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Atherosclerosis preferentially develops at average low shear stress (SS) locations. SS-related signaling maintains lumen dimensions by inducing outward arterial remodeling. Prolonged plaque accumulation at low SS predilection locations explains an inverse relation between wall thickness (WT) and SS. No data exist on WT-SS relations when lumen narrowing and loss of compensatory remodeling commence.In 14 patients, an angiographically normal artery (stenosis <50%) was investigated with ANGiography and ivUS (ANGUS) to provide 3D lumen and wall geometry. Selection of segments >5 mm in length, in between side branches, yielded 25 segments in 12 patients. SS at the wall was calculated by computational fluid dynamics. WT smaller than 0.2*lumen diameter was defined as normal. Largest arc of normal WT defined reference cross sections. Lumen area relative to the reference cross sections defined area stenosis (AS). Average segmental AS smaller or greater than 10% defined preserved or narrowed lumen, respectively. Total vessel area relative to the reference defined vascular remodeling (VR). For the preserved lumens (n=11, AS=1.7+/-5.6%, P=NS), axially averaged WT and SS were inversely related (slope, -0.46+/-0.55 mm/Pa, P<0.05) and VR was positive (7+/-9%, P<0.05). Narrowed segments (n=13, 1 excluded, AS=18+/-6%, P<0.05) showed no relation between WT and SS or vascular remodeling.In patient coronary arteries, the often-reported inverse WT-SS relationship appears restricted to lumen preservation and positive vascular remodeling. Its disappearance with lumen narrowing suggests a growing importance of non-SS-related plaque progression.

Purpose: Intra-coronary near-infrared spectroscopy (NIRS) is capable of identifying lipid core-containing plaques, which can subsequently be quantified as a lipid core burden index (LCBI). Currently, no data are available on the long-term prognostic value of NIRS in patients with coronary artery disease (CAD). Methods: In this prospective, observational study, NIRS imaging was performed in a non-culprit coronary artery in 203 patients referred for angiography due to stable angina pectoris (SAP) or acute coronary syndrome (ACS). Results: The one-year cumulative incidence of the primary endpoint (the composite of all-cause mortality, non-fatal ACS, stroke and unplanned coronary revascularization) was 10.4%. Cumulative one-year rates in patients with an LCBI equal to and above the median (43.0) versus those with LCBI values below the median, were 16.7% versus 4.0% (P=0.003) (adjusted hazard ratio, 4.04; 95% confidence interval, 1.33-12). The relation between LCBI and the primary endpoint was similar in SAP and ACS patients (p-value for heterogeneity=0.14). Similar results were observed for the secondary endpoints of all-cause mortality or non-fatal ACS (8.8% vs. 1.0%, P=0.010), all-cause mortality, non-fatal ACS or stroke (11.8% vs. 1.0%, P=0.002) and all-cause mortality, non-fatal ACS or unplanned coronary revascularization (13.7% vs. 4.0%, P=0.014). KM curves for the primary endpoint Conclusion: CAD patients with a LCBI equal to or above the median of 43.0, as assessed by NIRS in a non-culprit coronary artery, had a four-fold risk of adverse cardiovascular events during one-year follow-up. Apparently, the LCBI as assessed in a non-culprit vessel, reflects vascular vulnerability of the larger coronary tree. Our results should be (externally) validated in a larger sample.

Background Despite the well-established benefits of secondary cardiovascular prevention, the importance of concurrent medical therapy in clinical trials of coronary revascularization is often overlooked. Objectives The goal of this study was to assess compliance with guideline-directed medical therapy (GDMT) in clinical trials and its potential impact on the comparison between percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG). Methods The Cochrane Central Register of Controlled Trials and MEDLINE were searched from 2005 to August 2017. Clinical trial registries and reference lists of relevant studies were also searched. Randomized controlled trials comparing PCI with drug-eluting stents versus CABG and reporting medical therapy after revascularization were included. The study outcome was compliance with GDMT, defined as the following: 1) any antiplatelet agent plus beta-blocker plus statin (GDMT1); and 2) any antiplatelet agent plus beta-blocker plus statin plus angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (GDMT2). Data collection and analysis were performed according to the methodological recommendations of The Cochrane Collaboration. Results From a total of 439 references, 5 trials were included based on our inclusion and exclusion criteria. Overall, compliance with GDMT1 was low and decreased over time from 67% at 1 year to 53% at 5 years. Compliance with GDMT2 was even lower and decreased from 40% at 1 year to 38% at 5 years. Compliance with both GDMT1 and GDMT2 was higher in PCI than in CABG at all time points. Meta-regression suggested an association between lower use of GDMT1 and adverse clinical outcomes in PCI versus CABG at 5 years. Conclusions Compliance with GDMT in contemporary clinical trials remains suboptimal and is significantly lower after CABG than after PCI, which may influence the comparison of clinical trial endpoints between those study groups.

No abstract is provided for this article.

<h3>Introduction</h3> Macrophages play an important role in clearing inhaled particles and bacteria from the lung, thus maintaining its sterility. Defective phagocytosis of bacteria has been demonstrated in both alveolar and monocyte-derived macrophages (MDMs) from COPD patients and may play a role in the aetiology of the frequent exacerbator phenotype. We hypothesised that defective phagocytosis may also be associated with lower airway bacterial colonisation (LABC) and other clinical parameters in stable COPD. <h3>Methods</h3> Whole blood and sputa were collected from stable patients in the London COPD cohort. Stable COPD was defined as no symptom-defined exacerbations recorded on prospectively completed diary cards in the preceding four weeks and subsequent two weeks. Monocytes were isolated from the whole blood and cultured with GM-CSF (2 ng/ml) for 12 days to generate MDMs. MDM phagocytosis of fluorescently-labelled polystyrene beads, <i>Haemophilus influenzae</i> (HI) and <i>Streptococcus</i><i>pneumoniae</i> (SP) was measured by fluorimetry. LABC was defined as detection of HI, SP or <i>Moraxella catarrhalis</i> (MC) in sputum using quantitative PCR. <h3>Results</h3> MDMs were cultured from 26 COPD patients. 54% were male, mean age 70.0 years (SD 8.3), FEV1 predicted 55.3% (20.3), 46% were current smokers, median daily inhaled corticosteroid (ICS) dose was 1000 (640–2000) mcg (beclomethasone equivalent dose) and median exacerbation frequency per year was 1.8 (1.0–2.9) based on diary card events. Phagocytosis of HI was significantly less with increasing exacerbation frequency (p=0.002, r=–0.58, Figure 1), although no significant associations were demonstrated between exacerbation frequency and phagocytosis of inert beads or SP (p=0.27 and p=0.22 respectively). 13 patients (50%) with LABC did not demonstrate any significant difference in phagocytosis of either beads (p=0.29), HI (p=0.66) or SP (p=0.88) compared with non-colonised patients. There was no significant association between phagocytosis of beads, HI or SP with age, FEV₁%predicted, smoking pack year history, ICS dose or BMI (all p&gt;0.05). <h3>Conclusion</h3> In stable COPD patients, decreasing phagocytosis of HI was associated with increasing exacerbation frequency. Phagocytosis was not related to LABC suggesting that macrophage activity alone may not determine bacteria colonisation. Further work is needed to elucidate the mechanisms of reduced phagocytosis in COPD and its relationship to exacerbation frequency.

No abstract is provided for this article.

No abstract is provided for this article.

No abstract is provided for this article.

<h3>BACKGROUND</h3> Bronchiectasis is a chronic inflammatory lung disease associated with increased production of oxidants due mostly to neutrophilic inflammation. Induction of heme oxygenase (HO-1) by reactive oxygen species is a general cytoprotective mechanism against oxidative stress. HO-1 catabolises heme to bilirubin, free iron and carbon monoxide (CO). Exhaled CO measurements may therefore reflect an oxidative stress and be clinically useful in the detection and management of inflammatory lung disorders. <h3>METHODS</h3> The levels of exhaled CO of 42 non-smoking patients with bronchiectasis treated or not treated with inhaled corticosteroids were compared with CO levels in 37 normal non-smoking subjects. <h3>RESULTS</h3> Levels of exhaled CO were raised in patients with bronchiectasis, both those treated with inhaled corticosteroids (n = 27, median 5.5 ppm, 95% CI 5.16 to 7.76) and those not treated with inhaled corticosteroids (n = 15, median 6.0 ppm, 95% CI 4.74 to 11.8), compared with normal subjects (n = 37, median 3.0 ppm, 95% CI 2.79 to 3.81, p = 0.0024). There was no correlation between exhaled CO and HbCO levels (<i>r</i> = 0.42, p = 0.12) in normal subjects (n = 7), nor between the urine cotinine concentration and exhaled CO levels (<i>r</i> = 0.2, p = 0.12). <h3>CONCLUSIONS</h3> Increased levels of exhaled CO may reflect induction of HO-1 and oxidative stress in bronchiectasis. Measurement of exhaled CO may be useful in the management of bronchiectasis and possibly other chronic inflammatory lung disorders.

Immediately after stent/scaffold implantation, quantitative coronary angiography (QCA) in comparison to optical coherence tomography (OCT) more severely underestimates the lumen diameter (LD) in Absorb than in XIENCE. This OCT-QCA discrepancy has not been evaluated at long-term follow-up. The present study aimed to assess the accuracy of QCA with reference to OCT in Absorb as compared to XIENCE.We assessed two-year QCA and OCT in the ABSORB Japan randomised trial (Absorb n=87, XIENCE n=44). The accuracy of QCA parameters was assessed with reference to OCT measurements. OCT-QCA luminal dimensions were compared in matched cross-sections at both edges of the scaffolds (n=127) and stents (n=78). OCT-QCA late lumen loss (LLL) was also assessed using the Bland-Altman method. The systematic error of LD on QCA in Absorb was -0.092 mm (relative difference -3.3%) with a random error of 0.473 mm, whereas in XIENCE the systematic error was -0.018 mm (-0.5%) with a random error of 0.477 mm. These OCT-QCA discrepancies did not differ between Absorb and XIENCE (p=0.275) at two-year follow-up. QCA tended to underestimate LLL more in Absorb than in XIENCE (QCA-LLL minus OCT-LLL: -0.180±0.308 mm vs. -0.058±0.322 mm, p=0.058) at two-year follow-up, although this comparison was not statistically powered.The two-year dimensional measurements on QCA had minor and insignificant systematic errors between both devices. A discrepancy between QCA-LLL and OCT-LLL would raise a question as to whether this parameter is appropriate for the comparative assessment of device performance.