This is the first evidence that loss of cardiac KLF15 in CKD induced LVH is associated with unchecked trophic and fibrotic signalling, and that ACE inhibition ameliorates loss of cardiac KLF15.
In conclusion, Ang II and ACE1 expression in cardiac tissue was inhibited by NGN in L-NAME-treated rats, which may contribute to the inhibitory effects of NGN on left ventricular hypertrophy that is induced by pressure overload.
Angiotensin-converting enzyme insertion/deletion polymorphism, 24-h blood pressure profile and left ventricular hypertrophy in hypertensive individuals: a cross-sectional study.
We measured leucocyte telomere length (LTL) by Southern blot and analysed ACE I/D genotypes in 1249 subjects with hypertension and left ventricular hypertrophy (LVH).
Taken together, our results demonstrated significant association of ACE gene I/D polymorphism with LVH risk, especially in East Asians, and this association was more pronounced in studies involving males and untreated subjects.
Also, ACE and the 12 other genotypes did not affect risk of the primary composite endpoint or its components stroke, myocardial infarction, and cardiovascular death, or treatment differences between losartan and atenolol on these endpoints, as assessed by Cox proportional hazards models including baseline Framingham risk score and LVH.
An association between the insertion/deletion polymorphism of the angiotensin-converting enzyme (ACE) gene and the progression of left ventricular hypertrophy in patients with hypertrophic cardiomyopathy has been reported.
The aim of the study was to evaluate the prevalence of hypertension, left ventricular hypertrophy, hypertensive retinopathy in patients treated with haemodialysis and to evaluate the association between the polymorphism of RAAS genes: ACE I/D, AGT M235T AT1R A1166C, CYP112 (-344) and the systemic complications of arterial hypertension such as hypertensive retinopathy, left ventricular hypertrophy and also mortality in haemodialysis patients.
To assess the relationship between I/D polymorphism of the ACE gene and the severity of LVH assessed by echocardiography (Echo) in patients with type 2 diabetes mellitus.
The study investigated whether the insertion/deletion (I/D) polymorphism of ACE gene and the A/B polymorphism of the CMA gene are related to the regression of LVH in essential hypertension patients who were participants in a long-term trial of therapy with benazepril.
The effect of angiotensin receptor blockade ARB on the regression of left ventricular hypertrophy in hemodialysis patients: comparison between patients with D allele and non-D allele ACE gene polymorphism.
The ACE I/D and ACE 2350 G>A polymorphisms were in strong linkage disequilibrium and were independently associated with LVH, suggesting that ACE is likely to be a QTL for LVH.
The ACE I/D and ACE 2350 G>A polymorphisms were in strong linkage disequilibrium and were independently associated with LVH, suggesting that ACE is likely to be a QTL for LVH.
ACE I/D and ACE 2350 G>A polymorphisms are in strong linkage disequilibrium and are associated with LVH, suggesting that ACE is likely to be a QTL for LVH.
DNA analysis of the ACE gene deletion polymorphism showed those with the deletion/deletion (D/D) genotype had a greater progression of left ventricular hypertrophy compared to those carrying the other ACE genotypes (increase in hypertrophy: 6.2 +/- 3.3 vs. 1.7 +/- 4.2 mm; p < 0.01, D/D vs. I/D genotype; 2.8 +/- 5.8 mm; p = ns, D/D vs. I/I genotype).
Other studies found an interaction between ACE inhibitors and the ACE insertion/deletion (I/D) polymorphism, which resulted in differences in AT(1) receptor mRNA expression, left ventricular hypertrophy and arterial stiffness between different genetic variants.