Publications

The impact of final kissing balloon inflation (FKBI) after percutaneous coronary intervention (PCI) of bifurcation lesions on long-term clinical outcomes remains controversial. We sought to determine the impact of FKBI on four-year outcomes after PCI of distal left main (LM) bifurcation lesions.The EXCEL trial compared PCI with everolimus-eluting stents and coronary artery bypass graft surgery (CABG) in patients with left main (LM) disease. We examined four-year clinical outcomes after PCI of distal LM bifurcation lesions according to use of FKBI. The primary endpoint was the composite rate of death, myocardial infarction (MI), or stroke. The major secondary endpoint was the composite rate of death, MI, stroke, or ischaemia-driven revascularisation (IDR). Among 948 patients randomised to PCI, 759 had distal LM lesions treated, 430 of which were treated with one stent and 329 of which were treated with two or more stents. The four-year rates of the primary and major secondary endpoints were similar with versus without FKBI in both the one-stent and ≥2-stent groups in both unadjusted and adjusted analyses.In the EXCEL trial, the performance of FKBI after PCI of distal LM bifurcation lesions was not associated with improved four-year clinical outcomes regardless of whether one stent or ≥2 stents were implanted.

An increased concentration of nitric oxide (NO) in the exhaled air of asthmatic patients may reflect inflammation of the airways, and exhaled NO may, therefore, be useful in monitoring asthma control and the optimal use of anti-inflammatory treatment. We have studied the effect of reducing and then increasing the dose of inhaled steroid on exhaled NO, lung function and symptoms in 14 asthmatic patients treated with twice daily budesonide. Baseline measurements were made at the end of a 2 week run-in period, 2 weeks after the daily dose of budesonide was reduced by 200 micrograms daily, and 2 weeks after the dose was then increased by 200 micrograms daily. Exhaled NO increased significantly compared with baseline after the dose was reduced by 200 micrograms daily (from 122 +/- 13 to 246 +/- 52 ppb); whereas, there was no significant decrease in spirometry or change in peak flow variability. There was also a significant increase in symptoms at night, but no change during the day or in the number of rescue doses of inhaled beta 2-agonist. The level of exhaled NO decreased when the dose of inhaled steroids was increased, and this was associated with a reduction in diurnal variability of peak expiratory flow, and in nocturnal symptoms. Our study suggests that exhaled nitric oxide may be a useful means of monitoring control of asthma. Further longitudinal studies in patients of differing asthma severity are now indicated.

Infrared Dark Clouds (IRDCs) are cold, high mass surface density and high density structures, likely to be representative of the initial conditions for massive star and star cluster formation. CO emission from IRDCs has the potential to be useful for tracing their dynamics, but may be affected by depleted gas phase abundances due to freeze-out onto dust grains. Here we analyze C18O J=1-0 and J=2-1 emission line data, taken with the IRAM 30m telescope, of the highly filamentary IRDC G035.39.-0033. We derive the excitation temperature as a function of position and velocity, with typical values of ~7K, and thus derive total mass surface densities, Sigma_C18O, assuming standard gas phase abundances and accounting for optical depth in the line, which can reach values of ~1. The mass surface densities reach values of ~0.07 g/cm^2. We compare these results to the mass surface densities derived from mid-infrared (MIR) extinction mapping, Sigma_SMF, by Butler & Tan, which are expected to be insensitive to the dust temperatures in the cloud. With a significance of >10sigma, we find Sigma_C18O/Sigma_SMF decreases by about a factor of 5 as Sigma increases from ~0.02 to ~0.2 g/cm^2, which we interpret as evidence for CO depletion. Several hundred solar masses are being affected, making this one of the most massive clouds in which CO depletion has been observed directly. We present a map of the depletion factor in the filament and discuss implications for the formation of the IRDC.

No abstract is provided for this article.

The acute impact in vivo from a selfexpanding stent on the vessel wall has not been sufficiently evaluated.We sought to compare acute in vivo injury on the vessel wall and the clinical impact between a self-expanding coronary stent and conventional balloon-expandable stents immediately after stent implantation.We included 40 patients (45 vessels) with stable or unstable angina who were assigned to either the self-expanding stent (vProtect Luminal Shield) group (n = 9; Group 1) or the conventional balloon-expandable stent group (n = 36; Group 2). Optical coherence tomography (OCT) was performed after stent deployment, as were qualitative and quantitative assessments of tissue prolapse, intrastent dissection, edge dissection and incomplete stent apposition.Tissue prolapse was visible in all vessels in both groups. The corrected tissue prolapse area by stent length was larger in Group 2 than in Group 1 (0.06 +/- 0.06 vs. 0.02 +/- 0.01 mm(2); p < 0.001). Intrastent dissection was more frequently seen in Group 2 (33/36 vs. 4/9 vessels; p = 0.004) and the mean length of the dissection flap was greater in Group 2 than in Group 1 (277.6 +/- 110.0 vs. 76.9 +/- 103.7 microm; p < 0.001). Although edge dissection was not detected in Group 1, it was visible in 19/36 vessels (52.8%) in Group 2. The frequency of incomplete stent apposition was not significantly different between Group 2 and Group 1 (23/36 vs. 7/9 vessels, p = 0.7), but the mean depth of incomplete stent apposition was greater in Group 2 than in Group 1 (268.2 +/- 72.1 vs. 178.2 +/- 156.7 microm, p = 0.03).A selfexpanding stent was associated with less intrastent dissection and edge dissection than conventional balloon-expandable stents with OCT.

The development of the heparin-coated (HC)-stent should be viewed against the backdrop of the early unfavorable results with noncoated stents in the pre-intravascular ultrasound and pre-ticlopidine era. Notwithstanding, results of pilot and randomized trials show a surprisingly low incidence of (sub)acute stent thrombosis under challenging circumstances, such as acute coronary syndromes. Considering the quite low incidence of early complications with noncoated second-generation stents, it may require large trials to prove the clinical efficacy of the heparin- coating against noncoated devices. However, even if the "added value" of the heparin-coating will never be clinically proven, it has helped to enhance the penetration of stent therapy in interventional cardiology. Unlike the situation in 1992, very few cardiologists will now disagree with the statement that stents contribute to the state-of-the-art treatment of patients with angina pectoris or acute myocardial infarction. A preliminary comparison of available trials also suggests that the heparin-coated Palmaz-Schatz stent (Cordis Corp., Waterloo, Belgium) is as effective as the noncoated stent plus abciximab treatment.

The T lymphocyte-mediated immune response to Mycobacterium tuberculosis infection in the parietal pleura of patients with tuberculous pleurisy is unknown. The aim of this study was to investigate the immune response in the parietal pleura of tuberculous pleurisy compared with nonspecific pleuritis. We have measured the numbers of inflammatory cells particularly T-cell subsets (Th1/Th2/Th17/Treg cells) in biopsies of parietal pleura obtained from 14 subjects with proven tuberculous pleurisy compared with a control group of 12 subjects with nonspecific pleuritis. The number of CD3+, CD4+ and CCR4+ cells and the expression of RORC2 mRNA were significantly increased in the tuberculous pleurisy patients compared with the nonspecific pleuritis subjects. The number of toluidine blue+ cells, tryptase+ cells and GATA-3+ cells was significantly decreased in the parietal pleura of patients with tuberculous pleurisy compared with the control group of nonspecific pleuritis subjects. Logistic regression with receiver operator characteristic (ROC) analysis for the three single markers was performed and showed a better performance for GATA-3 with a sensitivity of 75%, a specificity of 100% and an AUC of 0.88. There was no significant difference between the two groups of subjects in the number of CD8, CD68, neutrophil elastase, interferon (IFN)-γ, STAT4, T-bet, CCR5, CXCR3, CRTH2, STAT6 and FOXP3 positive cells. Elevated CD3, CD4, CCR4 and Th17 cells and decreased mast cells and GATA-3+ cells in the parietal pleura distinguish patients with untreated tuberculous pleurisy from those with nonspecific pleuritis.

Background: Patients with both diabetes mellitus (DM) and chronic kidney disease (CKD) are a subpopulation characterized by ultrahigh ischemic and bleeding risk after the percutaneous coronary intervention (PCI). There are limited data on the impact of ticagrelor monotherapy among these patients. Methods: In this post hoc analysis of the GLOBAL-LEADERS trial, the treatment effects of the experimental (one-month dual-antiplatelet therapy [DAPT] followed by 23-month ticagrelor monotherapy) versus the reference regimen (12-month DAPT followed by 12-month aspirin alone) were analyzed according to DM/CKD status. The primary endpoint was a composite endpoint of all-cause death or new Q-wave myocardial infarction at two-years. The patient-oriented composite endpoint (POCE) was defined as the composite of all-cause death, any stroke, site-reported MI and any revascularization, whereas net adverse clinical events (NACE) combined POCE with BARC type 3 or 5 bleeding events. Results: At two years, the DM+/CKD+ patients had significantly higher incidences of the primary endpoint (9.5% versus 3.1%, adjusted HR 2.16; 95%CI [1.66-2.80], p&lt;0.001), BARC type 3 or 5 bleeding events, stroke, site-reported myocardial infraction, all revascularization, POCE, and NACE, compared with the DM-/CKD- patients. Among the DM+/CKD+ patients, after adjustment, there were no significant differences in the primary endpoints between the experimental and reference regimen. The experimental regimen was associated with lower rates of POCE (20.6% versus 25.9%, HR 0.74; 95%CI [0.55-0.99], p=0.043, p trend =0.155) and NACE (22.7% versus 28.3%, HR 0.75; 95%CI [0.56-0.99], p=0.044, p trend =0.310), mainly driven by a lower rate of all revascularization, as compared with the reference regimen. The landmark analysis showed that while the experimental and reference regimen had similar rates of all the clinical endpoints during the first year, the experimental regimen was associated with significantly lower rates of POCE (5.8% versus 11.0%, HR 0.49; 95%CI [0.29-0.82], p=0.007, p trend =0.040) and NACE (5.8% versus 11.2%, HR 0.48; 95%CI [0.29-0.82], p=0.007, p trend =0.013) in the second year. Conclusion: Among patients with both DM and CKD, ticagrelor monotherapy was not associated with lower rates of all-cause death or new Q-wave, or major bleeding complications; however, it was associated with lower rates of POCE and NACE. These findings should be interpreted as hypothesis-generating. Clinical Trial Registration: ClinicalTrials.gov (NCT01813435).