Angiotensin II type‐I receptor and ACE polymorphisms and risk of myocardial infarction in men and women

Kee, Frank; Morrison, Caroline; Poirier, Odette; McCrum, Evelyn; Mallet, Christine; Nicaud, Viviane; McMaster, Dorothy; Dallongeville, Jean; Fruchart, J.C.; Evans, Alun

doi:10.1046/j.1365-2362.2000.00741.x

Cited by 25 publications

(25 citation statements)

References 26 publications

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“…30,31 Some of the contradictory findings concerning AT1R polymorphism and the risk of MI and hypertension may be due has not been found as an independent risk factor for MI or hypertension in either sex. 33,34 Our results are consistent with these reports and we found no difference in the distribution of the A/C1166 genotype or allele frequency between the patients and the control group in either sex.…”

Section: 7±04 Ns No Significant Difference Was Found Among Three Gesupporting

confidence: 92%

Association Between A/C1166 Gene Polymorphism of the Angiotensin II Type 1 Receptor and Biventricular Functions in Patients With Acute Myocardial Infarction

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et al. 2006

Circ J

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cute myocardial infarction (AMI) is characterized by loss of contractile tissue and changes in ventricular geometry. 1 The presence of congestive heart failure or left ventricular (LV) systolic dysfunction is probably the most important risk factor in patients with AMI. 2 The development of right ventricular (RV) dysfunction has been reported following LV myocardial infarction (MI), 3,4 and is also associated with increased risk of shock, arrhythmia, and death. 5,6 After MI, the process of LV remodeling begins rapidly, usually within the first few hours after an infarct, and continues to progress. 7 Furthermore, it is known that the renin -angiotensin -aldosterone system (RAS) and angiotensin-converting enzyme (ACE) activity contribute to the remodeling process. 8 Angiotensin II (ATII) is the final effector of the RAS. It is a vasoactive peptide and leads to growth promotion, fibroblast proliferation, and the most potent vasoactive and salt-retaining effector peptide of the RAS, which is involved in blood pressure homeostasis and cardiovascular pathophysiology. Two subtypes of cell surface receptors, ATII type 1 receptor (AT1R) and ATII type 2 receptor Circulation Journal Vol. 70, October 2006 (AT2R), have been identified. Most of the actions of ATII are mediated by AT1, which is particularly prominent in the myocardium. 9,10 Although a number of polymorphisms of the AT1R gene have been identified, one of the most widely studied is an A-C substitution at position 1166 (A/C1166). 11 Two-dimensional (D) and Doppler echocardiography is a reliable tool for the diagnosis of systolic and diastolic dysfunction. The Doppler echocardiographic myocardial performance index (MPI) called the "Tei index", combining time intervals of LV contraction and relaxation, has been shown to be a powerful predictor of death and congestive heart failure after MI. 12,13 This index can be obtained easily, is reproducible and independent of the ventricular geometry, and has been shown to have potential for clinical application in the assessment of overall cardiac function in various disorders. 14 Poulsen et al recently reported that the LVMPI was a powerful predictor of death or congestive heart failure after MI, 15 and Moller et al showed that the RVMPI was increased in the acute phase of MI and was significantly correlated with indices of RV systolic dysfunction. 16 In a previous study, we reported higher LVMPI and RVMPI in patients with the DD genotype than in patients with the ID genotype of the ACE gene after anterior AMI. 17 Although there have been several association studies of the polymorphism of AT1R (A/C1166) in clinical endpoints, such as MI, 18 hypertension, 11 aortic stiffness, 19 and LV mass, 20 to our knowledge the relationship between AT1R polymorphism and biventricular function in anterior Methods and ResultsThe study group comprised 132 consecutive patients who were admitted to the coronary care unit with their first acute anterior MI. Systolic and diastolic diameters, volumes, inflow properties, ejection fraction an...

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Section: 7±04 Ns No Significant Difference Was Found Among Three Gesupporting

confidence: 92%

Association Between A/C1166 Gene Polymorphism of the Angiotensin II Type 1 Receptor and Biventricular Functions in Patients With Acute Myocardial Infarction

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et al. 2006

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“…Three studies (two in Caucasians 22,25 and one in Asians 29 ) for which the genotype distributions in the controls were significantly deviated from HWE were excluded.…”

Section: Sensitivity Analysismentioning

confidence: 99%

A systematic review and meta-analysis of the association between angiotensin II type 1 receptor A1166C gene polymorphism and myocardial infarction susceptibility

Zheng

Shi

et al. 2012

J Renin Angiotensin Aldosterone Syst

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Background and aim: Many reported studies have been conducted to investigate the association of angiotensin II type 1 receptor (AT1R) A1166C gene polymorphism with myocardial infarction (MI) susceptibility. However, the results from those reports are still conflicting. This meta-analysis was performed to study the relationship between AT1R A1166C gene polymorphism and MI risk. Method: The databases of PubMed, Embase, and Cochrane Library were searched as of 1 March 2012, and eligible investigations were recruited into this meta-analysis. Results: Eighteen investigations were identified for the analysis of association between AT1R A1166C gene polymorphism and MI risk, 11 in Caucasians, three in Asians, two in Africans, one in the population of Brazil and one in the population of Durban, South Africa . There was a marked association between AT1R C allele and MI susceptibility for overall populations (odds ratio (OR)=1.12, 95% confidence interval (CI): 1.01-1.25, p=0.03), and AT1R AA genotype was associated with a lower risk of MI in overall populations (OR=0.87, 95% CI: 0.78-0.98, p=0.02). However, AT1R A1166C gene polymorphism was not associated with MI risk in the sub-groups of Caucasians, Asians, Africans, Brazil and Durban populations. Conclusions: C allele is a risk factor for the MI susceptibility in overall populations, and AA genotype might be a protective factor against the MI risk in overall populations. However, more case-control association investigations on larger, stratified populations are required in the future.

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“…The rationale of intensive investigation of these polymorphisms was that an enhanced activity of the RAAS, associated with these polymorphisms, might subsequently lead to adverse physiologic consequences such as an increased cardiovascular risk. The AGT 1 R A1166C and AGT M235T polymorphisms have been associated with increased RAAS activity and CAD risk [35,36,37,38,39], although we have to take into account that negative results have been published as well [40,41,42,43]. The most comprehensively studied RAAS polymorphism in relationship with CAD is the ACE insertion/deletion (ACE I/D) polymorphism.…”

Section: Raas Polymorphisms and Cadmentioning

confidence: 99%

The Renin-Angiotensin-Aldosterone System: Approaches to Guide Angiotensin-Converting Enzyme Inhibition in Patients with Coronary Artery Disease

et al. 2008

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Drugs that modulate the renin-angiotensin-aldosterone system (RAAS) play an important role in modern cardiovascular prevention strategies. Inhibitors of the RAAS, in particular angiotensin-converting enzyme (ACE) inhibitors, have been proven to be beneficial in specific patient groups, including patients with hypertension, heart failure, diabetes mellitus and stable coronary artery disease. Although clinical trials demonstrated a rather consistent beneficial effect of ACE inhibitors across groups of patients based on clinical characteristics, the variability in treatment response on the individual patient level is extensive. Recent publications suggest that genetic polymorphisms in the RAAS are related to cardiovascular risk. Genetic variability also seems associated with the response to ACE inhibitor therapy, and can probably be used to tailor treatment. This review discusses several approaches to guide ACE inhibitor therapy in patients with coronary artery disease. In addition, the potential impact of pharmacogenetics regarding this particular topic is highlighted.

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Angiotensin II type‐I receptor and ACE polymorphisms and risk of myocardial infarction in men and women

Abstract: Some of the contradictory findings concerning the ACE polymorphism and the risk of MI may be due to heterogeneity in the risk between men and women. The AT1R1196 polymorphism is not an independent risk factor for MI in either sex.

Cited by 25 publications

References 26 publications

Association Between A/C1166 Gene Polymorphism of the Angiotensin II Type 1 Receptor and Biventricular Functions in Patients With Acute Myocardial Infarction

Association Between A/C1166 Gene Polymorphism of the Angiotensin II Type 1 Receptor and Biventricular Functions in Patients With Acute Myocardial Infarction

A systematic review and meta-analysis of the association between angiotensin II type 1 receptor A1166C gene polymorphism and myocardial infarction susceptibility

The Renin-Angiotensin-Aldosterone System: Approaches to Guide Angiotensin-Converting Enzyme Inhibition in Patients with Coronary Artery Disease

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