Gene–Gene Interaction in the RAS System in the Predisposition to Myocardial Infarction in Elder Population of St. Petersburg (Russia)

Fomicheva, Ekaterina; Gukova, Svetlana P.; Larionova-Vasina, Valentina I.; Kovalev, Y.; Schwartz, E.I.

doi:10.1006/mgme.1999.2924

Cited by 21 publications

(11 citation statements)

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“…In 14 studies [13], [29]–[32], [35], [37]–[39], [44], [47], [49], [53], the WHO criteria were used, and, in four studies, CHD was diagnosed based on a clinical diagnosis [6], [33], [45]. Controls arose from the source population of the cases in 21 studies [6], [8], [13], [29], [31]–[33], [35]–[38], [45], [47], [49]–[53], [55], while hospital-based/not population-based controls were used in 17 studies [7], [10], [11], [30], [34], [39]–[44], [46], [48], [54], [56]–[58].…”

Section: Resultsmentioning

confidence: 99%

The M235T Polymorphism in the AGT Gene and CHD Risk: Evidence of a Hardy-Weinberg Equilibrium Violation and Publication Bias in a Meta-Analysis

et al. 2008

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BackgroundThe M235T polymorphism in the AGT gene has been related to an increased risk of hypertension. This finding may also suggest an increased risk of coronary heart disease (CHD).Methodology/Principal FindingsA case-cohort study was conducted in 1,732 unrelated middle-age women (210 CHD cases and 1,522 controls) from a prospective cohort of 15,236 initially healthy Dutch women. We applied a Cox proportional hazards model to study the association of the polymorphism with acute myocardial infarction (AMI) (n = 71) and CHD. In the case-cohort study, no increased risk for CHD was found under the additive genetic model (hazard ratio [HR] = 1.20; 95% confidence interval [CI], 0.86 to 1.68; P = 0.28). This result was not changed by adjustment (HR = 1.17; 95% CI, 0.83 to 1.64; P = 0.38) nor by using dominant, recessive and pairwise genetic models. Analyses for AMI risk under the additive genetic model also did not show any statistically significant association (crude HR = 1.14; 95% CI, 0.93 to 1.39; P = 0.20). To evaluate the association, a comprehensive systematic review and meta-analysis were undertaken of all studies published up to February 2007 (searched through PubMed/MEDLINE, Web of Science and EMBASE). The meta-analysis (38 studies with 13284 cases and 18722 controls) showed a per-allele odds ratio (OR) of 1.08 (95% CI, 1.01 to 1.15; P = 0.02). Moderate to large levels of heterogeneity were identified between studies. Hardy-Weinberg equilibrium (HWE) violation and the mean age of cases were statistically significant sources of the observed variation. In a stratum of non-HWE violation studies, there was no effect. An asymmetric funnel plot, the Egger's test (P = 0.066), and the Begg-Mazumdar test (P = 0.074) were all suggestive of the presence of publication bias.Conclusions/SignificanceThe pooled OR of the present meta-analysis, including our own data, presented evidence that there is an increase in the risk of CHD conferred by the M235T variant of the AGT gene. However, the relevance of this weakly positive overall association remains uncertain because it may be due to various residual biases, including HWE-violation and publication biases.

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Section: Resultsmentioning

confidence: 99%

The M235T Polymorphism in the AGT Gene and CHD Risk: Evidence of a Hardy-Weinberg Equilibrium Violation and Publication Bias in a Meta-Analysis

et al. 2008

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“…In support of this conclusion, some reports have described a synergistic interaction between genes of the RAS associated with a higher risk of AMI. Ludwig et al [16] and Fomicheva et al [17] observed a significant interaction between the AGT and ACE genes. Tiret et al [33] and van Geel et al [34] found a significant association between ACE and AGTR1, and Á lvarez et al [35] have demonstrated an interaction between AGT and AGTR1.…”

Section: Discussionmentioning

confidence: 97%

“…Interactions among mutations of these three genes of the RAS may play a role in the development of AMI. While several studies have independently identified gene interactions (ACE vs. AGT, AGT vs. AGTR1 and ACE vs. AGTR1) suggestive of a higher risk for myocardial infarction in different populations [15][16][17], there is still no consensus on this matter. These reports have generally investigated only one combination of gene-to-gene interaction and no study has yet examined all possible interactions within the same population.…”

Section: Introductionmentioning

confidence: 95%

Genotypic interactions of renin–angiotensin system genes in myocardial infarction

Araújo

Goulart

Cordeiro

et al. 2005

International Journal of Cardiology

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“…Specifically, the D allele of the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism is associated with QT-related ECG abnormalities in myocardial infarction [5] and with ventricular fibrillation [6]. Therefore, ACE-DD genotype and other RAS polymorphisms, angiotensin type 1 receptor-A1166C (AT1R-A1166C) and angiotensinogen-M235T (AGT-M235T), and within-RAS gene-gene interactions, may contribute to QT prolongation in ESRD patients [7][8][9][10].…”

mentioning

confidence: 98%

Renin-angiotensin polymorphisms and QTc interval prolongation in end-stage renal disease

Raizada¹,

Skipper²,

Luo³

et al. 2005

Kidney International

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Gene–Gene Interaction in the RAS System in the Predisposition to Myocardial Infarction in Elder Population of St. Petersburg (Russia)

Cited by 21 publications

References 42 publications

The M235T Polymorphism in the AGT Gene and CHD Risk: Evidence of a Hardy-Weinberg Equilibrium Violation and Publication Bias in a Meta-Analysis

The M235T Polymorphism in the AGT Gene and CHD Risk: Evidence of a Hardy-Weinberg Equilibrium Violation and Publication Bias in a Meta-Analysis

Genotypic interactions of renin–angiotensin system genes in myocardial infarction

Renin-angiotensin polymorphisms and QTc interval prolongation in end-stage renal disease

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