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ibrillation and may therefore not be interpretable in the equivalent manner as BP in sinus rhythm. The 2008 European Society of Cardiology/European Society of Hypertension guidelines recommend the first-line prescription of two antihypertensive drugs in single-pill combinations (SPCs), also known as fixed-dose combinations, for the treatment of most patients with hypertension. This recommendation is based on a large amount of data, which shows that first-line treatment with SPCs supports reaching blood pressure targets rapidly and reducing cardiovascular outcome risk while keeping the therapeutic strategies as simple as possible and fostering adherence and persistence. As this approach constitutes a big shift from the stepped-care approaches that have been dominant for many years, practicing physicians have expressed concerns about using SPCs as first-line agents. In this review, we will discuss the barriers to the uptake of this recommendation. We will also offer suggestions to reduce the impact of these barriers and address specific concerns that have been raised.

The current study examines the placental and maternal lipid profile and expression of genes involved in placental lipid metabolism in women with preeclampsia.

The current study includes normotensive control women (n = 40) and women with preeclampsia (n = 39). Preeclampsia women were further classified into women delivering at term preeclampsia (T-PE; n = 15) and preterm preeclampsia (PT-PE; n = 24).

There were no significant differences in maternal lipid profile between the T-PE and normotensive control groups. Maternal plasma VLDL (P < 0.05) and ratios of total cholesterol  HDL (P < 0.05), atherogenic index [log (triglycerides/HDL)] (P < 0.01) and apolipoprotein B  apolipoprotein A (P < 0.05) were higher in the PT-PE group as compared with the normotensive control group. Placental total cholesterol and HDL levels were higher (P < 0.05) in the T-PE as compared with the normotensive control group. Higher placental triglycerides (P < 0.05) were observed in PT-PE group compared with T-PE rly in women delivering preterm. Lower expression of genes involved in placental fatty acid oxidation and transport was also observed in preeclampsia.

To determine whether there is an interaction between knowledge about hypertension and awareness of hypertension on the treatment and control of hypertension in three regions of South India at different stages of epidemiological transition (see Video, Supplemental Digital Content 1, http//links.lww.com/HJH/B426).

Using a cross-sectional design, we randomly selected villages within each of rural Trivandrum, West Godavari, and Chittoor. Sampling was stratified by age group and sex. We measured blood pressure and administered a questionnaire to determine knowledge and awareness of hypertension. Logistic regression was used to assess associations of awareness and knowledge about hypertension with its treatment and control in participants with hypertension, while examining for statistical interaction.

Among a total of 11 657 participants (50% male; median age 45 years), 3455 had hypertension. In analyses adjusted for age and sex, both knowledge score [adjusted odds ratio (aOR) 1.14 [95% confidence interval (CI) 1.12--1.17)] and awareness [aOR 104 (95% CI 82--134)] were associated with treatment for hypertension. Similarly, both knowledge score [aOR 1.10; 95% CI (1.08--1.12)] and awareness [aOR 13.4; 95% CI (10.7--16.7)], were positively associated with control of blood pressure in those with hypertension, independent of age and sex. There was an interaction between knowledge and awareness on both treatment and control of hypertension (P of attributable proportion <0.001 for each).

Health education to improve knowledge about hypertension and screening programs to improve awareness of hypertension may act in an additive fashion to improve management of hypertension in rural Indian populations.

Health education to improve knowledge about hypertension and screening programs to improve awareness of hypertension may act in an additive fashion to improve management of hypertension in rural Indian populations.

Few echocardiographic studies have focused on regression of left ventricular hypertrophy (LVH) in patients with renal artery stenosis after revascularization, with inconsistent results. We performed a systematic meta-analysis of these studies in order to offer a comprehensive information on this topic.

The PubMed, OVID-MEDLINE, and Cochrane library databases were analyzed to search English-language articles published from 1 January 1990 up to 31 March 2020. Studies were identified by crossing the following terms 'renal artery stenosis', 'renovascular hypertension', 'fibromuscular dysplasia', 'renal artery stenting', 'renal artery surgery' with 'cardiac damage', 'hypertensive heart disease' 'left ventricular mass', 'left ventricular hypertrophy', 'echocardiography'.

A total of 726 hypertensive patients with renal artery stenosis (mean age 61 years, 64% men, 98% treated, 10% with fibromuscular dysplasia) were included in 13 studies. Baseline and postintervention pooled mean LVM values were 220 ± 15 and 20ase in absolute and indexed LV mass index as well by a lower risk of LVH. Limitations include high prevalence of modest renal artery stenosis (≥50%); small sample of fibromuscular dysplasia; lack of randomized design of most studies.

The aim of this study was to identify demographic and clinical risk factors for mortality in patients with antineutrophil cytoplasmic antibodies-associated vasculitides (AAVs) in a Peruvian tertiary referral hospital.

Medical records of patients with AAV according to classification criteria or diagnosed by an experienced rheumatologist, covering the period between January 1990 and December 2018, were reviewed. Granulomatosis with polyangiitis, microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis, and renal-limited vasculitis were included. Selleck PF-477736 of mortality were demographic factors, clinical manifestations, antineutrophil cytoplasmic antibodies status, diagnosis, disease categorization, the 2009 Five Factor Score (FFS), and treatment. Cox regression models were used to determine the risk factors for mortality. Univariable and multivariable analyses using a backward selection method were performed.

One hundred ninety-six patients were included; female-to-male ratio was nts.

Ocular involvement was protective, whereas 2009 FFS ≥ 1 and renal and lung involvement were predictive factors of mortality in Peruvian AAV patients.

Previous investigations showed inconsistent results for comparison in clinical outcomes between patients with 3-vessel disease (3VD) treated with percutaneous coronary intervention (PCI) and coronary artery bypass graft (CABG) surgery. A systematic review and meta-analysis is essential to compare the clinical outcomes of PCI with CABG surgery for patients with 3VD.

We systematically searched on PubMed and Web of Science for articles which compared PCI with CABG for patients with 3VD and published from January 1989 to January 2020. We computed the hazard ratios (HRs) and 95% confidence intervals (CIs) for individual clinical outcomes.

This study indicated that the PCI group was associated with a 1.51-fold higher risk of all-cause mortality compared with the CABG group in patients with 3VD (HR 1.51, 95% CI 1.38-1.65). In addition, the PCI group showed a 3.08-fold and 2.94-fold higher risk compared with the CABG group in risks of myocardial infarction (MI) and target-vessel revascularization (TVR), respectively (MI HR 3.08, 95% CI 2.61-3.63; TVR HR 2.94, 95% CI 1.94-4.46).

In conclusion, in patients with 3VD, PCI was consistently associated with higher rates of all-cause mortality, MI, and TVR, compared with CABG.

In conclusion, in patients with 3VD, PCI was consistently associated with higher rates of all-cause mortality, MI, and TVR, compared with CABG.Chemokine (C-C motif) ligand 6 (CCL6), one of the small cytokines in the CC chemokine family, has been reported to involve in renal ischemia-reperfusion (I/R) injury. However, the role of CCL-6 in myocardial I/R injury is nonelucidated. In this study, we used in vitro H9c2 cell model to investigate the overall contributions of CCL6 to myocardial I/R injury. #link# We found the elevated level of CCL6 from the reanalysis of data set GSE-4105 and in hypoxia-reoxygenation (H/R)-injured H9c2 cells. CCL6 silencing attenuated the cardiomyocyte apoptosis induced by H/R injury, whereas exogenous CCL6 treatment aggravated the apoptosis of H/R-injured H9c2 cells. During CCL6 administration, the expression of numerous long noncoding RNAs was differentially regulated. Quantitative RT-Polymerase chain reaction assay demonstrated that insulin-like growth factor 2 (IGF2)-Antisense (AS) had the highest induction by CCL6 addition. IGF2-AS silencing alleviated the apoptosis of H/R-injured H9c2 cells. Collectively, we have identified a potential mechanism by which high expression of CCL6 contributes to the H/R-induced apoptosis in H9c2 cells through enhancing the expression of IGF2-AS. These findings also give evidence of the feasibility of CCL6 or long noncoding RNA IGF2-AS as a potential target for modulation or therapeutic intervention in myocardial I/R injury.Emerging evidence has demonstrated that long non-coding RNAs (lncRNAs) are related to the pathogenesis of atherosclerosis (AS). We aimed to investigate the roles and molecular mechanisms of myocardial infarction-associated transcript (MIAT) in the proliferation, migration and invasion of oxidized low-density lipoprotein (ox-LDL)-induced vascular smooth muscle cells (VSMCs). Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to determine the levels of MIAT, microRNA490-3p (miR-490-3p) and Intercellular Adhesion Molecule 1 (ICAM1). Cell Counting Kit-8 (CCK-8) assay was carried out to assess cell proliferation. Transwell assay was employed to evaluate cell migration and invasion. Western blot assay was performed to measure the protein levels of proliferating cell nuclear antigen (PCNA), N-cadherin, matrix metalloprotein-9 (MMP9) and ICAM1. Dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull-down assays were conducted to verify the relationship between miR-490-3p and MIAT or ICAM1. MIAT was elevated in AS patients' serum and ox-LDL-induced VSMCs. MIAT knockdown suppressed cell proliferation, migration and invasion in ox-LDL-stimulated VSMCs. link2 MIAT acted as a sponge of miR-490-3p and miR-490-3p deficiency overturned the inhibition of MIAT knockdown on VSMC proliferation, migration and invasion. ICAM1 was a direct target of miR-490-3p and ICAM1 silencing repressed the proliferation, migration and invasion of ox-LDL-stimulated VSMCs. Moreover, ICAM1 overexpression reversed the impacts of MIAT knockdown on ox-LDL-induced VSMC proliferation, migration and invasion. MIAT knockdown could depress cell proliferation, migration and invasion via miR-490-3p/ICAM1 axis in ox-LDL-induced VSMCs.Resveratrol is well known to exhibit vascular relaxant and antihypertensive effects. link3 In this study, we determined the effects of resveratrol on the modulation of cytosolic [Ca] level and adenosine 5'-triphosphate-induced Ca release from the sarcoplasmic reticulum (SR) in rat aortic smooth muscle cells (ASMCs) and explored its underlying mechanisms. In this article, cytosolic [Ca] and SR [Ca] in ASMCs were determined by Fluo-4/acetoxymethyl and Mag-Fluo-4/acetoxymethyl respectively. Resveratrol (20, 50, and 100 µM) caused a rapid and substantial reduction in cytosolic [Ca] in ASMCs bathed in normal Hank's Balanced Salt Solution or Ca-free Hank's Balanced Salt Solution. Pretreatment with resveratrol reduced adenosine 5'-triphosphate-induced SR Ca release and SR Ca content. In the cells bathed in Na-free physiological saline, which favors the reverse mode of the Na-Ca exchanger (NCX), resveratrol induced an increase in cytosolic [Ca] and SR [Ca]. However, its effect on cytosolic [Ca] was inhibited by the selective NCX inhibitor, SEA0400.