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No abstract is provided for this article.

The non-uniform extent and distribution of atherosclerotic plaque at bifurcations have been described by necropsy studies and they are related to local blood-flow disturbances. Systematic evaluation of plaque extent and distribution upstream and downstream of major coronary side-branches has not yet been evaluated in vivo.We used intravascular ultrasound imaging in 41 patients with atherosclerotic disease to study the region of 73 major coronary side-branches at 2 mm increments proximal and distal to the side-branch (657 images: 73 at origin of side-branch; 292 proximal; 292 distal). The maximum (MXT) and minimum (MINT) plaque thickness and the plaque burden percentage (% PB) were measured in all the segments. The angle of distribution of maximum plaque thickness with respect to the origin of the side-branch was determined in each cross-section and assigned to S1 when located on the semicircle in the direction of the origin of the side-branch and to S2 when located on the opposite wall.The mean value of maximum plaque thickness and the plaque burden percentage were similar at the origin and in the two adjacent segments proximal and distal to the side-branch (1.0 +/- 0.48 mm, 1.06 +/- 0.48 mm and 0.98 +/- 0.48 mm; 45 +/- 19%, 46 +/- 19% and 44 +/- 18%). In distal sites of analysis, the plaque was more frequently eccentric in comparison to proximal sites (presence of an arc of plaque-free wall: 79% versus 62% in very distal and in very proximal sites respectively; p < 0.05). The prevalence of maximum plaque in S2 was higher at the origin (84%) and in adjacent distal segments (86%) as compared with the adjacent proximal segments (60%; p < 0.0001).The distribution of plaque is influenced by the origin of a major coronary side-branch in patients with coronary atherosclerosis: in distal sites the location of maximum plaque is almost always eccentrically distributed on the wall opposite the take-off.

Abstract IFN-γ is crucial for protection against M. tuberculosis (Mtb). Previously we reported that signaling through SLAM on Mtb-stimulated cells induced CREB activation increasing IFN-γ. Here, we deeply investigated the potential relationship between SLAM-CREB and IFN-γ. After Mtb-stimulation, most of the IFN-γ+ cells co-expressed SLAM and pCREB (48,68 ± 11,18), whereas a smaller percentage of T cells expressed one of the two molecules. These results demonstrate that the induction of IFN-γ mediated by SLAM in TB depends, at least in part, on CREB activation. It was reported that SLAM signaling would induce the activation of the protein kinase Erk. To analyze the signaling pathways induced by SLAM that contribute to CREB activation and IFN-γ secretion in TB, we studied Erk phosphorylation after SLAM activation. The addition of PD90059 (an Erk inhibitor) to Mtb stimulated cells inhibited the percentage of IFN-γ+pCREB+ T cells, indicating that Erk could be involved on CREB activation. Moreover, the addition of PD90059 to Mtb±α-SLAM stimulated cells significantly decreased IFN-γ production (% inhibition: 71,6 ± 7,4). Finally, α-SLAM induced Erk activation in Mtb stimulated cells. These results demonstrate that IFN-γ production induced by SLAM signaling on Mtb stimulated cells is, at least in part, mediated by Erk and CREB phosphorylation. These data contribute new information about the molecular basis operating during SLAM activation that leads to IFN-γ production in human TB.

No abstract is provided for this article.

The Academic Research Consortium (ARC) and the Standardized Data Collection for Cardiovascular Trials Initiative have recently published updated clinical and angiographic endpoint definitions for percutaneous coronary intervention trials. The aim of this document is to provide practical guidance to facilitate and harmonize the implementation of those definitions in randomized trials or registries, as well as to foster consistency among independent adjudication committees. The authors compared the ARC-2 and Standardized Data Collection for Cardiovascular Trials Initiative definitions to identify areas of consistency, complex scenarios, and definitions in need of further standardization. Furthermore, the authors compared the fourth universal definition of myocardial infarction with the ARC-2 definition of myocardial infarction. The Society for Cardiovascular Angiography and Interventions definition of periprocedural myocardial infarction was also compared with the ARC-2 definition and the fourth universal definition of myocardial infarction. An in-depth assessment was done for each individual clinical endpoint to guide clinical investigators on reporting and classifying clinical adverse events. Finally, the authors propose standard streamlined data capture templates for reporting and adjudicating death, myocardial infarction, stroke, revascularization, stent or scaffold thrombosis, and bleeding.

First generation drug-eluting stents have considerably reduced in-stent restenosis and broadened the applications of percutaneous coronary interventions for the treatment of coronary artery disease. The polymer is an integral part of drug-eluting stents in that, it controls the release of an antiproliferative drug. The main safety concern of first generation drug-eluting stents with permanent polymers—stent thrombosis—has been caused by local hypersensitivity, delayed vessel healing, and endothelial dysfunction. This has prompted the development of newer generation drug-eluting stents with biodegradable polymers or even polymer-free drug-eluting stents. Recent clinical trials have shown the safety and efficacy of drug-eluting stents with biodegradable polymer, with proven reductions in very late stent thrombosis as compared to first generation drug-eluting stents. However, the concept of using a permanent metallic prosthesis implies major drawbacks, such as the presence of a foreign material within the native coronary artery that causes vascular inflammation and neoatherosclerosis, and also impedes the restoration of the vasomotor function of the stented segment. Bioresorbable scaffolds have been introduced to overcome these limitations, since they provide temporary scaffolding and then disappear, liberating the treated vessel from its cage. This update article presents the current status of these new technologies and highlights their future perspectives in interventional cardiology.

The purpose of this study was to compare measurements by MetriCath to intravascular ultrasound (IVUS) and quantitative coronary angiography (QCA). The MetriCath system consists of a low‐pressure (200 mm Hg) balloon catheter connected to a pressure transducer and infusion pump linked to a computer that records pressure‐volume curves. Cross‐sectional area of blood vessels is obtained directly from the unrestrained and in‐stent pressure‐volume measurements. We compared stent cross‐sectional area measurements by MetriCath, IVUS, and QCA in a porcine stented coronary artery model. Comparison of area measurements in 14 stents showed no significant differences between the three methods ( P = 0.66). On average, values differed 0.37 ± 0.60 mm 2 between MetriCath and QCA, 0.13 ± 0.55 mm 2 between MetriCath and IVUS, and 0.22 ± 0.80 mm 2 between IVUS and QCA. This corresponds to 6.2% ± 10%, 3.0% ± 9.0%, and 3.1% ± 12.9% relative difference from the average of two corresponding measurements. Linear regression analysis showed excellent correlation between measurements (r = 0.99 for all comparisons). The differences in in‐stent area measurements between MetriCath and both QCA and IVUS were small. Considering the ease and rapidity of obtaining MetriCath results, this technique may form an alternative to the others in evaluating stent expansion. Based on these findings, clinical evaluation seems warranted. Cathet Cardiovasc Intervent 2002;57:2–9. © 2002 Wiley‐Liss, Inc.