Angiotensin I-converting enzyme gene polymorphism, coronary artery disease and myocardial infarction. An angiographically controlled study

Pfohl, Martin; Koch, Matthias; Prescod, S.; Haase, K.K.; Häring, Hans Ulrich; Karsch, K. R.

doi:10.1053/euhj.1999.1543

Cited by 35 publications

(26 citation statements)

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“…4,38 In contrast, the data that support the contention that the D allele could also be a general marker of CVD are controversial. Positive studies [7][8][9][10][11][12][13][14] have in fact been contradicted not only by negative results basically for all types of CVD [15][16][17][18] (for reviews, see Koch et al 19 and Samani et al 45 ) but also by a study showing an association of the D allele with longevity in centenarians. 46 The mechanisms responsible for the supposed predisposition to developing CVD also remain largely speculative, because (1) the D/I polymorphism is located in intron 16 (ie, a noncoding region); (2) no change in the kinetic properties of ACE in relation with this polymorphism was documented 47 ; and (3) the contention that the higher ACE plasma levels associated with the D allele enhances Ang II generation in vivo 31 has been challenged.…”

Section: Discussionmentioning

confidence: 99%

“…5,6 The D allele has thereafter been associated with other CVD, including dilated and ischemic cardiomyopathy, coronary and carotid artery disease, coronary artery spasm, restenosis, left ventricular hypertrophy in hypertensives, left ventricular dysfunction, and, more recently, atherosclerotic renovascular hypertension. [7][8][9][10][11][12][13][14] However, opposite results for almost every clinical association have also been published, and therefore the value of the D/I genotyping for the purpose of cardiovascular risk stratification has been challenged [15][16][17][18][19][20][21][22][23] (for reviews, see Butler et al 24 and Agerholm-Larsen et al 25 ). Furthermore, the mechanisms by which the D allele would lead to a generalized increase in CVD risk remain largely speculative.…”

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confidence: 99%

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Exclusion of the ACE D/I Gene Polymorphism as a Determinant of Endothelial Dysfunction

et al. 2001

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Abstract-A deletion/insertion (D/I) polymorphism within the ACE gene may increase the risk of cardiovascular events through still unknown mechanisms. The latter may involve increased angiotensin II-induced NO breakdown and/or reduced agonist-mediated NO release. We therefore investigated whether the D allele of the ACE gene affects endothelium-dependent vasodilatation in mild-to-moderate primary hypertensive patients and healthy normotensive subjects. We compared in a cross-sectional study the forearm blood flow response of the 3 D/I genotypes with 5 incrementally increasing doses of the endothelium-dependent vasodilator acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 g ⅐ 100 mL Ϫ1 ⅐ min Ϫ1) in 142 subjects: 103 mild-to-moderate uncomplicated primary hypertensives (49.3Ϯ9.1 years old, 152Ϯ11/99Ϯ5 mm Hg) and 39 normotensives (44.6Ϯ15.3 years old, 122Ϯ12/78Ϯ6 mm Hg). We also assessed the endothelium-independent vasodilatation in the forearm, as blood flow response to 3 incrementally increasing doses of sodium nitroprusside (1, 2, and 4 g ⅐ 100 mL Ϫ1 ⅐ min Ϫ1 ). The overall genotype distribution was II, nϭ10; ID, nϭ70; and DD, nϭ62. It did not differ significantly between primary hypertensives and normotensives. A significant blunting of endothelium-dependent vasodilatation in primary hypertensive patients compared with normotensive subjects (PϽ0.001) was found. No effect of the DI genotype on endothelium-dependent and -independent vasodilatation was detected. Thus, these results obtained in a relatively large population do not support the contention that the D allele is associated with a blunting of either stimulated endothelial NO or donated NO responses in both mild-to-moderate primary hypertensive patients and normotensive subjects. (Hypertension. 2001;37:293-300.)

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Exclusion of the ACE D/I Gene Polymorphism as a Determinant of Endothelial Dysfunction

et al. 2001

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“…12,13 Studies using the ACE I/D polymorphism have shown a dose effect of the D allele as a genetic risk factor for circulatory dysfunction and vasoconstriction, [14][15][16][17][18] but other authors present controversial results or do not describe any significant association. [19][20][21][22][23][24][25] It is believed that this intronic (noncoding) polymorphism may be a marker for another genetic locus (or loci) with more functional significance. Extensive haplotyping of the region has evaluated the promoter region and a number of exons.…”

Section: Introductionmentioning

confidence: 99%

Análise da tendência temporal de dano renal agudo entre pacientes graves conforme polimorfi smos I/D e -262A > T da enzima conversora da angiotensina

Pedroso

Paskulin²,

Dias³

et al. 2010

J. Bras. Nefrol.

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Multiple organ failure syndrome and acute renal dysfunction share many of physiologic factors involved in their development. Recent studies correlate the susceptibility to organ dysfunction in critically ill patients with genetic inheritance. Many of them consider ACE gene could be a possible candidate to elucidate a genetic risk predisposition or a genetic factor. We aimed to examine the effects of I/D and -262A > T ACE polymorphisms in the renal function in ill southern Brazilians patients. A multi-organic worldwide known failure score, the SOFA (sequential organ failure assessment), was used to determine the basal health state at first day (ICU admission). Considering admission SOFA score and trend of renal function (measured by daily renal SOFA scores, with daily measure of serum creatinine and diuresis), we hypothesize that ACE polymorphisms could influence in the trend of renal function in ICU patients. A total of 153 critically ill adult patients (79 men) were included in this study. We monitored the patients daily during their entire ICU and post-ICU (hospital) stay (measured from the ICU admission day to a maximum of 224 days). We observed progression to renal failure (SOFA scores 3 and 4) in first seven days of ICU stay and need for dialysis. The general genotypic frequencies in our sample were II = 0.17; ID = 0.46; DD = 0.37 and AA = 0.30; AT = 0.55; TT = 0.15, and the allelic frequencies were I = 0.40; D = 0.60 and A = 0.56; T = 0.44. This is the first study to verify the influence of I/D and -262A > T ACE polymorphisms in acute renal dysfunction among critically ill patients. No significant association was found between genotypes or allele frequencies and the trend of the renal function. The I/D and -262A > T ACE polymorphisms have no significant impact on the trend of renal function during the first week of ICU stay, neither any influence in mortality in critically ill patients.

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“…MI is a multifactorial disease, influenced by environmental and genetic factors (18). These factors differ in each population.…”

Section: Introductionmentioning

confidence: 99%

Investigation of Angiotensin Converting Enzyme Gene Polymorphism and Blood Lipid Peroxidation with MI Patients in Turkish Population

Kayhan¹,

Peker²

2004

Biotechnology & Biotechnological Equipment

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Angiotensin I-converting enzyme gene polymorphism, coronary artery disease and myocardial infarction. An angiographically controlled study

Cited by 35 publications

References 36 publications

Exclusion of the ACE D/I Gene Polymorphism as a Determinant of Endothelial Dysfunction

Exclusion of the ACE D/I Gene Polymorphism as a Determinant of Endothelial Dysfunction

Análise da tendência temporal de dano renal agudo entre pacientes graves conforme polimorfi smos I/D e -262A > T da enzima conversora da angiotensina

Investigation of Angiotensin Converting Enzyme Gene Polymorphism and Blood Lipid Peroxidation with MI Patients in Turkish Population

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