Blood Pressure Variability: Marker or Predictor of Cardiovascular Risk?

Background: Regardless of the mean blood pressure value, short-term and long-term BP variability (BPV) are associated with the development and progression of target organ damage and predictors of cardiovascular complications and mortality. The purpose of the present study was to evaluate the prognostic significance of increased BPV in patients with arterial hypertension (AH). Methods and Results: The study consisted of two stages. In the first stage, a retrospective analysis of 365 ABPM results was carried out. As a result of the analysis, 271 patients aged 56.1±10.0 years with uncontrolled AH Grades 1-3 (ESC/ESH, 2018) were included in this study. Depending on the values of BPV, AH patients were divided into two groups: Group 1 consisted of patients with normal BPV (n=145), and Group 2 consisted of patients with increased BPV (n=126). The second stage included 91 patients with uncontrolled hypertension without permanent antihypertensive therapy who had increased BPV. We found statistically significant differences in BP between the AH patients with normal BPV and increased BPV. Thus, in the group with normal BPV, compared with increased BPV, the parameters of the average 24-h systolic BP (SBP), daytime SBP, and nighttime SBP were statistically lower (141±14.6 vs. 147.2±20.2 mmHg, P<0.004; 142.8±15.1 vs. 148.4±20.7 mmHg, P<0.01; and 136.2±15.5 vs. 143.8±21.4 mmHg, P<0.001; respectively). A statistically significant moderate direct correlation was found between the average 24-h SBP and the average 24-h and daytime SBP variability (SBPV) (rs=0.49 and rs=0.40 respectively, P<0.001 in all cases). A statistically significant moderate to weak direct correlation also was found between the average daytime SBP, and the average 24-h and daytime SBPV (rs=0.45 and rs=0.37, respectively, P<0.001 in all cases). A moderate direct correlation was found between nighttime SBP and 24-hour SBPV (rs=0.52, P<0.001) and between nighttime SBP and daytime SBPV (rs=0.42, P<0.001). Weak direct correlations were found between the average 24-h SBPV and central SBP (SBPc) (rs=0.34, P<0.001), as well as between the average 24-h and daytime SBPV and central pulse pressure (PPc) (rs=0.33 and rs=0.32, respectively, P<0.001 in all cases). A weak direct correlation was found between carotid intima-media thickness (CIMT) and the average 24-h and daytime SBPV (rs=0.37 [P<0.001] and rs=0.3 [P=0.04]). Conclusion: The increased BPV is associated with impaired diurnal blood pressure profile (DBPP) and structural and functional changes in blood vessels, in particular, an increase in SBPc and PP in the aorta, and CIMT thickening, which characterizes increased BPV as a predictor of vascular remodeling in patients with uncontrolled AH

A new dynamical mechanism of incomplete fusion in heavy-ion collision

The incomplete fusion has been proved as the formation and emission of the $\alpha$ particle by the increase in the rotational energy of the very mass-asymmetric dinuclear system. The results of the dinuclear system model have confirmed that the incomplete fusion in heavy-ion collisions occurs at a large orbital angular momentum ($L > 30 \hbar$) due to the strong increase of the intrinsic fusion barrier.Comment: 6 pages, 11 figure

Conformations of acyclic sulfites

1. Dialkyl sulfites in liquids, vapors, and solutions are represented by structures with trans-trans- and trans-gauche-conformations of the chain R-O-S-O-R. 2. Diaryl sulfites exist in a trans-gauche conformation. © 1974 Consultants Bureau

Conformation of 2-aryl groups in 1, 3-dioxanes

On the basis of the data of the method of dipole moments and the Kerr effect, 2-(p-X-phenyl)-1, 3-dioxanes and 5, 5-dichloro-2-(p-X-phenyl)-1,3-dioxanes, where X=Cl or NO2, have a chair conformation with an equatorial phenyl group, the plane of which coincides with the plane of symmetry of the dioxane ring. © 1975 Plenum Publishing Corporation

The Kinetics and Mechanism of the Sulfur Dioxide Oxidation by the Oxygen in the Presence of the Cobalt and Nickel Complexes, Fixed on Polymer Matrix

Catalytic sulphur dioxide oxidation by oxygen on the cobalt and nickel complexes fixed on polyetheleneamine was investigated. On the base of kinetics study it was established that SO2 and oxygen interact in inner sphere mechanism. UV-spectra and quantum-chemical calculations are presented, and on the base of them the ways of oxygen activation are discussed

Conformations of certain ethylene ketals with vicinal C-Hal bonds

The g⇌t equilibrium is displaced toward the less polar gauche form in the ethylene ketals of 2-chlorocyclohexanone and 2-bromocyclohexanone, and in the chloro- and bromoacetaldehydes. © 1978 Plenum Publishing Corporation

Sulfate group polarization and polarizability and the conformations of the dimethyl sulfates

1. Polarity and polarizability parameters have been determined for the sulfate group. 2. In solution, the dimethylsulfate molecule shows trans-trans conformation of the C-O-S-O-C chain. © 1977 Plenum Publishing CorporationPlenum Publishing Corporation

Inhibition of plasmin-mediated TAFI activation may affect development but not progression of abdominal aortic aneurysms

Objective: Thrombin-activatable fibrinolysis inhibitor (TAFI) reduces the breakdown of fibrin clots through its action as an indirect inhibitor of plasmin. Studies in TAFI-deficient mice have implicated a potential role for TAFI in Abdominal Aortic Aneurysm (AAA) disease. The role of TAFI inhibition on AAA formation in adult ApoE-/- mice is unknown. The aim of this paper was to investigate the effects of TAFI inhibition on AAA development and progression. Methods: Using the Angiotensin II model of AAA, male ApoE-/- mice were infused with Angiotensin II 750ng/kg/min with or without a monoclonal antibody inhibitor of plasmin-mediated activation of TAFI, MA-TCK26D6, or a competitive small molecule inhibitor of TAFI, UK-396082. Results: Inhibition of TAFI in the Angiotensin II model resulted in a decrease in the mortality associated with AAA rupture (from 40.0% to 16.6% with MA-TCK26D6 (log-rank Mantel Cox test p = 0.16), and 8.3% with UK-396082 (log-rank Mantel Cox test p = 0.05)). Inhibition of plasmin-mediated TAFI activation reduced the incidence of AAA from 52.4% to 30.0%. However, late treatment with MA-TCK26D6 once AAA were already established had no effect on the progression of AAA in this model. Conclusions: The formation of intra-mural thrombus is responsible for the dissection and early rupture in the angiotensin II model of AAA, and this process can be prevented through inhibition of TAFI. Late treatment with a TAFI inhibitor does not prevent AAA progression. These data may indicate a role for inhibition of plasmin-mediated TAFI activation in the early stages of AAA development, but not in its progression

Localization of type 1 diabetes susceptibility to the MHC class I genes HLA-B and HLA-A

The major histocompatibility complex (MHC) on chromosome 6 is associated with susceptibility to more common diseases than any other region of the human genome, including almost all disorders classified as autoimmune. In type 1 diabetes the major genetic susceptibility determinants have been mapped to the MHC class II genes HLA-DQB1 and HLA-DRB1 (refs 1-3), but these genes cannot completely explain the association between type 1 diabetes and the MHC region. Owing to the region's extreme gene density, the multiplicity of disease-associated alleles, strong associations between alleles, limited genotyping capability, and inadequate statistical approaches and sample sizes, which, and how many, loci within the MHC determine susceptibility remains unclear. Here, in several large type 1 diabetes data sets, we analyse a combined total of 1,729 polymorphisms, and apply statistical methods - recursive partitioning and regression - to pinpoint disease susceptibility to the MHC class I genes HLA-B and HLA-A (risk ratios >1.5; Pcombined = 2.01 × 10-19 and 2.35 × 10-13, respectively) in addition to the established associations of the MHC class II genes. Other loci with smaller and/or rarer effects might also be involved, but to find these, future searches must take into account both the HLA class II and class I genes and use even larger samples. Taken together with previous studies, we conclude that MHC-class-I-mediated events, principally involving HLA-B*39, contribute to the aetiology of type 1 diabetes. ©2007 Nature Publishing Group