The selective hydrogenation of furfural at ambient temperature has been investigated using a Pd/TiO
2
catalyst. The effect of the solvent was studied and high activity and selectivity to ...2-methylfuran and furfuryl alcohol was observed using octane as solvent but a number of byproducts were observed. The addition of Ru to the PdTiO
2
catalyst decreased the catalytic activity but improved the selectivity towards 2-methylfuran and furfuryl alcohol with decreased byproduct formation. Variation of the Ru/Pd ratio has shown an interesting effect on the selectivity. The addition of a small amount of Ru (1 wt%) shifted the selectivity towards furfuryl alcohol and 2-methylrofuran. Further increasing the Ru ratio decreased the catalytic activity and also showed a very poor selectivity to 2-methylfuran.
The selective hydrogenation of furfural at ambient temperature has been investigated using a Pd/TiO
2
catalyst.
Although rupture of thin-cap fibroatheroma (TCFA) underlies most myocardial infarctions, reliable TCFA identification remains challenging. Virtual-histology intravascular ultrasound (VH-IVUS) and ...optical coherence tomography (OCT) can assess tissue composition and classify plaques. However, direct comparisons between VH-IVUS and OCT are lacking and it remains unknown whether combining these modalities improves TCFA identification.
Two hundred fifty-eight regions-of-interest were obtained from autopsied human hearts, with plaque composition and classification assessed by histology and compared with coregistered ex vivo VH-IVUS and OCT. Sixty-seven regions-of-interest were classified as fibroatheroma on histology, with 22 meeting criteria for TCFA. On VH-IVUS, plaque (10.91±4.82 versus 8.42±4.57 mm(2); P=0.01) and necrotic core areas (1.59±0.99 versus 1.03±0.85 mm(2); P=0.02) were increased in TCFA versus other fibroatheroma. On OCT, although minimal fibrous cap thickness was similar (71.8±44.1 μm versus 72.6±32.4; P=0.30), the number of continuous frames with fibrous cap thickness ≤85 μm was higher in TCFA (6.5 1.75-11.0 versus 2.0 0.0-7.0; P=0.03). Maximum lipid arc on OCT was an excellent discriminator of fibroatheroma (area under the curve, 0.92; 95% confidence interval, 0.87-0.97) and TCFA (area under the curve, 0.86; 95% confidence interval, 0.81-0.92), with lipid arc ≥80° the optimal cut-off value. Using existing criteria, the sensitivity, specificity, and diagnostic accuracy for TCFA identification was 63.6%, 78.1%, and 76.5% for VH-IVUS and 72.7%, 79.8%, and 79.0% for OCT. Combining VH-defined fibroatheroma and fibrous cap thickness ≤85 μm over 3 continuous frames improved TCFA identification, with diagnostic accuracy of 89.0%.
Both VH-IVUS and OCT can reliably identify TCFA, although OCT accuracy may be improved using lipid arc ≥80° and fibrous cap thickness ≤85 μm over 3 continuous frames. Combined VH-IVUS/OCT imaging markedly improved TCFA identification.
Background: Coronary computed tomography angiography (CCTA) is now widely used in the diagnosis of coronary artery disease since it is a rapid, minimally invasive test with a diagnostic accuracy ...comparable to coronary angiography. However, to meet demands for increasing spatial and temporal resolution, higher x-ray radiation doses are required to circumvent the resulting increase in image noise. Exposure to high doses of ionizing radiation with CT imaging is a major health concern due to the potential risk of radiation-associated malignancy. Given its increasing use, a number of dose saving algorithms have been implemented to CCTA to minimize radiation exposure to “as low as reasonably achievable (ALARA)” without compromising diagnostic image quality.
Objective: The purpose of this review is to outline the most recent advances and current status of dose saving techniques in CCTA.
Method: PubMed, Medline, EMBASE and Scholar databases were searched to identify feasibility studies, clinical trials, and technology guidelines on the technical advances in CT scanner hardware and reconstruction software.
Results: Sub-millisievert (mSv) radiation doses have been reported for CCTA due to a combination of strategies such as prospective electrocardiogram-gating, high-pitch helical acquisition, tube current modulation, tube voltage reduction, heart rate reduction, and the most recent novel adaptive iterative reconstruction algorithms.
Conclusion: Advances in radiation dose reduction without loss of image quality justify the use of CCTA as a non-invasive alternative to coronary catheterization in the diagnosis of coronary artery disease.
Aim
To conduct a meta‐analysis and systematic review to examine the effects of glucagon‐like peptide‐1 receptor agonists (GLP‐1RAs) on clinical biomarkers of inflammation and oxidative stress in ...patients with type 2 diabetes.
Methods
Medline, Embase and the Cochrane Library were searched for randomised controlled trials (RCTs) that examined changes with GLP‐1RAs in a priori selected biomarkers of inflammation: C‐reactive protein (CRP), adiponectin, tumour necrosis factor‐alpha (TNFα), plasminogen activator inhibitor‐1, interleukin‐6, leptin; and of oxidative stress: malondialdehyde (MDA); 8‐iso‐prostaglandin F2α; and 8‐hydroxy‐2′‐deoxyguanosine (8‐OHdG).
Results
We included 40 eligible RCTs (n = 6749) with a median follow‐up of 6 months, a mean participant age of 53.1 years, 56.3% females, glycated haemoglobin (HbA1c) 55.6 mmol/mol, body mass index 28.8 kg/m2 and diabetes duration 7.46 years. Analysis of GLP‐1RAs versus standard diabetes therapies or placebo revealed significant reductions in CRP, TNFα and MDA, and significant increases in adiponectin for (mean difference −0.54 mg/L −0.75, −0.34; standard mean difference SMD −0.39 −0.62, −0.15; SMD −0.84 −1.61, −0.06 and SMD 0.30 0.12, 0.49, respectively 95% confidence intervals). Systolic blood pressure decreased significantly and was significantly and strongly correlated with a reduction in CRP. Homeostatic model assessment of insulin resistance was also significantly correlated with a reduction in CRP, but HbA1c was not.
Conclusions
There is strong evidence supporting clinically relevant anti‐inflammatory and antioxidant effects of GLP‐1RAs. This may be used to guide future targeted clinical use of GLP‐1RAs and the development of medications seeking to target the cardioprotective properties of GLP‐1RAs.
The purpose of this study was to determine whether thin-capped fibroatheromata (TCFA) identified by virtual histology intravascular ultrasound (VH-IVUS) are associated with major adverse cardiac ...events (MACE) on individual plaque or whole patient analysis.
Post-mortem studies have identified TCFA as the substrate for most myocardial infarctions. However, little is known about the natural history of individual TCFA and their link with MACE. VH-IVUS provides a method of identifying plaques in vivo that are similar (although not identical) to histologically defined TCFA, and has been validated in human atherectomy and post-mortem studies.
One hundred seventy patients with stable angina or troponin-positive acute coronary syndrome referred for percutaneous coronary intervention (PCI) were prospectively enrolled and underwent 3-vessel VH-IVUS pre-PCI and also post-PCI in the culprit vessel. MACE consisted of death, myocardial infarction, or unplanned revascularization.
In all, 30,372 mm of VH-IVUS were analyzed. Eighteen MACE occurred in 16 patients over a median follow-up of 625 days (interquartile range: 463 to 990 days); 1,096 plaques were classified, and 19 lesions resulted in MACE (13 nonculprit lesions and 6 culprit lesions). Nonculprit lesion factors associated with nonrestenotic MACE included VHTCFA (hazard ratio HR: 7.53, p = 0.038) and plaque burden >70% (HR: 8.13, p = 0.011). VHTCFA (HR: 8.16, p = 0.007), plaque burden >70% (HR: 7.48, p < 0.001), and minimum luminal area <4 mm(2) (HR: 2.91, p = 0.036) were associated with total MACE. On patient-based analysis, the only factor associated with nonrestenotic MACE was 3-vessel noncalcified VHTCFA (HR: 1.79, p = 0.004).
VH-IVUS TCFA was associated with nonrestenotic and total MACE on individual plaque analysis, and noncalcified VHTCFA was associated with nonrestenotic and total MACE on whole-patient analysis, demonstrating that VH-IVUS can identify plaques at increased risk of subsequent events. The preservation of the association between VHTCFA and MACE despite various analyses emphasizes its biological importance.
BACKGROUND—Mitochondrial DNA (mtDNA) damage occurs in both circulating cells and the vessel wall in human atherosclerosis. However, it is unclear whether mtDNA damage directly promotes atherogenesis ...or is a consequence of tissue damage, which cell types are involved, and whether its effects are mediated only through reactive oxygen species.
METHODS AND RESULTS—mtDNA damage occurred early in the vessel wall in apolipoprotein E–null (ApoE) mice, before significant atherosclerosis developed. mtDNA defects were also identified in circulating monocytes and liver and were associated with mitochondrial dysfunction. To determine whether mtDNA damage directly promotes atherosclerosis, we studied ApoE mice deficient for mitochondrial polymerase-γ proofreading activity (polG/ApoE). polG/ApoE mice showed extensive mtDNA damage and defects in oxidative phosphorylation but no increase in reactive oxygen species. polG/ApoE mice showed increased atherosclerosis, associated with impaired proliferation and apoptosis of vascular smooth muscle cells, and hyperlipidemia. Transplantation with polG/ApoE bone marrow increased the features of plaque vulnerability, and polG/ApoE monocytes showed increased apoptosis and inflammatory cytokine release. To examine mtDNA damage in human atherosclerosis, we assessed mtDNA adducts in plaques and in leukocytes from patients who had undergone virtual histology intravascular ultrasound characterization of coronary plaques. Human atherosclerotic plaques showed increased mtDNA damage compared with normal vessels; in contrast, leukocyte mtDNA damage was associated with higher-risk plaques but not plaque burden.
CONCLUSIONS—We show that mtDNA damage in vessel wall and circulating cells is widespread and causative and indicates higher risk in atherosclerosis. Protection against mtDNA damage and improvement of mitochondrial function are potential areas for new therapeutics.
We investigated the predictors, aetiology and long-term outcomes of acute kidney injury (AKI) following urgent percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS). Acute kidney ...injury occurred in 198 (7.2%) of 2917 patients: 14.1% of AKI cases were attributed to cardiogenic shock and 5.1% were classified as atheroembolic renal disease (AERD). Significant risk factors for AKI included age (odds ratio OR 1.05, 95% confidence limits CI 1.03-1.06), diabetes (OR 1.73, 95% CI 1.20-2.47), hypertension (OR 1.43, 95% CI 1.03-2.00), heart failure (OR 3.01, 95% CI 1.58-5.57), femoral access (OR 1.50, 95% CI 1.03-2.15), cardiogenic shock (OR 2.03, 95% CI 1.19-3.37) and ST-elevation myocardial infarction (STEMI) (OR 3.89, 95% CI 2.80-5.47). One-year mortality after AERD was 44.4% and renal replacement therapy (RRT) requirement 22.2% (compared with mortality 33.3% and RRT requirement 7.4%, respectively, in all other AKI patients). Mortality at 1 year was associated with AKI (OR 4.33, 95% CI 2.89-6.43), age (OR 1.08, 95% CI 1.06-1.09), heart failure (OR 1.92, 95% CI 1.05-3.44), femoral access (OR 2.05, 95% CI 1.41-2.95) and cardiogenic shock (OR 3.63, 95% CI 2.26-5.77). Acute kidney injury after urgent PCI is strongly associated with worse outcomes. Atheroembolic renal disease has a poor outcome and a high likelihood of long-term RRT requirement.
To assess compliance with European Society of Cardiology (ESC) secondary prevention recommendations in a nationwide contemporary population with diabetes mellitus (DM) and coronary artery disease.
We ...conducted a retrospective observational study using linked health data in patients across Wales with DM undergoing percutaneous coronary intervention (2012–2017). The follow-up was for one year. We analysed the clinical characteristics, medications, target levels for HbA1c, low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C) and blood pressure against the ESC prevention guidelines.
Overall, 3478 patients with diabetes had available data at 1-year post-PCI. Only 43% had HbA1c levels <53 mmol/L, but 81% had blood pressure < 140/80 (current ESC targets).
Prescribing frequency of the newer hypoglycaemic agents (glucagon-like peptide-1 receptor agonists and sodium-glucose co-transporter 2 inhibitors) was suboptimal, with a higher rate in patients with HbA1c ≥53 mmol/mol.
Only 51% & 27% of the patients had LDL-C levels <1.8 &1.4 mmol/L (2016 & 2019 guidelines recommendations respectively), and 55% & 34% had non-HDL-C levels <2.6 & 2.2 mmol/L (2016 & 2019 guidelines respectively). Of the uncontrolled LDL-C patients, 42% (2016 target) and 35% (2019 target) were prescribed high-intensity statins. Females were more likely to have LDL-C targets above the recommended level.
Achievement of ESC treatment goals in this very-high risk cohort for DM and hyperlipidaemia was far from optimal, with a low prescription rate of the guidelines-recommended therapy. Target goals for hypertension were met more frequently. An up-to-date analysis reflecting the current practice against the most recent guidelines is warranted.
•There is a clinical gap between real-life CV risk factors management and the recommendations laid in the guidelines.•P rescription rate of medications with previous personal experience is higher than relatively newer ones.•Females have a lower probability of achieving the recommended LDL-C targets and is less likely to be followed up.•Secondary prevention optimization is more efficient when managed by specialists rather than primary care physicians
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