Publications

We tested whether fractional flow reserve (FFR) discriminates between suboptimally and optimally deployed stents. Latex tubes (diameter ⊘ = 4 mm) with diameter stenosis 40% (n = 3), 50% (n = 3) and 60% (n = 3) were tested in a pulsatile flow system, using water. Measurements were done at baseline (n = 9; FFR/QCA) and after suboptimal (SOD; 3‐mm balloon at 8 atm) and optimal (OD; 4 mm balloon at 16 atm) deployment of a 35‐mm stent (n = 6; FFR/QCA/IVUS). Varying Q from 150 to 50 ml/min increased FFR by 2–7%. Conversely, at 100 ml/min, FFR increased by only 0.8% from SOD to OD ( P < 0.05). Extrapolating data to blood flow, the gain in FFR from SOD to OD is less than 5% for Q = 100 ml/min, while FFR may increase by 15–20% by changes in blood flow from 50 to 150 ml/min. We conclude that IVUS and QCA are more appropriate for the assessment of optimal stent deployment. Cathet Cardiovasc Intervent 2001;54:363–375. © 2001 Wiley‐Liss, Inc.

Objectives The aim of this study was to report the frequency, patient and lesion-related characteristics, and outcomes of subclinical, nonculprit plaque ruptures in the PROSPECT (Providing Regional Observations to Study Predictors of Events in the Coronary Tree) study. Background Plaque rupture and subsequent thrombosis is the most common cause of acute coronary syndrome (ACS). Secondary, subclinical, nonculprit plaque ruptures have been seen in both stable patients and patients with ACS; however, reports of the natural history of these secondary plaque ruptures are limited. Methods After successful stenting in 697 patients with ACS, 3-vessel grayscale and intravascular ultrasound virtual histology (IVUS-VH) was performed in the proximal-mid segments of all 3 coronary arteries as part of a prospective multicenter study. Results Among 660 patients with complete IVUS data, 128 plaque ruptures were identified in 105 nonculprit lesions in 100 arteries from 93 patients (14.1%). Although the minimum lumen area (MLA) was similar, the plaque burden was significantly greater in nonculprit lesions with a plaque rupture compared with nonculprit lesions without a plaque rupture (66.0% [95% confidence interval: 64.5% to 67.4%] vs. 56.0% [95% confidence interval: 55.6% to 56.4%]; p < 0.0001). IVUS-VH analysis revealed that a nonculprit lesion with a plaque rupture was more often classified as a fibroatheroma than a nonculprit lesion without a plaque rupture (77.1% vs. 51.4%; p < 0.0001). Independent predictors of a plaque rupture were lesion length (per 10 mm; odds ratio: 1.30; p < 0.0001), plaque burden at the MLA site (per 10%; odds ratio: 2.56; p < 0.0001), vessel area at the MLA site (per 1 mm2; odds ratio: 1.13; p < 0.0001), and VH–thin-cap fibroatheroma (odds ratio: 1.80; p = 0.016). During 3 years of follow-up, the incidence of overall major adverse cardiac events did not differ significantly between the patients with and patients without subclinical, nonculprit plaque ruptures. Conclusions Secondary, nonculprit plaque ruptures were seen in 14% of patients with ACS and were associated with a fibroatheroma phenotype with a residual necrotic core but not with adverse outcomes if patients were treated with optimal medical therapy as part of a multicenter study. (Providing Regional Observations to Study Predictors of Events in the Coronary Tree [PROSPECT]; NCT00180466)

Context. The formation processes of massive stars are still unclear but a picture is emerging involving accretion disks and molecular outflows in what appears to be a scaled-up version of low-mass star formation. A census of outflow activity towards massive star-forming clumps in various evolutionary stages has the potential to shed light on massive star formation (MSF). Aims. We conducted an outflow survey towards ATLASGAL clumps using SEDIGISM data and aimed to obtain a large sample of clumps exhibiting outflows in different evolutionary stages. Methods. We identify the high-velocity wings of the 13CO lines toward ATLASGAL clumps by (1) extracting the simultaneously observed 13CO and C18O spectra from SEDIGISM, and (2) subtracting Gaussian fits to the scaled C18O from the 13CO, line after considering opacity broadening. Results. We have detected high-velocity gas towards 1192 clumps out of a total sample of 2052, giving an overall detection rate of 58%. Outflow activity has been detected in the earliest quiescent clumps (i.e., 70$μ$m weak), to the most evolved HII region stages i.e., 8$μ$m bright with MSF tracers. The detection rate increases as a function of evolution (quiescent=51%, protostellar=47%, YSO=57%, UCHII regions=76%). Conclusion. Our sample is the largest outflow sample identified so far. The high-detection rate from this large sample is consistent with previous results and supports that outflows are a ubiquitous feature of MSF. The lower detection rate in early evolutionary stages may be due to that outflows in the early stages are weak and difficult to detect. We obtain a statistically significant sample of outflow clumps for every evolutionary stage, especially for outflow clumps in the 70$μ$m dark stage. This suggests that the absence of 70$μ$m emission is not a robust indicator of starless/pre-stellar cores.

No abstract is provided for this article.

The aim of this study was the external validation of the updated logistic clinical SYNTAX score for two-year all-cause mortality after PCI in the GLOBAL LEADERS trial.The GLOBAL LEADERS trial was an investigator-initiated, prospective randomised, multicentre, open-label trial comparing two strategies of antiplatelet therapy in 15,991 patients undergoing PCI. As a predefined analysis, we studied the first 4,006 consecutive patients enrolled between July 2013 and April 2014 for whom the anatomic SYNTAX scores were calculated by an independent core lab. The updated logistic clinical SYNTAX score was available in 3,271 patients. Patients were divided into quintiles according to the score. The C-statistic of the updated logistic clinical SYNTAX score for two-year all-cause mortality was 0.71 (95% confidence interval [CI]: 0.64-0.77). The updated logistic clinical SYNTAX score identified patients at very high risk for two-year all-cause mortality after PCI. Although it systematically overestimated two-year all-cause mortality, predicted and observed two-year all-cause mortality in the majority of the patients (four out of five quintiles) were in agreement.Overall discrimination for two-year all-cause mortality of the updated logistic clinical SYNTAX score is either borderline acceptable or possibly helpful. Calibration in the majority of patients is appropriate. The score is potentially useful in selecting enriched high-risk populations.

<b>Introduction:</b> COPD is a chronic inflammatory lung disease, associated with elevated neutrophilic inflammation. The IL-36 family belongs to the IL-1 superfamily consisting of 3 agonists (IL-36α, β, γ) and 2 antagonists (IL-36RA and IL-38); their role in COPD is unclear. Here, we examined their role in COPD, examining the cellular source and effects of these cytokines within the lung. <b>Methods:</b> Human small airway epithelial cells (SAEC), small airway fibroblasts (SAF) and tissue resident macrophages (TMφ) were extract from lung tissue from non-smokers (NS) and COPD patients. Cytokines were measured by ELISA and gene expression by RT-PCR. Lung cells were treated with IL-36γ (100 ng/ml). <b>Results:</b> IL-36γ, but not IL-36α/β, was significantly elevated in bronchoalveolar lavage fluid (p=0.032) and nasal fluid (p=0.042) of COPD patients (n=9-18) compared to NS (n=8-13). IL-36RA was significantly decreased in sputum samples from COPD patients (P=0.006) (n=13). IL-36RA gene expression was significantly decreased in COPD TMφ (n=8) compared to NS (n=5) (p=0.0048); IL-38 was undetectable. SAEC were the major source of IL-36γ (n=8) (P=0.0001). Treatment of TMφ, SAEC and SAF with IL-36γ led to release of the neutrophil chemokines CXCL1/8, as well as IL-6, GM-CSF and MMP-9; SAF released the highest concentrations, suggesting these as major effector cell. <b>Conclusions:</b> These data suggest IL-36γ is elevated within the lungs of COPD patients and released from SAEC. IL-36γ activates SAF to release neutrophil chemokines and MMPs, which can cause disease pathobiology. Loss of IL-36RA may further exacerbate these effects. Inhibitors of IL-36 signalling may prove to be useful anti-inflammatory treatments in COPD.

No abstract is provided for this article.

Bleeding and myocardial infarction (MI) after percutaneous coronary intervention are independent risk factors for mortality. This study aimed to investigate the association of all-cause mortality after percutaneous coronary intervention with site-reported bleeding and MI, when considered as individual, repeated, or combined events.We used the data from the GLOBAL LEADERS trial (GLOBAL LEADERS: A Clinical Study Comparing Two Forms of Anti-Platelet Therapy After Stent Implantation), an all-comers trial of 15 968 patients undergoing percutaneous coronary intervention. Bleeding was defined as Bleeding Academic Research Consortium (BARC) 2, 3, or 5, whereas MI included periprocedural and spontaneous MIs according to the Third Universal Definition.At 2-year follow-up, 1061 and 498 patients (6.64% and 3.12%) experienced bleeding and MI, respectively. Patients with a bleeding event had a 10.8% mortality (hazard ratio [HR], 5.97 [95% CI, 4.76-7.49]; P<0.001), and the mortality of patients with an MI was 10.4% (HR, 5.06 [95% CI, 3.72-6.90]; P<0.001), whereas the overall mortality was 2.99%. Albeit reduced over time, MI and even minor BARC 2 bleeding significantly influenced mortality beyond 1 year after adverse events (HR of MI, 2.32 [95% CI, 1.18-4.55]; P=0.014, and HR of BARC 2 bleeding, 1.79 [95% CI, 1.02-3.15]; P=0.044). The mortality rates in patients with repetitive bleeding, repetitive MI, and both bleeding and MI were 16.1%, 19.2%, and 19.0%, and their HRs for 2-year mortality were 8.58 (95% CI, 5.63-13.09; P<0.001), 5.57 (95% CI, 2.53-12.25; P<0.001), and 6.60 (95% CI, 3.44-12.65; P<0.001), respectively. De-escalation of antiplatelet therapy at the time of BARC 3 bleeding was associated with a lower subsequent bleeding or MI rate, compared with continuation of antiplatelet therapy (HR, 0.32 [95% CI, 0.11-0.92]; P=0.034).The fatal impact of bleeding and MI persisted beyond one year. Additional bleeding or MIs resulted in a poorer prognosis. De-escalation of antiplatelet therapy at the time of BARC 3 bleeding could have a major safety merit. These results emphasize the importance of considering the net clinical benefit including ischemic and bleeding events. Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01813435.