Antihypertensive treatment modulates the association between the D/I ACE gene polymorphism and left ventricular hypertrophy: a meta-analysis

Abstract

This meta-analysis attempted to derive pooled estimates for the putative association between echocardiographic or electrocardiographic left ventricular hypertrophy and the deletion/insertion (D/I) polymorphism of the angiotensin-I converting enzyme. Casecontrol studies were combined, using the Mantel and Haenszel approach. Joint P-values for continuous variables were calculated by Stouffer's method. Continuous measurements of left ventricular mass, which were reported in different units, were expressed on a percentage scale using the within-study mean of the II genotype as the denominator. The computerised database used for this analysis, included 28 reports with an overall sample size of 6638 subjects. The prevalence of the D allele was significantly lower in Japanese (37.2%) than in Caucasians (56.2%). A funnel plot including 12 casecontrol studies (4094 subjects) suggested that no publication bias was present. Overall, left ventricular hypertrophy was not associated with the D allele. Compared with the II genotype, the excess risks of left ventricular hypertrophy associated with DD and DI geno-

A Translational Approach to Hypertensive Heart Disease

“…In this regard, a meta-analysis of case-control and association studies has shown that the D allele of the insertion/deletion polymorphism of the angiotensinconverting enzyme (ACE) gene behaved as an LVH marker in untreated hypertensive patients. 26 In addition, recent findings suggest that the concomitant presence of the D allele of the insertion/deletion polymorphism of the ACE gene and the C allele of the A1166C polymorphism of the AT 1 receptor gene synergistically increased predisposition to diastolic dysfunction/failure in hypertensive patients. 27 Of interest, the C allele of the A1166C polymorphism of the AT 1 receptor gene has been found to be associated with enhanced LV chamber stiffness in HHD patients.…”

The genetic epidemiology of neurodegenerative disease

“…However, there is only relatively little empirical evidence that publication bias actually represents a common or significant source of error in current publications investigating the genetics of a number of disorders (e.g., refs. [6][7][8][9][10][11][12]. The sheer number of publications in the AD genetics literature, for example, reveals that nearly two-thirds represent "negative" articles, with the rest being "positive" or "suggestive," so that one can hardly speak of a preponderance of the positive (13).…”

Left ventricular structure in relation to the human SAH gene in the European Project on Genes in Hypertension

“…7 Left ventricular mass index (LVMI) increases with blood pressure and body mass index. 8 This phenotype might therefore more readily pick up association with variation in the SAH gene. In this study, we explored possible association between left ventricular structure and the GÀ1606A and À962ins/del polymorphisms in the human SAH gene.…”