Prognostic value of adenosine stress cardiovascular magnetic resonance in patients with low-risk chest pain

<p>Abstract</p> <p>Background</p> <p>Approximately 5% of patients with an acute coronary syndrome are discharged from the emergency room with an erroneous diagnosis of non-cardiac chest pain. Highly accurate non-invasive stress imaging is valuable for assessment of low-risk chest pain patients to prevent these errors. Adenosine stress cardiovascular magnetic resonance (AS-CMR) is an imaging modality with increasing application. The goal of this study was to evaluate the negative prognostic value of AS-CMR among low-risk acute chest pain patients.</p> <p>Methods</p> <p>We studied 103 patients, mean 56.7 ± 12.3 years of age, with chest pain and no electrocardiographic evidence of ischemia and negative cardiac biomarkers of necrosis, who were admitted to the Cardiac Decision Unit of our institution. All patients underwent AS-CMR. A negative AS-CMR was defined as absence of all the following: regional wall motion abnormalities at rest; perfusion defects during stress (adenosine) and rest; and myocardial scar on late gadolinium enhancement images. The patients were followed for a mean of 277 (range 161-462) days. The primary end point was defined as the combination of cardiac death, nonfatal acute myocardial infarction, re-hospitalization for chest pain, obstructive coronary artery disease (>50% coronary stenosis on invasive angiography) and coronary revascularization.</p> <p>Results</p> <p>In 14 patients (13.6%), AS-CMR was positive. The remaining 89 patients (86.4%), who had negative AS-CMR, were discharged. No patient with negative AS-CMR reached the primary end-point during follow-up. The negative predictive value of AS-CMR was 100%.</p> <p>Conclusion</p> <p>AS-CMR holds promise as a useful tool to rule out significant coronary artery disease in patients with low-risk chest pain. Patients with negative AS-CMR have an excellent short and mid-term prognosis.</p

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

TLQAP: A topology and link quality assessment protocol for efficient node allocation on wireless testbeds

In this paper we present Topology and Link Quality Assessment Protocol (TLQAP), which we have implemented as a wireless testbed management framework component, that is used to inspect link quality between wireless testbed nodes and appropriately map them to user experiment requirements. TLQAP is mainly an OSI layer 2 design for fixed location, non RF-isolated wireless testbed deployments, which assesses interconnection topology and link quality by estimating packet delivery ratio (PDR) and transmission delay at each node for all requested channel, rate and transmission power combinations. Moreover, TLQAP builds a measurement history log and creates a channel utilization profile, in the context of each testbed node, for all the nearby testbed-external devices that operate independently in the region and are not under the management framework control. The analysis of this information enables TLQAP to choose the channels that have the highest probability of being free during an experiment. TLQAP OSI layer 2 component has been implemented in the click modular router framework and the controller component has been integrated with OMF management framework for wireless testbeds. To outline TLQAP benefits, we have performed experiments on our ORBIT node testbed and we compare it to an existing application level measuring tool. Copyright 2009 ACM

A new slicing scheme for efficient use of wireless testbeds

The gradually growing need for testbed use so as networking algorithms to be validated in real environments, has given rise to optimal utilization of testbed resources. Despite the fact that, many laboratories around the globe have deployed testbeds, so as experimenters have the opportunity to test their algorithms, the majority of those testbeds suffer from bad management that prevents users from efficiently exploiting testbed's resources. Moreover, as the number of testbed users increases, experimenters needs for more sophisticated allocation of testbed resources are growing. Toward, this direction, we propose a managerial framework that exploits testbed utilization by introducing slicing over frequency spectrum. This new framework will allow a more sophisticated way to optimally control and manage network resources of a testbed. Lab's website: http://nitlab.inf.uth.gr

Towards maximizing wireless testbed utilization using spectrum slicing

As experimentation becomes one of the de-facto approaches for benchmarking, researchers are turning to testbeds to test, review and verify their work. As a result, several research laboratories build wireless testbeds, in order to offer their researchers a real environment to test their algorithms. As testbeds become more and more popular, the need for a managerial tool that will not only provide a unified way for defining and executing an experiment and collecting experimental results, but that will also serve as many users as possible maximizing the utilization of its resources, is growing. In this spirit, we propose a scheme that exploits wireless testbeds functionality by introducing spectrum slicing of the testbed resources. This scheme can be incorporated inside OMF, an already existing wireless testbeds managerial framework, which is widely used by many researchers. © Institute for Computer Sciences, Social Informatics and Telecommunications Engineering 2011

Publish/subscribe over information centric networks: A Standardized approach in convergence

Originally conceived as a "network of hosts", the Internet is evolving into an Internet of services, an Internet of media, an Internet of people and an Internet of "things". This implies a strategic shift from "host-centri" to "content-centric" and "data-centric" networking. CONVERGENCE proposes to enhance the Internet with a novel, information-centric, publish-subscribe service model, based on the Versatile Digital Item (VDI): a common container for all kinds of digital content, derived from the MPEG-21 standard. Results in terms of standardization activities and software implementation are presented

Publish/subscribe over information centric networks: A Standardized approach in convergence

Originally conceived as a "network of hosts", the Internet is evolving into an Internet of services, an Internet of media, an Internet of people and an Internet of "things". This implies a strategic shift from "host-centri" to "content-centric" and "data-centric" networking. CONVERGENCE proposes to enhance the Internet with a novel, information-centric, publish-subscribe service model, based on the Versatile Digital Item (VDI): a common container for all kinds of digital content, derived from the MPEG-21 standard. Results in terms of standardization activities and software implementation are presented

The 12q14 microdeletion syndrome: additional patients and further evidence that HMGA2 is an important genetic determinant for human height.

Characteristic features of the 12q14 microdeletion syndrome include low birth weight, failure to thrive, short stature, learning disabilities and Buschke-Ollendorff lesions in bone and skin. This report on two additional patients with this microdeletion syndrome emphasizes the rather constant and uniform phenotype encountered in this disorder and refines the critical region to a 2.61 Mb interval on 12q14.3, encompassing 10 RefSeq genes. We have previously shown that LEMD3 haploinsufficiency is responsible for the Buschke-Ollendorff lesions and now provide strong evidence that a heterozygous deletion of HMGA2 is causing the growth failure observed in this disorder. The identification of an intragenic HMGA2 deletion in a boy with proportionate short stature and the cosegregation of this deletion with reduced adult height in the extended family of the boy further underscore the role of HMGA2 in regulating human linear growth