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Numerous advances and innovative therapies have been introduced in interventional cardiology over the recent years, since the first introduction of balloon angioplasty, but bioresorbable scaffold is certainly one of the most exciting and attracting one. Despite the fact that the metallic drug-eluting stents have significantly diminished the re-stenosis ratio, they have considerable limitations including the hypersensitivity reaction to the polymer that can cause local inflammation, the risk of neo-atherosclerotic lesion formation which can lead to late stent failure as well as the fact that they may preclude surgical revascularization and distort vessel physiology. Bioresorbable scaffolds overcome these limitations as they have the ability to dissolve after providing temporary scaffolding which safeguards vessel patency. In this article we review the recent developments in the field and provide an overview of the devices and the evidence that support their efficacy in the treatment of CAD. Currently 3 devices are CE marked and in clinical use. Additional 24 companies are developing these kind of coronary devices. Most frequently used material is PLLA followed by magnesium.

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Objectives The study compared, by intravascular ultrasound (IVUS), acute gain (AG) at the site of the pre-procedural minimal lumen area (MLA) achieved by either the Absorb (Abbott Vascular, Santa Clara, California) scaffold or the Xience stent and identified the factors contributing to the acute performance of these devices. Background It is warranted that the acute performance of Absorb matches that of metallic stents; however, concern exists about acute expansion and lumen gain with the use of Absorb. Methods Of a total of 501 patients (546 lesions) in the ABSORB II (ABSORB II Randomized Controlled Trial) randomized trial, 445 patients with 480 lesions were investigated by IVUS pre- and post-procedure. Comparison of MLA pre- and post-procedure was performed at the MLA site by matching pre- and post-procedural IVUS pullbacks. Results Lower AG on IVUS (lowest tertile) occurred more frequently in the Absorb arm than in the Xience arm (3.46 mm2 vs. 4.27 mm2, respectively; p < 0.001; risk ratio: 3.04; 95% confidence interval: 1.94 to 4.76). The plaque morphology at the MLA cross-section was not independently associated with IVUS acute gain. The main difference in AG in MLD by angiography was observed at the time of device implantation (Xience vs. Absorb, Δ+1.50 mm vs. Δ+1.23 mm, respectively), whereas the gain from post-dilation was similar between the 2 arms (Δ+0.16 mm vs. Δ+0.16 mm) when patients underwent post-dilation, although expected balloon diameter was smaller in the Absorb arm than in the Xience arm (p = 0.003) during post-dilation. Conclusions At the site of the pre-procedural MLA, the increase of the lumen post-procedure was smaller in the Absorb-arm than in the Xience arm. To achieve equivalent AG to Xience, the implantation of Absorb may require more aggressive strategies at implantation, pre- and post-dilation than the technique used in the ABSORB II trial. (ABSORB II Randomized Controlled Trial [ABSORB II]; NCT01425281)

Objective: To investigate relations of several circulating chemokines with extent and phenotype of coronary atherosclerosis and with 1-year clinical outcome.Methods: Intravascular ultrasound virtual histology (IVUS-VH) imaging of a coronary artery was performed in 581 patients. Monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1α (MIP-1α), MIP-1β and regulated upon activation normal T cell expressed and secreted (RANTES) were measured in plasma.Results: Higher MCP-1, MIP-1α and lower RANTES were associated with coronary plaque burden. Higher MCP-1, MIP-1α and lower RANTES were associated with the presence of IVUS-VH-derived thin-cap fibroatheroma lesions. RANTES was associated with major adverse cardiac events.Conclusions: RANTES is a promising biomarker that is inversely associated with coronary plaque burden and vulnerability, as well as with death and acute coronary syndrome.Trial registration: ClinicalTrials.gov identifier: NCT01789411.

Conference Abstract| January 01 1986 Influence of Autonomic Blockade on Cardiovascular effects of Infused Adenosine in Man B Clarke; B Clarke 1Department of Clinical Pharmacology, Cardiothoracic Institute, Brompton Hospital, London SW3 6HP Search for other works by this author on: This Site PubMed Google Scholar T-B Conradson; T-B Conradson 1Department of Clinical Pharmacology, Cardiothoracic Institute, Brompton Hospital, London SW3 6HP Search for other works by this author on: This Site PubMed Google Scholar CMS Dixon; CMS Dixon 1Department of Clinical Pharmacology, Cardiothoracic Institute, Brompton Hospital, London SW3 6HP Search for other works by this author on: This Site PubMed Google Scholar PJ Barnes PJ Barnes 1Department of Clinical Pharmacology, Cardiothoracic Institute, Brompton Hospital, London SW3 6HP Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (1986) 71 (s15): 45P. https://doi.org/10.1042/cs071045P Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation B Clarke, T-B Conradson, CMS Dixon, PJ Barnes; Influence of Autonomic Blockade on Cardiovascular effects of Infused Adenosine in Man. Clin Sci (Lond) 1 January 1986; 71 (s15): 45P. doi: https://doi.org/10.1042/cs071045P Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1986 The Biochemical Society and the Medical Research Society1986 Article PDF first page preview Close Modal You do not currently have access to this content.

Background— Surveillance conventional coronary angiography (CCA) is recommended 2 to 6 months after stent-supported left main coronary artery (LMCA) percutaneous coronary intervention due to the unpredictable occurrence of in-stent restenosis (ISR), with its attendant risks. Multislice computed tomography (MSCT) is a promising technique for noninvasive coronary evaluation. We evaluated the diagnostic performance of high-resolution MSCT to detect ISR after stenting of the LMCA. Methods and Results— Seventy-four patients were prospectively identified from a consecutive patient population scheduled for follow-up CCA after LMCA stenting and underwent MSCT before CCA. Until August 2004, a 16-slice scanner was used (n=27), but we switched to the 64-slice scanner after that period (n=43). Patients with initial heart rates &gt;65 bpm received β-blockers, which resulted in a mean periscan heart rate of 57±7 bpm. Among patients with technically adequate scans (n=70), MSCT correctly identified all patients with ISR (10 of 70) but misclassified 5 patients without ISR (false-positives). Overall, the accuracy of MSCT for detection of angiographic ISR was 93%. The sensitivity, specificity, and positive and negative predictive values were 100%, 91%, 67%, and 100%, respectively. When analysis was restricted to patients with stenting of the LMCA with or without extension into a single major side branch, accuracy was 98%. When both branches of the LMCA bifurcation were stented, accuracy was 83%. For the assessment of stent diameter and area, MSCT showed good correlation with intravascular ultrasound ( r =0.78 and 0.73, respectively). An intravascular ultrasound threshold value ≥1 mm was identified to reliably detect in-stent neointima hyperplasia with MSCT. Conclusions— Current MSCT technology, in combination with optimal heart rate control, allows reliable noninvasive evaluation of selected patients after LMCA stenting. MSCT is safe to exclude left main ISR and may therefore be an acceptable first-line alternative to CCA.

Both the sirolimus-(SES) and paclitaxel-eluting (PES) stents have been shown to reduce restenosis rates when used in relatively simple lesions. This study aimed to evaluate the results of a consecutive series of patients treated with drug-eluting stent implantation for de novo bifurcation lesions, and compared outcomes with respect to stenting strategy and stent type.From April 2002 to September 2003, all patients at our institution were treated with drug-eluting stent implantation. A consecutive series of 144 patients were treated for 167 de novo bifurcation lesions with SES, followed by 104 patients treated with PES for 113 lesions.Clinical follow-up at 6 months was obtained in 99% patients with survival-free of major adverse cardiac events (MACE) of 93.7% for SES versus 85.8% for PES, p=0.05. By multivariate analysis, factors predictive for MACE were age, diabetes mellitus, previous CABG, multivessel disease, treatment for acute myocardial infarction, and treatment with PES. Survival-free of target lesion revascularization (TLR) was 95.7% for SES versus 86.8% for PES, p=0.01, with stent type being the only independent predictor. Technique of stenting was not a predictor of either MACE or TLR.MACE rates for both the SES and PES are low compared with historical data of bare metal stents. The most effective techniques for bifurcation stenting remain undefined. Our data suggests a higher need for TLR for the PES compared with the SES, however further randomized studies are needed to fully evaluate both stenting strategy, and any difference between the stents.

Respiratory virus infections are commonly associated with COPD exacerbations, but little is known about the mechanisms linking virus infection to exacerbations. Pathogenic mechanisms in stable COPD include oxidative and nitrosative stress and reduced activity of histone deacetylase-2 (HDAC2), but their roles in COPD exacerbations is unknown. We investigated oxidative and nitrosative stress (O&NS) and HDAC2 in COPD exacerbations using experimental rhinovirus infection.Nine subjects with COPD (Global Initiative for Chronic Obstructive Lung Disease stage II), 10 smokers, and 11 nonsmokers were successfully infected with rhinovirus. Markers of O&NS-associated cellular damage, and inflammatory mediators and proteases were measured in sputum, and HDAC2 activity was measured in sputum and bronchoalveolar macrophages. In an in vitro model, monocyte-derived THP-1 cells were infected with rhinovirus and nitrosylation and activity of HDAC2 was measured.Rhinovirus infection induced significant increases in airways inflammation and markers of O&NS in subjects with COPD. O&NS markers correlated with virus load and inflammatory markers. Macrophage HDAC2 activity was reduced during exacerbation and correlated inversely with virus load, inflammatory markers, and nitrosative stress. Sputum macrophage HDAC2 activity pre-infection was inversely associated with sputum virus load and inflammatory markers during exacerbation. Rhinovirus infection of monocytes induced nitrosylation of HDAC2 and reduced HDAC2 activity; inhibition of O&NS inhibited rhinovirus-induced inflammatory cytokines.O&NS, airways inflammation, and impaired HDAC2 may be important mechanisms of virus-induced COPD exacerbations. Therapies targeting these mechanisms offer potential new treatments for COPD exacerbations.

Six normal male subjects, ages 28–40 years, were studied on separate days during increasing infusions with adenosine, 40–120 μ g kg ‐1 min ‐1 , before and during infusions of two xanthine derivatives, theophylline (mean plasma concentration 9 mg 1 –1 ) and enprofylline (mean plasma concentration 3 mg 1 –1 ). The study was double‐blind, randomized, placebo controlled. Cardio‐respiratory variables were measured non‐invasively. Adenosine by itself increased heart rate ( P &lt; 0.05), skin temperature ( P &lt; 0.05), resting minute ventilation ( P &lt; 0.01) and decreased estimated P a, CO2 ( P &lt; 0.01). Compared with placebo enprofylline increased heart rate ( P &lt; 0.05) and shifted the heart rate and ventilation dose–response curves of adenosine upwards ( P &lt; 0.05 and P &lt; 0.02, respectively). Theophylline did not by itself affect heart rate but significantly ( P &lt; 0.05) reduced the heart rate response to adenosine. Compared with placebo theophylline caused a small increase in minute ventilation ( P &lt; 0.05) and flattened the dose‐response curves of the effects of adenosine on ventilation ( P &lt; 0.01) and P a, CO2 , ( P &lt; 0.01). Theophylline also reduced abdominal and chest discomfort caused by adenosine permitting significantly ( P &lt; 0.05) higher infusion rates of adenosine. These findings suggest that, with equipotent bronchodilating plasma concentrations, theophylline can inhibit while enprofylline augments some cardio‐respiratory stimulant effects of infused adenosine in man.