Plasma level and gene polymorphism of angiotensin-converting enzyme in relation to myocardial infarction.

Cambien, François; Costerousse, Olivier; Tiret, Laurence; Poirier, Odette; Lecerf, Laure; Gonzales, Marie-Françoise; Evans, Alun; Arveiler, Dominique; Cambou, Jean-Pierre; Luc, Gérald

doi:10.1161/01.cir.90.2.669

Cited by 223 publications

(133 citation statements)

References 14 publications

Supporting

Mentioning

121

Contrasting

Unclassified

Order By: Relevance

“…Several studies have suggested that the D allele of ACE I/D dimorphism confers increased risk of developing CVDs. 7,22,25 At the same time, considerable negative evidence exists on this question. An analysis of 11 000 cases and controls showed no relationship between MI and the I/D dimorphism.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies on the association of ACE I/D dimorphism and the risk of developing CVDs, such as essential hypertension (EH) [9][10][11][12][13][14][15][16][17][18] and myocardial infarction (MI), [19][20][21][22][23][24][25][26][27][28] have generated inconsistent information. This instigated a search for new polymorphisms in the ACE gene to identify better markers or actual functional variants.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Association of the angiotensin-converting enzyme (ACE) gene G2350A dimorphism with essential hypertension

et al. 2003

View full text Add to dashboard Cite

Although the angiotensin converting enzyme (ACE) is a strong candidate gene for hypertension, the extensively studied insertion-deletion dimorphism in intron 16 was not found to be associated with it. Several new polymorphisms in the ACE gene were identified, among which a dimorphism in exon 17, ACE G2350A, has a significant effect on plasma ACE concentrations. To assess the value of genotyping the ACE G2350A dimorphism in a genetically homogeneous population, we carried out a retrospective, case-control study of dimorphism G2350A for a putative association with essential hypertension (EH) in a Gulf population (Emirati)-an ethnic group characterized by no alcohol intake and no cigarette smoking. We investigated a sample population of 254 Emirati, comprising 136 normotensive controls, and 118 patients with clinical diagnoses of EH. ACE G2350A alleles were visualized by assays based on polymerase chain reaction and restriction endonuclease analysis. The ACE G2350A dimorphism showed an association with EH (v 2 ¼ 6.71, 2 df, P ¼ 0.05). Further analysis revealed that the ACE G/G 2350 genotype was positively associated (OR ¼ 1.06-3.07, P ¼ 0.02) with EH. This is the first association study of the ACE G2350A dimorphism with EH, and the positive result might indicate that ACE could be a QTL for EH as originally thought.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Association of the angiotensin-converting enzyme (ACE) gene G2350A dimorphism with essential hypertension

et al. 2003

View full text Add to dashboard Cite

show abstract

“…Several studies on the association of ACE I/D polymorphism and the risk for myocardial infarction (MI) (Bohn et al, 1993;Cambien et al, 1994;Evans et al, 1994;Soubrier and Cambien, 1994;Cambian and Evans, 1995;Lindpainter et al, 1995;Ferrieres et al, 1999;O' Mally et al, 1999;Keavney et al, 2000), have generated inconAssociation study of the angiotensin-converting enzym e (ACE) gene G2350A dim orphism with m yocardial infarction sistent information. This has stimulated a search for new polymorphisms in the ACE gene to identify better markers or actual functional variants.…”

Section: Introductionmentioning

confidence: 99%

Association study of the angiotensin-converting enzyme (ACE) gene G2350A dimorphism with myocardial infarction

Iqbal

Saeed²,

Mehboobali³

et al. 2004

Exp Mol Med

View full text Add to dashboard Cite

“…10 IL-6 is known to be involved in the stimulation of matrix-degrading enzymes, for example, metalloproteinases. 11In parallel, the renin-angiotensin system (RAS) has been suggested to be involved in the development of acute coronary syndromes, based on the observations that (1) increased circulating levels of renin were associated with a higher incidence of myocardial infarction (MI), 12 (2) genetic polymorphisms of the ACE gene revealed a higher risk for coronary events for the ACE/ID phenotype, as compared with the DD-phenotype, 13,14 and (3) clinical trials in patients with left ventricular dysfunction demonstrated that long-term ACE inhibition reduces the incidence of MI. 15,16 The present study investigated the localization of angiotensin II (Ang II), the Ang II type 1 (AT 1 ) receptor, and ACE within human coronary atherosclerotic plaques.…”

mentioning

confidence: 99%

Expression of Angiotensin II and Interleukin 6 in Human Coronary Atherosclerotic Plaques

et al. 2000

View full text Add to dashboard Cite

Background-Patients with an activated renin-angiotensin system (RAS) or genetic alterations of the RAS are at increased risk of myocardial infarction (MI). Administration of ACE inhibitors reduces the risk of MI, and acute coronary syndromes are associated with increased interleukin 6 (IL-6) serum levels. Accordingly, the present study evaluated the expression of angiotensin II (Ang II) in human coronary atherosclerotic plaques and its influence on IL-6 expression in patients with coronary artery disease. Methods and Results-Immunohistochemical colocalization of Ang II, ACE, Ang II type 1 (AT 1 ) receptor, and IL-6 was examined in coronary arteries from patients with ischemic or dilated cardiomyopathy undergoing heart transplantation (nϭ12), in atherectomy samples from patients with unstable angina (culprit lesion; nϭ8), and in ruptured coronary arteries from patients who died of MI (nϭ13). Synthesis and release of IL-6 was investigated in smooth muscle cells and macrophages after Ang II stimulation. Colocalization of ACE, Ang II, AT 1 receptor, and IL-6 with CD68-positive macrophages was observed at the shoulder region of coronary atherosclerotic plaques and in atherectomy tissue of patients with unstable angina. Ang II was identified in close proximity to the presumed rupture site of human coronary arteries in acute MI. Ang II induced synthesis and release of IL-6 shortly after stimulation in vitro in macrophages and rat smooth muscle cells. Conclusions-Ang II, AT 1 receptor, and ACE are expressed at strategic sites of human atherosclerotic coronary arteries, suggesting that Ang II is produced primarily by ACE within coronary plaques. The observation that Ang II induces IL-6 and their colocalization with the AT 1 receptor and ACE is consistent with the notion that the RAS may contribute to inflammatory processes within the vascular wall and to the development of acute coronary syndromes. (Circulation. 2000;101:1372-1378.)Key Words: interleukins Ⅲ angiotensin Ⅲ angina Ⅲ myocardial infarction Ⅲ arteries Ⅲ receptors R upture of atherosclerotic plaques occurs predominantly at the edges of the plaque's fibrous cap, the shoulder region, that is, areas of accumulated inflammatory cells, for example, macrophages, T-lymphocytes, and mast cells in close proximity to vascular smooth muscle cells (SMC). [1][2][3][4][5][6] The activated inflammatory cells stimulate their neighboring cells to erode the extracellular matrix through the release of inflammatory cytokines. The decay of the framework that forms the plaque cap leads to plaque rupture 1,7,8 and resembles the morphological correlate of an acute coronary syndrome. Serum levels of interleukin 6 (IL-6) are increased in patients with unstable angina 9 and may trigger the onset of an acute coronary syndrome. 10 IL-6 is known to be involved in the stimulation of matrix-degrading enzymes, for example, metalloproteinases. 11In parallel, the renin-angiotensin system (RAS) has been suggested to be involved in the development of acute coronary syndromes, based on the observat...

show abstract

Plasma level and gene polymorphism of angiotensin-converting enzyme in relation to myocardial infarction.

Abstract: These results extend our previous findings and indicate that plasma ACE level may be a risk factor for MI, independent of the ACE I/D polymorphism.

Cited by 223 publications

References 14 publications

Association of the angiotensin-converting enzyme (ACE) gene G2350A dimorphism with essential hypertension

Association of the angiotensin-converting enzyme (ACE) gene G2350A dimorphism with essential hypertension

Association study of the angiotensin-converting enzyme (ACE) gene G2350A dimorphism with myocardial infarction

Expression of Angiotensin II and Interleukin 6 in Human Coronary Atherosclerotic Plaques

Contact Info

Product

Resources

About