22 research outputs found
Association of polymorphisms within the Renin-Angiotensin System with metabolic syndrome in a cohort of Chilean subjects
Association of T174M polymorphism of angiotensinogen gene with essential hypertension: a meta-analysis
Polymorphisms of the insertion / deletion ACE and M235T AGT genes and hypertension: surprising new findings and meta-analysis of data
The influence of GSTM1-null, TS-del6bp, XRCC1-A751C gene polymorphisms on overall survival in colorectal cancer patients related to the TNM parameters: A Romanian single-center study
[PP.24.10] THE D1 (C/T) - D2 (THR22ALA) - MTHFR (C677T) GENETIC MODEL ASSOCIATED WITH HYPOTHYROIDISM AS A RISK FACTOR FOR INCREASED MATERNAL-FETAL MORBIDITY IN PREECLAMPSIA
THE T344C-CYP11B2 POLYMORPHISM AS A RISK FACTOR FOR PREECLAMPSIA IN ROMANIAN PREGNANT WOMEN. ASSOCIATION WITH M235T (AGT) AND I/D (ACE) POLYMORPHISMS: PP.24.487
Renin-angiotensin-aldosterone system genotypes and cardiac remodeling response to essential hypertension
Abstract
Background/Introduction
Cardiac remodeling represent a response to uncontrolled essential hypertension (EHT). The morphological response is expressed by left ventricular (LV) mass index values and/or relative wall thickness (RWT) >0.42. Functionally response is expressed by isolated alteration of LV diastolic function (E/A<1).
Purpose
We aimed to establish the association between anatomical and functional adaptation to EHT, with two genetic variants of the renin-angiotensin-aldosterone system (RAAS): M235T-AGT and A3123C-R2 AngII.
Methods
In 139 hypertensive subjects cohort, we determined the M235T-AGT and A3123C-R2 AngII genotypes, using polymerase chain reaction-restriction fragment length polymorphism methods. The relationship between the studied RAAS gene polymorphisms and morphological and functional cardiac remodeling was assessed by multiple logistic regressions.
Results
We found that the C/C, A/C genotypes of the A3123C-R2 AngII polymorphism were statistically significantly associated with RWT<0.42 (p=0.033), so hypertensive patients carrying this genotype had a 2.7-fold increased risk to have a non-concentric type of cardiac response. The association was maintained even after adjustment for confounders - age, body mass index (BMI), systolic blood pressure (BP), and diastolic BP (p=0.008). We found statistically significant associations between LV diastolic dysfunction in hypertensive patients cohort carrying the T/T, M/T genotypes (M235T-AGT polymorphism) (p=0.037). Moreover, the association remained statistically significant even after adjustment for age, BMI, systolic BP, and diastolic BP (p=0.039). We could not identify any statistically significant associations between M235T-AGT, A3123C-R2 AngII polymorphisms, and LV mass index.
Conclusion(s)
Non-concentric type of cardiac response to essential hypertension was associated with A3123C-R2 AngII polymorphism. M235T-AGT polymorphism was found to be statistically significantly associated with alteration of LV diastolic function.
Funding Acknowledgement
Type of funding sources: Public Institution(s). Main funding source(s): “Iuliu Hatieganu” University of Medicine and Pharmacy Cluj-Napoca, as part of Doctoral Research Projects (DRP) 2016
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INTERACTION BETWEEN MATERNAL AND FETAL RAAS GENE POLYMORPHISMS ON THE RISK OF PREECLAMPSIA: PP.22.415
P5360Cardiovascular adaptation characteristics in women with preeclampsia
Abstract
Introduction
Even in normal pregnancies, physiologic functional and structural cardiovascular adjustments are required for progression of a successful pregnancy. In preeclamptic patients, these pregnancy-induced adaptive processes are intensified. It has been suggested that preeclampsia should be regarded as a failed stress test, a marker for increased later life cardiovascular risk.
Purpose
To differentiate between cardiovascular remodelling patterns in preeclamptic vs. normal pregnancies, using echocardiography and digital photoplethysmography.
Material
We conducted a single-center case–control study, performing cardiovascular assessment during last trimester of pregnancy in 56 pregnant women with preeclamsia (PE) and 62 healthy pregnant women, without CV risk factors.
Echocardiography was performed to characterize left ventricular (LV) remodelling patterns and to assess LV systolic and dyastolic function. Also, digital photoplethysmography was used to determine stiffness index (SI) and vascular age (VA). Data between groups were compared.
Results
The two groups were matched by age (30.42±6.37 vs 29.96±5.18 y/o, p=0.74), body mass index (29.84±5.31 vs. 28.53±5.33g, p=0.30), and parity (primiparous 33 vs. 25, p=0.47, multiparous 23 vs. 27, p=0.78). The prevalence of LV hypertrophy, expressed as LV mass (185.75±39.61 vs. 144.85±28.81 g, p=0.0023) and LV relative wall thickness (0.49±0.08 vs. 0.42±0.069), was higher in preeclamptic women, corresponding to higher blood pressure values (systolic blood pressure 164.27±20.09 vs 114±18.04 mmHg, p=0.0014, dyastolic blood pressure 103.22±14.13 vs. 72.83±11.34 mmHg, p=0.0015). The most common remodeling type in preeclamptic group was concentric hypertrophy (28/56, 50%), while in normal pregnancy group, normal geometry (21/62, 34%) and concentric remodeling (21/62, 34%), were more frequently encountered. No significant differences between groups were found in terms of LV ejection fraction, while dyastolic LV function, depicted through transmitral flow parameters, varied only when E/A ratio was measured (1.38±0.34 vs. 1.62±0.46, p=0.03). In preeclamptic women, SI was increased (9.27±1.86 vs. 7.13±1.86 m/s, p=0.0091), with a significantly higher VA also (47.44±21.61 vs. 28.75±7.51y/o, p=0.0001), for a similar maternal age of the study groups.
Conclusions
We documented a higher prevalence of LV hypertrophy, with the concentric remodelling pattern predominance, as well as a significantly advanced vascular age due to an increased arterial stiffness, among preeclamptic group. Follow-up of these patients may reveal features, or cut-off values, useful to early identify a population that may benefit from early interventions to prevent cardiovascular disease.
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