increased risk of coronary heart disease, but whether it is a risk factor for underlying atherosclerosis remains unclear. Therefore, we examined to see whether the ACE gene deletion polymorphism was associated with carotid wall thickening and atherosclerotic plaque formation in a large randomly selected community population. A total of 1111 subjects, aged 27 to 77 years, with an equal male:female ratio and equal numbers in each age decile, were randomly selected from the Perth community population. Mean common carotid intima-medial wall thickness (IMT) and focal plaque formation were assessed by high-resolution B-mode ultrasound.

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“…Then the right side was used as representative because the coefficient of variation was significantly lower than in the left side (right vs left side: 3.4 vs 4.2%). Using digitized still images of the arteries taken during scanning, IMT was measured in the far wall of the right CCA at sites of the most advanced atherosclerotic lesions, identified as diffuse and continuous projections with the greatest distance between the lumen -intimal interface and the media -adventitial interface but without atherosclerotic plaque, which was defined as localized lesions of thickness $ 2.0 mm (35,36). These interfaces were manually traced and the mean value calculated as the mean of at least three still images obtained from the same section of the CCA.…”

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confidence: 99%

Change in von Willebrand factor and carotid intima-media thickness in hypothyroid patients with normal thyroid function after levothyroxine replacement therapy

Nagasaki

Inaba

Henmi

et al. 2004

European Journal of Endocrinology

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Objective: This study examined whether levothyroxine (L-T 4 ) replacement might affect serum markers of endothelium injury, including von Willebrand factor (vWF), factor VIII activity and thrombomodulin (TM), during normalization of increased intima-media thickness (IMT) in the common carotid artery (CCA) in hypothyroid patients after L-T 4 replacement therapy. Patients and methods: Thirty-three hypothyroid patients were examined for vWF, factor VIII, TM and CCA IMT before and after 1 year of normalization of thyroid function by L-T 4 replacement. CCA IMT was measured from digitized still images taken during scanning by high-resolution ultrasonography as an indicator of early atherosclerosis. Results: Serum factor VIII and vWF increased significantly during 1 year of normalization of thyroid function (from 122.7^9.4 to 151.3^18.8% (P , 0.05) and from 109.9^9.6 to 135.2^12.4% (P , 0.005) respectively), although these values all fell within the respective normal range. Serum TM, in contrast, did not change appreciably in response to L-T 4 treatment, moving from 2.57^0.15 to 2.74^0.18 ng/ml (P ¼ 0.086). During 1 year of a euthyroid state, all patients showed a significant decrease in CCA IMT (P , 0.0001). Change in serum vWF, but not in factor VIII or TM, showed a positive correlation with that of CCA IMT during L-T 4 replacement therapy. Furthermore, the change in serum vWF was significantly and independently associated with change in CCA IMT (r ¼ 0.490, P ¼ 0.0038).Conclusions: The present study demonstrated that the improvement of CCA IMT during L-T 4 treatment might have the potential to attenuate an elevation of vWF and to attenuate vascular injury by the cardiovascular effects of thyroid hormone in hypothyroid patients. 150 125-131 European Journal of Endocrinology

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Angiotensin-Converting Enzyme Gene Polymorphism Is Associated With Carotid Arterial Wall Thickness in Non–Insulin-Dependent Diabetic Patients

Abstract: The D allele of the ACE gene may be a risk factor for the development of wall thickening of the carotid but not the femoral artery in NIDDM patients.

Cited by 94 publications

References 18 publications

Risk factor–gene interaction in carotid atherosclerosis: effect of gene polymorphisms of renin-angiotensin system

Risk factor–gene interaction in carotid atherosclerosis: effect of gene polymorphisms of renin-angiotensin system

Angiotensin-Converting Enzyme Gene Polymorphism and Carotid Wall Thickening in a Community Population

Change in von Willebrand factor and carotid intima-media thickness in hypothyroid patients with normal thyroid function after levothyroxine replacement therapy

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