Publications

Intense investigation continues on the pathobiology of stent thrombosis (ST) because of its morbidity and mortality. Because little advance has been made in outcomes following ST, ongoing research is focused on further understanding predictive factors as well as ST frequency and timing in various patient subsets, depending upon whether a drug-eluting stent or bare-metal stent has been implanted. Although the preventive role of antiplatelet therapies remains unchallenged, new data on genomics and variability in response to antiplatelet therapy, as well as the effects of novel therapeutic agents and duration of therapy, have become available. The goal remains identification of patients at particularly increased risk of ST so that optimal prevention strategies can be developed and employed.

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Objectives. This study was designed to examine whether restenosis is related to the extent or mechanism of lumen improvement and to explore angiographic determinants of optimal atherectomy. Background. Directional atherectomy induces a greater extent of immediate gain and late loss but has not been found to yield a better late angiographic lumen than angioplasty in randomized trials. The difference in lumen renarrowing may be related to either the extent or the mechanism of immediate gain. The design of previous studies has precluded the detection of a device-specific effect on restenosis. Methods. A retrospective analysis was based on matching a prospectively collected series of 80 native coronary arteries successfully treated with atherectomy with a prospectively collected series of 80 native coronary arteries successfully treated with balloon angioplasty. Angiographic analysis was performed in 160 lesions to explore whether a specific device-related effect exists. Multivariate analyses were performed to determine the correlates of minimal lumen diameter at follow-up and late lumen loss and to identify the procedural characteristics for optimal atherectomy. Results. Matching resulted in two comparable groups with equivalent baseline clinical and stenosis characteristics. By study design, atherectomy and angioplasty resulted in similar mean (±SD) immediate lumen gain (1.15 ± 0.44 vs. 1.10 ± 0.40 mm, p = 0.50). However, lumen loss was more pronounced after atherectomy, and, thus, the minimal lumen diameter at follow-up differed significantly between the two groups (1.78 ± 0.57 vs. 2.00 ± 0.56 mm, p = 0.001). Device type was retained in the multivariate analysis as an independent predictor of late minimal lumen diameter and lumen loss. Multivariate analysis identified vessel size and immediate gain as determinants of optimal atherectomy. Conclusions. Restenosis is a consequence not only of the extent of lumen improvement but also of the mechanism of vessel wall injury (debulking vs. dilating). While performing atherectomy, the operator should strive for an optimal procedural result to accommodate an increased intimal hyperplastic response.

We aim to investigate the association between different types of statins, in particular simvastatin and atorvastatin, and long-term mortality after percutaneous coronary intervention (PCI).Between 2000 and 2005, a prospective cohort was constituted of 5,647 patients who underwent PCI. Type and doses of statin use were collected after the PCI procedure. Survival status was obtained from municipal civil registries. The primary endpoint was all-cause mortality. Secondary endpoints were cardiac and cancer mortality. Median follow-up was 5.0 years (range three to nine years). During follow-up 738 patients (13.1%) died. In total, 4,970 patients (88%) were on statin therapy four weeks after PCI of whom the majority used either atorvastatin (34%) or simvastatin (29%). Cumulative survival rates at eight years in the atorvastatin group were 83%, and 79% in the simvastatin group (log-rank, p=0.004). After adjustment, statin use was associated with a 50% mortality reduction (HR 0.49, 95% CI 0.40-0.59) and atorvastatin use was associated with lower total mortality than simvastatin use (adjusted HR 0.77, 95% CI 0.61-0.97). This was largely driven by cancer mortality (adjusted HR 0.59, 95% CI 0.38-0.91).In patients undergoing PCI the use of statins is associated with reduced mortality during prolonged follow-up. Patients using atorvastatin had a 23% lower mortality than those using simvastatin.

Background Although considered the gold standard, pressure wire‐derived fractional flow reserve (PW‐FFR) and instantaneous wave‐free ratio (PW‐iFR) are not sufficiently adopted. Vessel fractional flow reserve (vFFR) is a potentially less invasive surrogate. Aims To validate the diagnostic performance of vFFR against the wire‐based physiological assessments in real‐world clinical settings. Methods In this single‐center retrospective study, we analyzed 479 patients (586 vessels) who underwent PW‐FFR and vFFR in the same vessel, and evaluated the correlation between vFFR and PW‐FFR using PW‐FFR ≦ 0.80 as the reference. Additionally, we analyzed 378 patients (455 vessels) with vFFR, PW‐FFR, and PW‐iFR, and 93 patients (119 vessels) with vFFR, PW‐FFR, and resting full‐cycle ratio (RFR). Results The indications for coronary angiography were stable angina (92%), unstable angina (6.3%), and non‐ST‐elevation myocardial infarction (1.5%). The target vessels were the left anterior descending artery (61%), left circumflex artery (20%), and right coronary artery (19%). A good correlation was found between vFFR and PW‐FFR ( R = 0.67; p < 0.001) with a mean bias of 0.0068 ± 0.0786. vFFR demonstrated good accuracy at predicting PW‐FFR ≦0.80 (area under the curve [AUC] = 0.86; 95% confidence interval [CI]: 0.83‐0.89). At a vFFR cut‐off value of ≦0.80, the sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic accuracy for predicting PW‐FFR ≦0.80 were 78.8%, 82.5%, 77.6%, 83.5%, and 80.9%, respectively, with a Cohen's Kappa coefficient of 0.612. Similar results were observed for vFFR with PW‐iFR and RFR. Conclusion vFFR demonstrated good correlation and diagnostic performance compared with wire‐based physiological assessments.

Chronic obstructive pulmonary disease (COPD) is associated with colonisation of the lower airways with bacteria including Haemophilus influenzae (HI) and Streptococcus pneumoniae (SP), and increased numbers of highly activated lung macrophages (mφ) with reduced phagocytic ability. Mφ may exist as M1-like (classically-activated, pro-inflammatory) or M2-like (alternatively-activated, anti-inflammatory) states. In COPD, M1 mφ may be more prevalent leading to pro-inflammatory conditions in the lung. To test this monocyte-derived mφ from non-smokers (NS), smokers (S) and COPD patients were cultured in GM-CSF (G-mφ, M1-like) or M-CSF (M-mφ, M2-like) for 12 days (n=3-6). Mφ were exposed to oxidative stress via treatment with 1-200 µM H 2 O 2 for 24 h after which phagocytosis of fluorescently labelled inert beads, or heat killed H.influenzae (HI) or S.pneumoniae (SP) was measured fluorimetrically. In all groups, M- mφ displayed higher phagocytic capacity than G- mφ (p In M-mφ from COPD patients, oxidative stress caused a concentration-dependent reduction in phagocytosis of HI (p M-mφ from COPD patients were more susceptible to oxidative stress than G-mφ which may contribute to their reduced presence in the lung. This abnormality in M-mφ should be further studied to elucidate the mechanisms behind this effect. Funded by COPDMAP.

Intracoronary thermography is a technique that measures lumen wall temperatures for vulnerable plaque detection. In this paper the influence of vulnerable plaque composition on lumen wall temperatures was studied numerically. Concerning the vulnerable plaque heat generation, the location of the heat source and its heat production were varied. Concerning the heat transfer, the thermal properties of the lipid core and the location of the vasa vasorum were studied. The heat source location was the main determinant of the lumen wall temperature distribution. The strongest effect was noted when the heat producing macrophages were located in the shoulder region leading to focal spots of higher temperature. The maximal lumen wall temperature was mainly determined by the heat production of the macrophages and the cooling effect of blood. The insulating properties of the lipid core increased lumen wall temperatures when the heat source was located in the cap and the presence of vasa vasorum lowered the temperatures. These results show that the lumen wall temperature distribution is influenced by vulnerable plaque composition and that intracoronary thermography techniques require a high spatial resolution. To be able to couple temperature measurements to plaque vulnerability, intracoronary thermography needs to be combined with an imaging modality.

The computer-aided quantitative analysis of co-ronary obstructions from digitized coronary cineangiograms is described. First, the assessment of the percentage diameter reduction from single view angiograms is discussed. This method requires the delineation of the contours of the artery and the analysis of the diameter function. Next, a densitometric method is described to transform the brightness values in the digital image into cali-brated X-ray absorption profiles, thus creating the possibility to assess percentage area reduction of obstructions from single views.