Background Rupture of abdominal aortic aneurysm (rAAA) is associated with high case fatality rates, and risk of rupture increases with the AAA diameter. Heme oxygenase‐1 (gene HMOX1 , protein HO‐1) is a stress‐induced protein and induction has protective effects in the vessel wall. HMOX1 −/− mice are more susceptible to angiotensin II‐induced AAA formation, but the regulation in human nonruptured and ruptured AAA is only poorly understood. Our hypothesis proposed that HO‐1 is reduced in AAA and lowering is inversely associated with the AAA diameter. Methods and Results AAA walls from patients undergoing elective open repair (eAAA) or surgery because of rupture (rAAA) were analyzed for aortic HMOX1 /HO‐1 expression by quantitative real‐time polymerase chain reaction and Western blot. Aortas from patients with aortic occlusive disease served as controls. HMOX1 /HO‐1 expression was 1.1‐ to 7.6‐fold upregulated in eAAA and rAAA. HO‐1 expression was 3‐fold higher in eAAA specimen with a diameter >84.4 mm, whereas HO‐1 was not different in rAAA. Other variables that are known for associations with AAA and HO‐1 induction were tested. In eAAA, HO‐1 expression was negatively correlated with aortic collagen content and oxidative stress parameters H 2 O 2 release, oxidized proteins, and thiobarbituric acid reactive substances. Serum HO‐1 concentrations were analyzed in patients with eAAA, and maximum values were found in an aortic diameter of 55 to 70 mm with no further increase >70 mm, compared with <55 mm. Conclusions Aortic HO‐1 expression was increased in eAAA and rAAA. HO‐1 increased with the severity of disease but was additionally connected to less oxidative stress and vasoprotective mechanisms.
Aim Analyzing a 5-year experience of surgical treatment of cardiosurgical patients with atrial fibrillation (AF).Material and methods The study analyzed results of surgical treatment with extracorporeal circulation in 132 patients with AF who underwent the Maze-IV procedure using a radiofrequency ablator with transmurality feedback from 2013 through 2018.Results Two fatal outcomes were observed in the study group. These outcomes took place in the early postoperative period and were associated with progressive acute heart failure in patients with repeated surgery for mitral valve restenosis. 61.2% of the patients had no AF. Recurrent AF was observed during the first three years after surgery in association with withdrawal of the antiarrhythmic medication, which confirmed a need for long-term antiarrhythmic therapy. Analysis of risk factors for AF relapse identified significant predictors, including left ventricular dilatation larger than 5.5 cm at baseline and more than two-year duration of a history of arrhythmias.Conclusion The Maze-IV procedure proved an effective and safe method of surgical treatment in AF patients with acquired heart defects and ischemic heart disease, which allowed maintaining sinus rhythm in 61.2% of patients for 5 years. Preventive amiodarone saturation reduced the risk of AF relapse by 24.2 % (p=0.038) and incidence of postoperative arrhythmic complications by 34.9 % (p=0.008) in cardiosurgical patients.
The new approach for production prediction was developed and is described in the article which involves the clustering analysis aimed to well logs such that the reservoir and non-reservoir rocks are obtained (presented by various clusters) and the subsequent linkage among clusters' types, their thicknesses and production characteristics is found. It may be implemented for the prediction of the production for planned wells' ranking further. Such approach may provide the solution to various tasks. It may be used for the geological features' estimation. For example, clustering may be adjusted such that sedimentological interpretation becomes simpler, geological models may become more accurate since the machine interpretation was confirmed to be able to find the errors in human interpretation. Moreover, the necessity of implementation of the method was proved for production prediction by regression analysis when clustering results and dynamic characteristics are used simultaneously.
Angiotensin II (ANGII)‐induced endothelial dysfunction is recognized to be an important mediator of hypertension‐induced vascular remodeling. However, the mechanisms by which ANGII‐induced endothelial dysfunction contributes to this process are not fully understood. We addressed the role of angiotensin receptor type 1 (AT1R)/Akt1 signaling in endothelial cells in the genesis of vascular remodeling during ANGII‐induced hypertension. We employed two mice models, one lacking both isoforms of AT1 receptors on endothelial cells (AT1aREC−/−xAT1bR−/−) and a second model lacking endothelial Akt1 (Akt1Tie2−/−). Mice were infused with 1.5 mg/kg/day ANGII using osmotic minipumps. Systolic blood pressure (SBP) was measured using the tail‐cuff method. After 4 weeks, vascular remodeling was assessed using histology and endothelial function was measured using Mulvany myography. Matrix metalloproteinase 2 (MMP2) activity was determined with gelatin zymography and inflammatory cell count in vascular tissue by flow cytometry. After 4 weeks of ANGII infusion, AT1aREC−/−xAT1bR−/− mice had ~12 mmHg lower SBP compared to WT mice. The mice were protected from vascular remodeling and showed less aortic hypertrophy (P<0.01) and fibrosis (P<0.01). AT1aREC−/−xAT1bR−/− mice had more elastin (P<0.05) content and less MMP2 activity (P<0.01) in aorta. Endothelium‐dependent relaxation was ~35 % greater in AT1aREC−/−xAT1bR−/− compared to WTs. Inflammatory cell count (CD45+, TCR‐β+, CD4+ and CD8+ cells) was lower in aorta of AT1aREC−/−xAT1bR−/− mice (P<0.01) compared to WT mice. While AT1aREC−/−xAT1bR−/− mice were protected from vascular remodeling, mice lacking only one isoform of AT1R ‐ AT1aRwt/wtxAT1bR−/− or AT1aREC−/− xAT1bRwt/wt mice were not protected and did not differ from WT mice. Akt1Tie2−/− mice showed a similar protective vascular phenotype as AT1aREC−/−xAT1bR−/− mice. Experiments with cultured cells confirmed the importance of the AT1R/Akt1 axis in vascular remodeling. MMP2 activity was significantly (P<0.01) lower in ANGII‐stimulated human aortic smooth muscle cells co‐cultured with endothelial cells where Akt1 was silenced compared to control. Supplementation of endothelin‐1 (ET1) reversed this effect and led to activation of MMP2. Inhibition of ETa, but not ETb receptor, on smooth muscle cells blocked the activation of MMP2 in these cells. Experiments on isolated human aorta showed that ANGII‐stimulated aortas without endothelium had less (P<0.01) MMP2 activity compared to aortas with endothelium. Addition of ET1 reversed this effect, whereas inhibition of ETa, but not ETb, receptor blocked the activation of MMP2. We demonstrate that the endothelial AT1R/Akt1 axis mediates ANGII‐induced endothelial dysfunction, which causes ET1/ETa receptor dependent activation of MMP2. This axis appears to be the mechanistic link for enhanced vascular inflammation and consequent remodeling. Our findings advance the understanding of ANGII‐induced endothelial dysfunction and its contribution to vascular remodeling. Support or Funding Information Re...
Background Indication for prophylactic surgical abdominal aortic aneurysm (AAA) repair depends on the maximal aortic diameter. The lectin‐like oxidized low‐density lipoprotein receptor‐1 (LOX‐1) is the major receptor for uptake of oxidized low‐density lipoprotein cholesterol and is implicated in atherosclerosis. A soluble form of LOX‐1 (sLOX‐1) has been discussed as a novel biomarker in coronary artery disease and stroke. Herein, we assessed the regulation of aortic LOX‐1 as well as the diagnostic and risk stratification potential of sLOX‐1 in patients with AAA. Methods and Results Serum sLOX‐1 was assessed in a case–control study in AAA (n=104) and peripheral artery disease (n=104). sLOX‐1 was not statistically different between AAA and peripheral artery disease but was higher in AAA (β=1.28, P =0.04) after adjusting for age, atherosclerosis, type 2 diabetes, prescription of statins, β‐blockers, ACE inhibitors, and therapeutic anticoagulation. sLOX‐1 was not associated with the aortic diameter, AAA volume, or the thickness of the intraluminal thrombus. Aortic LOX‐1 mRNA expression tended to be higher in AAA when compared with disease, and expression was positively associated with cleaved caspase‐3, smooth muscle actin, collagen, and macrophage content. Conclusions In AAA, sLOX‐1 was differently affected by age, cardiometabolic diseases, and corresponding medical therapies. Comparison with nonatherosclerotic disease would be beneficial to further elucidate the diagnostic potential of sLOX‐1, although it was not useful for risk stratification. Aneurysmal LOX‐1 mRNA expression was increased and positively associated with smooth muscle cells and collagen content, suggesting that LOX‐1 is eventually not deleterious in human AAA and could counteract AAA rupture.
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