Margarita Torres-Tamayo

Estrogen effect on heart rate variability in hypertensive postmenopausal women

UNLABELLED Healthy postmenopausal women and hypertensive patients show an imbalance in the modulation of autonomic nervous control of the cardiovascular system, which may increase the cardiovascular risk. OBJECTIVE To examine the heart rate variability (HRV) response to estrogen replacement therapy (ERT) and its association with changes in metabolic variables in hypertensive postmenopausal women. METHODS A double-blind, placebo-controlled clinical trial was conducted in 30 hypertensive postmenopausal women receiving 180 mg/day of verapamil. The experimental group (n=16) received 0.625 mg OD of natural conjugated estrogens during 4 months, while control group (n=14) received a placebo. Lipids, lipoproteins, apolipoproteins, glucose and insulin were measured at 0, 2 and 4 months. HRV was determined in time and frequency domains using a 24-h Holter before and after ERT. RESULTS Significant higher values of spectral and non-spectral parameters of HRV, associated with a lower LF/HF ratio, were found at the end of 4 months of ERT. Multiple regression analysis revealed that estrogen treatment itself and changes in total cholesterol, LDL-cholesterol, glucose and waist circumference, contributed to the changes observed in indexes reflecting parasympathetic activity in time and frequency domains. CONCLUSIONS We conclude that ERT partially improves HRV favoring increased parasympathetic drive, and that part of the effect may be mediated by changes in metabolic variables.

Lipid plasma concentrations of HDL subclasses determined by enzymatic staining on polyacrylamide electrophoresis gels in children with metabolic syndrome.

BACKGROUND The antiatherogenic role of different HDL subclasses is still controversial. HDL particles of the same size can have different lipid contents in some physiopathological situations. However, little is known about the plasma lipid levels of HDL subclasses when they are separated by their hydrodynamic diameter. METHODS Triglycerides (Tg), phosphatidylcholine (Ph), and cholesterol (C) plasma concentrations of HDL subclasses, were determined by enzymatic staining on polyacrylamide gradient gel (PAGE) in 50 pediatric patients with metabolic syndrome (MS), and 50 control children paired by age and gender. Proteins of HDL subclasses were also stained for the assessment of the relative size distribution of HDL. RESULTS Relative HDL size distribution was shifted to small particles in MS pediatric patients when determined per protein. In contrast, cholesterol plasma concentrations corresponding to the HDL2b, 2a, 3a, and 3b subclasses were decreased; triglycerides of HDL3b and 3c, as well as plasma phospholipids from HDL3c, were elevated in MS patients as compared to controls. The C-to-Ph ratio, considered as indicative of HDL composition, was similar among the 5 HDL subclasses in control subjects, whereas this ratio gradually decreased from large HDL2b to small HDL3c in the MS group. Cholesterol plasma concentrations of HDL subclasses correlated with the components of the MS. CONCLUSIONS Lipids of HDL subclasses provide more and accurate information than the relative HDL size distribution determined by protein staining, and may contribute to understand better HDL metabolism and the coronary risk associated to these lipoproteins.

The Srb1+1050T Allele Is Associated with Metabolic Syndrome in Children but Not with Cholesteryl Ester Plasma Concentrations of High-Density Lipoprotein Subclasses

BACKGROUND Low cholesterol and phospholipid plasma levels of some high-density lipoprotein (HDL) subclasses have been described in children with metabolic syndrome. Scavenger receptor class B type I (SR-BI) has been proposed to be at the origin of such HDL alterations because of its key role on cholesteryl esters-HDL metabolism. However, the possible contribution of SR-BI has not been specifically explored in this kind of patients. METHODS Plasma lipid concentrations of HDL subclasses, i.e., triglycerides (TG), phosphatidylcholine (Ph), free cholesterol (FC), and total cholesterol (TC), were determined by enzymatic staining on polyacrylamide gradient gels (PAGE) in 39 pediatric patients with metabolic syndrome and 65 children as controls. Cholesteryl esters were estimated by the difference between TC and FC. Proteins of HDL subclasses were also stained for the assessment of the relative size distribution of HDL. For statistical analysis, the study population was grouped by Srb1 +1050C-->T polymorphism (rs5888) as carriers or noncarriers of the T allele, and data were corrected by metabolic syndrome status. RESULTS The Srb1 +1050T allele was associated with metabolic syndrome [odds ratio (OR)=2.18 (1.12-4.22), P=0.02]. Plasma TG corresponding to HDL3a, as well as the relative proportion of this HDL subclass, were slightly higher in carriers of the T allele as compared to CC homozygous subjects. Cholesteryl esters plasma concentrations of all HDL subclasses were comparable between T allele carriers and noncarriers after correction by metabolic syndrome status. CONCLUSIONS Srb1 +1050T was associated with metabolic syndrome, but T carrier subjects did not show important differences concerning HDL subclasses as compared to noncarriers.

Insulin Resistance in Adipose Tissue but Not in Liver Is Associated with Aortic Valve Calcification

Background. Insulin resistance is involved in the pathogenesis of cardiovascular disease, but its relationship with cardiovascular calcification has yielded conflicting results. The purpose of the present study was to investigate the role of hepatic and adipose tissue insulin resistance on the presence of coronary artery (CAC > 0) and aortic valve calcification (AVC > 0). Methods. In 1201 subjects (52% women, 53.6 ± 9.3 years old) without familiar and personal history of coronary heart disease, CAC and AVC were assessed by multidetector-computed tomography. Cardiovascular risk factors were documented and lipid profile, inflammation markers, glucose, insulin, and free fatty acids were measured. Hepatic insulin resistance (HOMA-IR) and adipose tissue insulin resistance (Adipo-IR) indices were calculated. Results. There was a significant relationship between HOMA-IR and Adipo-IR indices (r = 0.758, p < 0.001). Participants in the highest quartiles of HOMA-IR and Adipo-IR indices had a more adverse cardiovascular profile and higher prevalence of CAC > 0 and AVC > 0. After full adjustment, subjects in the highest quartile of Adipo-IR index had higher odds of AVC > 0 (OR: 2.40; 95% CI: 1.30–4.43), as compared to those in the lowest quartile. Conclusions. Adipo-IR was independently associated with AVC > 0. This suggests that abnormal adipose tissue function favors insulin resistance that may promote the development and progression of AVC.

Increased expression of miR-33a in monocytes from Mexican hypertensive patients in elevated carotid intima-media thickness

AbstractmiR-33a has been described as a key regulator in the initiation and progression of atherosclerosis. However, its role in arterial hypertension (HTA) has not been elucidated. Therefore, the aim of this study was to determine the association between the expression of miR-33a (5p and 3p) and the carotid intima-media thickness (cIMT) in samples of monocytes and serum from hypertensive patients. The miR-33a-5p and miR-33a-3p expression in monocytes and serum from Mexican hypertensive patients were examined by RT-PCR. This study involved 84 subjects (42 normotensive subjects and 42 patients with essential hypertension). Our study revealed that miR-33a-5p expression was significantly upregulated in the monocytes of hypertensive patients compared with the control group (p = 0.001), while miR-33a-3p was significantly downregulated (p = 0.013). miR-33a-5p upregulation [OR: 5.53, 95% CI: 2.01–15.20; p = 0.001], as well as miR-33a-3p downregulation [OR: 3.32, 95% CI: 1.45–7.60; p = 0.004] in monocytes, was associated with an increased risk of developing hypertension. In addition, miR-33a-5p upregulation in hypertensive patients was associated with an increased risk of presenting cIMT [OR: 5.99, 95% CI: 1.10–32.85; p = 0.039]. Moreover, we found no significant differences in the expression of both strands of miR-33a in serum of our patients. Our results showed an upregulation of miR-33a-5p and downregulation of miR-33a-3p in monocytes, these data are associated with cIMT, which could be a risk factor for the development of hypertension. In addition, upregulation of miR-33a-5p in monocytes from Mexican hypertensive patients could be involved in the development of atherosclerosis.