Publications

Two-year outcome of the use of paclitaxel-eluting stents in aorto-ostial lesions

Background Percutaneous treatment of stenoses involving aorto-ostial lesions is technically demanding and has been associated with lower procedural success and poorer clinical and angiographic outcomes when compared with non-ostial lesions. This study evaluated the immediate and long-term (2-year) outcome of aorto-ostial stenoses treated with paclitaxel-eluting stents (PES). Methods From February 2003 to December 2004, a total of 76 consecutive patients with 76 lesions underwent percutaneous intervention with PES for aorto-ostial lesions (right coronary artery, 37; left main, 26; saphenous vein graft, 13). All patients were clinically followed for the occurrence of major adverse cardiac events (MACE), defined as cardiac death, non-fatal myocardial infarction (MI), target lesion revascularization (TLR) or target vessel revascularization (TVR). Results All stents (1.7/lesion) were successfully deployed. Three lesions (3.9%) were pre-treated with debulking devices. Thirty-seven lesions (48.7%) were post-dilated with non-compliant balloons (balloon/artery ratio, 1.2). Stents were positioned protruding into the aortic lumen in 29 lesions (38.2%). Cumulative 2-year event-free survival was 68.4%. There was one angiographically-proven stent thrombosis occurring 427 days after TLR for restenosis after the index procedure. The restenosis rate at 7 months (median) was 20.0% and in-stent late lumen loss was 0.48 mm in 40 patients with angiographic follow-up. Conclusions Utilization of PES in this complex lesion subset is feasible and associated with favorable angiographic results at 7 months. However, the gradual increase in later events up to 2 years suggests that aorto-ostial disease remains problematic even in the era of drug-eluting stents.

Can machine learning improve risk prediction and individualise decision making between percutaneous and surgical revascularisation?

Background/Introduction In patients with three-vessel coronary artery disease (CAD) and/or left main (LM) CAD, individual risk prediction plays a key role in deciding between percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG). Purpose The aim of this study was to assess whether these individualised revascularization decisions can be improved by applying machine learning (ML) algorithms and integrating clinical, biological, and anatomical factors. Methods The present study consisted of patients enrolled in the SYNTAX study, which is a randomized trial comparing PCI and CABG in patients with complex coronary artery disease. ML algorithms were used to develop a prognostic index for 5-year death, which was combined, in the second stage, with assigned treatment (PCI or CABG), and pre-specified effect-modifiers: disease type (3-vessel or LMCAD) and anatomical SYNTAX score. The model’s discriminative ability to predict the risk of 5-year death and treatment benefit between PCI and CABG was cross-validated in the SYNTAX trial (n=1800 patients) and externally validated in the CREDO-KYOTO registry (n=7362), and then compared to the original SYNTAX score II 2020 (SS2020). Results The gradient boosting ML model identified the top 10 prognostic factors at the time of decision making as: age, creatinine clearance, left ventricular ejection fraction, peripheral vascular disease, C-reactive protein, hemoglobin, HbA1c, glucose, systolic and diastolic pressure. The ML model performed best for predicting 5-year all-cause death with C-indexes of 0.78 (95% CI 0.75-0.81) in cross-validation and 0.77 (95% CI 0.76-0.79) in external validation. The ML model discriminated 5-year mortality better than the SS2020 in the external validation cohort (vs C-index 0.72 for SS2020, p <0.001) and identified heterogeneity in the treatment benefit of CABG versus PCI (Figure). Conclusions An ML-based approach for identifying individuals who benefit from CABG or PCI is feasible and effective. Implementation of this model in health care systems—trained to collect large numbers of parameters—may harmonize decision making.Figure

Vélicités intracoronaires en cours d'angioplastie

No abstract is provided for this article.

Elective PTCA of totally occluded coronary arteries not associated with acute myocardial infarction; short-term and long-term results

Of 652 consecutive patients referred for coronary angioplasty between September 1980 and March 1984, 49 patients presented with total or functional 'occlusion' of the involved vessel. Total vessel occlusion was defined as absent anterograde filling beyond the lesion. Functional occlusion was defined as faint, late anterograde opacification of the distal segment in the absence of a discernible luminal continuity. In 39 patients, the total or functional occlusion represented a progression, without acute myocardial infarction, of a previously diagnosed stenotic lesion. The maximal potential duration of occlusion was estimated to be 4 weeks or less in 21 patients, more than 4 to 8 weeks in 12, and more than 8 weeks in 16. Dilation of the occluded artery was attempted in the left anterior descending coronary artery in 30 patients, in the right coronary artery in 8, in the circumflex coronary in 7 and in 4 jumpgrafts. For the whole group, angioplasty was successful in 28 patients (57%). The primary success rate with the functionally occluded vessel (81%) was significantly higher than with the total occlusion (45%). In 33 patients with an occlusion estimated to be of 8 weeks or less, angioplasty was successful in 65%. In the 16 patients with an occlusion estimated to be of more than 8 weeks duration, dilation was successful in 44%. Of the 21 patients in whom angioplasty was unsuccessful, 11 required surgery (1 urgent with persistent pain and ST elevation and 10 elective). Ten patients were maintained on medical treatment. Of the 28 patients in whom angioplasty was successful, 10 patients had recurrence of symptoms during follow-up (1–42 months). Four were kept on medical therapy, three required bypass surgery and three underwent repeat percutaneous transluminal coronary angioplasty (PTCA). After primary success, late angiographic studies obtained in 20 out of 28 patients showed reocclusion in 8. In conclusion, elective PTCA of totally occluded coronary arteries is feasible but the primary success rate is lower (57%) than that associated with conventional lesions. the long-term clinical results following successful angioplasty are satisfactory (64%), but the incidence of reocclusion is higher (40%).

Effects of a Potent Platelet-activating Factor Antagonist, SR27417A, on Allergen-induced Asthmatic Responses

Platelet-activating factor (PAF) is a lipid-derived mediator that has been implicated in the pathophysiology of airway inflammation in asthma. Its actions include chemotaxis and activation of inflammatory cells, particularly eosinophils. Inhaled PAF causes bronchoconstriction and increased airway responsiveness in human subjects. However, PAF antagonists have so far failed to show benefits in allergen challenge or in the treatment of chronic asthma. SR27417A is a novel PAF antagonist with increased potency compared with previously tested compounds. Twelve asthmatic subjects received treatment with either SR27417A or placebo for 1 wk in a double-blind crossover study. After treatment each subject underwent allergen challenge. Effects were assessed in terms of early and late asthmatic responses and allergen-induced effects on airway responsiveness. Baseline lung function and airway responsiveness were also examined. Treatment with SR27417A significantly attenuated the late asthmatic response (AUC LAR4–10h: 107 ± 24 after placebo, 79 ± 17 after SR27417A, p < 0.05; mean maximal percent fall in FEV1 LAR: 29 ± 6% after placebo, 23.5 ± 5.4% after SR27417A, p < 0.05). There were no effects on early asthmatic responses, allergen-induced airway responsiveness, or baseline lung measurements. SR27417A is the most potent PAF antagonist to date, and it has a modest inhibitory effect on the late asthmatic response. This suggests that PAF has a small role in allergic inflammation.

Are depredation rates by reef sharks influenced by fisher behaviour?

Shark depredation (damage to gear and loss of bait or hooked fish by a non-target species) is a common global occurrence. Depredation events by sharks can have negative impacts for the fishers, fishery targeted species and the sharks. It is, therefore important to better understand if learning behaviour of sharks can influence rates of depredation. Recreational fishers within the World Heritage Ningaloo Reef have reported increased rates of depredation by sharks over the last 5 years. This study aimed to determine if sharks are capable of learning to associate intensive recreational fishing activities with a food reward. We also aimed to test if sharks in areas frequently fished were more habituated to recreational fishing activities than those sharks within a no-take marine sanctuary. To simulate fishing activities baited underwater video systems were deployed in the morning (A.M.), midday, and afternoon (P.M.) for six consecutive days in Fished and Unfished sites. A significant decrease in time of arrival and time to first feed of sharks was seen across days at the Fished sites. The Unfished sites had very low numbers of sharks observed (n=3) and therefore was not statistically analysed. The relative abundance of sharks did not significantly increase across days, however there was a negative correlation between lemon sharks ( Negaprion sp . ) and whalers ( Carcharhinus sp.). Our study suggests sharks are capable of being classically conditioned to recreational fishing activities and depredation rates are influenced by fisher behaviour. We have highlighted possible mitigation strategies designed to un-condition sharks to recreational fishing, including modifying fishing practices, use of deterrents based on the sensitivity of shark senses and management strategies. The best approach is likely to be enabling fishers to become more knowledgeable of how and why shark depredation events happen and take appropriate steps to avoid them.

SBT‐CO₂: A NEW METHOD FOR THE DIAGNOSIS OF PULMONARY EMBOLISM?

The mechanism of directional coronary atherectomy

An attempt was made to assess the mechanism of directional coronary atherectomy using different methods of analysis. Quantitative coronary angiography was used as the gold standard to assess the immediate results of atherectomy, and a comparative quantitative analysis of atherectomy and balloon angioplasty was made. To determine whether the post-atherectomy cross-sectional area is close to a circle, we compared the area measurements obtained by edge detection with those obtained by videodensitometry. Finally, the extent of a ‘Dotter’ effect was established by quantitative angiography following crossing the stenosis with the atherectomy device. For the purpose of this study, the results of the first 113 successful atherectomy procedures were reviewed. In matched lesions, directional atherectomy induced a greater increase in minimal luminal diameter than balloon angioplasty (1.6 mm vs 0.8 mm; P < 0.0001 However, this luminal improvement is due to a substantial ‘Dotter’ effect induced by the bulky atherectomy device. Following atherectomy, only a slight difference in cross-sectional area measurements between edge detection and videodensitometry (mean difference: 0.28 mm2 was found. Histologic examination of an atherectomized coronary artery showed a near-circular post atherectomy area geometry. In conclusion, directional atherectomy is a very effective device with a substantially better initial result than balloon angioplasty. However, insertion of this bulky device itself causes an important ‘Dotter’effect.

Effect of coronary occlusion during percutaneous transluminal angioplasty on systolic and diastolic left ventricular function

No abstract is provided for this article.

Local buckling of stainless steel plates in fire

Against the Dutch Hypothesis: Asthma and Chronic Obstructive Pulmonary Disease Are Distinct Diseases

Bronchial mucosal inflammation and illness severity in response to experimental rhinovirus infection in COPD

BackgroundRespiratory viral infection causes chronic obstructive pulmonary disease (COPD) exacerbations. We previously reported increased bronchial mucosa eosinophil and neutrophil inflammation in patients with COPD experiencing naturally occurring exacerbations. But it is unclear whether virus per se induces bronchial mucosal inflammation, nor whether this relates to exacerbation severity.ObjectivesWe sought to determine the extent and nature of bronchial mucosal inflammation following experimental rhinovirus (RV)-16–induced COPD exacerbations and its relationship to disease severity.MethodsBronchial mucosal inflammatory cell phenotypes were determined at preinfection baseline and following experimental RV infection in 17 Global Initiative for Chronic Obstructive Lung Disease stage II subjects with COPD and as controls 20 smokers and 11 nonsmokers with normal lung function. No subject had a history of asthma/allergic rhinitis: all had negative results for aeroallergen skin prick tests.ResultsRV infection increased the numbers of bronchial mucosal eosinophils and neutrophils only in COPD and CD8+ T lymphocytes in patients with COPD and nonsmokers. Monocytes/macrophages, CD4+ T lymphocytes, and CD20+ B lymphocytes were increased in all subjects. At baseline, compared with nonsmokers, subjects with COPD and smokers had increased numbers of bronchial mucosal monocytes/macrophages and CD8+ T lymphocytes but fewer numbers of CD4+ T lymphocytes and CD20+ B lymphocytes. The virus-induced inflammatory cells in patients with COPD were positively associated with virus load, illness severity, and reductions in lung function.ConclusionsExperimental RV infection induces bronchial mucosal eosinophilia and neutrophilia only in patients with COPD and monocytes/macrophages and lymphocytes in both patients with COPD and control subjects. The virus-induced inflammatory cell phenotypes observed in COPD positively related to virus load and illness severity. Antiviral/anti-inflammatory therapies could attenuate bronchial inflammation and ameliorate virus-induced COPD exacerbations. Respiratory viral infection causes chronic obstructive pulmonary disease (COPD) exacerbations. We previously reported increased bronchial mucosa eosinophil and neutrophil inflammation in patients with COPD experiencing naturally occurring exacerbations. But it is unclear whether virus per se induces bronchial mucosal inflammation, nor whether this relates to exacerbation severity. We sought to determine the extent and nature of bronchial mucosal inflammation following experimental rhinovirus (RV)-16–induced COPD exacerbations and its relationship to disease severity. Bronchial mucosal inflammatory cell phenotypes were determined at preinfection baseline and following experimental RV infection in 17 Global Initiative for Chronic Obstructive Lung Disease stage II subjects with COPD and as controls 20 smokers and 11 nonsmokers with normal lung function. No subject had a history of asthma/allergic rhinitis: all had negative results for aeroallergen skin prick tests. RV infection increased the numbers of bronchial mucosal eosinophils and neutrophils only in COPD and CD8+ T lymphocytes in patients with COPD and nonsmokers. Monocytes/macrophages, CD4+ T lymphocytes, and CD20+ B lymphocytes were increased in all subjects. At baseline, compared with nonsmokers, subjects with COPD and smokers had increased numbers of bronchial mucosal monocytes/macrophages and CD8+ T lymphocytes but fewer numbers of CD4+ T lymphocytes and CD20+ B lymphocytes. The virus-induced inflammatory cells in patients with COPD were positively associated with virus load, illness severity, and reductions in lung function. Experimental RV infection induces bronchial mucosal eosinophilia and neutrophilia only in patients with COPD and monocytes/macrophages and lymphocytes in both patients with COPD and control subjects. The virus-induced inflammatory cell phenotypes observed in COPD positively related to virus load and illness severity. Antiviral/anti-inflammatory therapies could attenuate bronchial inflammation and ameliorate virus-induced COPD exacerbations.

Small airways and exercise-induced bronchoconstriction (EIB) in elite athletes

Background EIB is particularly frequent in elite athletes and represents a distinct phenotype of clinical asthma (Parsons JP et al. 2013) . Baseline spirometry and clinical symptoms have been shown to be poorly predictive of EIB (Bonini M et al. 2007) . Small airways (SA) represent a relevant topic in Respiratory Medicine and their involvement in chronic inflammatory pulmonary diseases has been extensively studied. However, the role of SA in EIB still needs to be clarified. Aim To assess if SA function and inflammation may be considered reliable predictive markers of EIB in elite athletes. Methods Study procedures of this ongoing study are summarized in Fig.1. Results Out of the 40 athletes representing the powered study population, 10 Caucasian males (mean age: 31.9±9 yrs) were studied. Baseline spirometry was normal in all subjects (FEV1 107.4±12.1%; FVC 110.3±15.2%; FEV1/FVC 81.6±5.9%). Seven athletes were atopic and 3 referred respiratory symptoms. Two athletes showed a positive response (FEV1 fall >10%) to the EVH challenge. Exhaled nitric oxide alveolar concentration was significantly higher in the two athletes with EIB. No differences were detected in spirometric values, clinical symptoms, airways resistance and reactance between subjects with- or without EIB. Conclusions Preliminary data seem to suggest a role of SA inflammation in predicting EIB. This research hypothesis should be supported by the completion of the study.

Elastic local post-buckling of elliptical tubes

The elastic local post-buckling behaviour of elliptical tubes under compression is analysed in this paper. A brief outline of the local, distortional and global buckling behaviour of EHS tubes is firstly provided, where it is shown that local buckling modes govern the stability of short to intermediate length tubes while distortional modes control the stability of intermediate length to moderately long tubes and global buckling dominates the behaviour of longer tubes. Following this, an in-depth numerical study employing shell finite element modelling, of the elastic local post-buckling behaviour of compressed elliptical hollow section (EHS) tubes is presented. It is concluded that EHS tubes with a low to moderate aspect ratio can support loads up to their limit loads but are imperfection sensitive (shell-type behaviour), while EHS tubes with a moderate to high aspect ratio can carry loads higher than their limit loads (plate-type behaviour) and are imperfection insensitive. The slope of the ascending post-buckling path increases with the EHS aspect ratio and can reach values up to 40% of the slope of the linear primary path. The bound imperfection amplitude concept, separating the imperfection amplitude ranges where the EHS tube is sensitive and insensitive, is proposed. It is also found that, for increasing EHS aspect ratio, the compressive stresses grow and accumulate near the zones of minimum radius of curvature while the zones of maximum radius of curvature possess an approximately uniform and relatively low compressive stress level. Therefore, it is expected that an approach based on the effective width concept widely used for the evaluation of the strength of flat plates may be adapted to the design of EHS tubes with moderate to high aspect ratios.

Randomized comparison of laser guidewire and mechanical guidewires for recanalization of chronic total coronary occlusions; the TOTAL trial, final result and follow-up at 30 days

No abstract is provided for this article.

Comparison of everolimus-eluting bioresorbable scaffolds with everolimuseluting metallic stents for treatment of coronary artery stenosis: Three-year follow-up of the ABSORB II randomized trial

At the time of the Absorb II study design in July 2011, commercialization of the Absorb scaffold (Abbott Vascular, Santa Clara, CA) was just starting, following approval with CE mark in December 2010. At that time, clinical evidence of the everolimus-eluting Absorb scaffold had been attained without the use of a comparator. There was a need to conduct a trial with the metallic comparator that was at that time the best-in-class drug-eluting stent. The aims of the trial were to assess the additional value of the technology in order to generate evidence-based data that would support the introduction of this novel device in clinical practice and to guide interventional cardiologists in its early use.

Asthma

Effect of platelet-activating factor on airway vascular permeability: possible mechanisms

We studied the effects of the potent inflammatory mediator, platelet-activating factor (PAF), on vascular permeability in airways (and other tissues) of guinea pigs by measuring extravasation of circulating Evans blue dye. PAF caused a dose-dependent increase in vascular permeability. At 1 ng/kg iv, PAF caused an increase in Evans blue extravasation of 220% (P less than 0.05) in the trachea, with the greatest effect at a dose of 100 ng/kg (858%; P less than 0.01). Histamine (150 micrograms/kg iv) caused a 320% increase over base line in the trachea and 200% in main bronchi; this effect was equivalent to that induced by 10 ng/kg PAF in the trachea and 1 ng/kg in main bronchi. The duration of effect of PAF was greatest in main bronchi (less than 10 min). Platelet depletion with a cytotoxic antibody, or the cyclooxygenase inhibitor, indomethacin, or the cyclooxygenase-lipoxygenase inhibitor, BW 7556, did not affect the vascular permeability response to PAF. The PAF-receptor antagonist, BN 52063, inhibited Evans blue extravasation in the airways in a dose-dependent manner, with complete inhibition at 5 mg/kg. Thus PAF-induced airway vascular leakage is mediated by specific receptors but not by products of arachidonic acid metabolism or by platelets. Increased airway microvascular leakage induced by PAF may lead to plasma extravasation and airway edema, factors that may contribute to the airway narrowing and hyperresponsiveness induced by PAF.