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The Key To Find Staurosporine Pointed Out In 2 Simple Actions

Intravascular thermography is a functional imaging method whereby temperature heterogeneity within plaque is detected, in contrast to the anatomical and morphological imaging observed with IVUS and OCT imaging systems. Inflammation plays a critical role in the initiation and pathogenesis of atherosclerosis [36]. The heat released by activated macrophages present in the TCFA can be detected and may help in identifying active inflammation GSK126 concentration and therefore predicting ACS [37]. In an ex-vivo study, thermistor catheters were used to detect temperatures at 20 sites per plaque and investigators reported a surface temperature variation of 0.2�C0.3��C, despite close (<1 mm) proximity of temperature sensors to each other. The temperature correlated positively with cell density (mostly macrophages) and inversely with the distance of the cell clusters from the luminal surface [37]. The first clinical device currently available to detect temperature heterogeneity in patients with CAD is a 0.014-in. thermocoil guide wire with a motorized pullback and data acquisition system. The tip of the wire contains a thermal sensor with temperature resolution of 0.03��C. The second device is a thermosense OTW catheter with a pullback system and a console. There are four thermistor sensors at the distal end of the catheter that expand after disengaging in the coronary artery to cover a 9-mm-width of the endoluminal surface. It has been shown in a preclinical study that <a href="">Transducin temperature heterogeneity of the plaque is related to plaque composition and more specifically determined by the total macrophage mass of the plaque [38]. Intraplaque temperature heterogeneity was observed in 20, 40, and 67% of the patients with stable angina, unstable angina, and myocardial infarction, respectively. Temperature difference (��T) between the atherosclerotic plaque and healthy vascular wall increased progressively, being lowest in patients with stable angina (��T: 0.106��C �� 0.110��C), and highest in those with unstable angina (��T: 0.683��C �� 0.347��C) and myocardial infarction (��T: 1.472��C �� 0.691��C). Thermal heterogeneity was not correlated to the degree of stenosis and no temperature heterogeneity was observed in the control vessels [39]. In another study, ��T was shown to be a strong predictor of adverse outcome after successful angioplasty [40]. The study followed 86 patients for 17 �� 7 months after successful PCI and reported that a temperature difference of >0.5��C post PCI significantly increased the risk of an adverse clinical event (41% if ��T of >0.5��C vs. 7% if ��T <0.5% ��C). At present it is not clear if temperature difference within the plaques is related solely to plaque vulnerability or to the complex interaction of patient's medication or indeed systemic inflammation.</div>
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