No description available.

ABSTRACT Background Sudden cardiac arrest in young athletes is a tragic event that can potentially be reduced through the implementation of a pre-participation screening program. While the absolute contents of this program are debated, consensus does exist, that should such a program be implemented, a reduction in mortality will be found. The emphasis of any pre-participation screening is found in a history and basic physical examination, with or without routine electrocardiogram testing. This is based on the understanding that 90% of sudden cardiac arrests are attributable to an underlying cardiac pathology with the majority being hypertrophic cardiomyopathy. Debate continues around the cost effectiveness of such a program but there is no doubt that in a society that is promoting an active lifestyle and with the pressure of competitive sport at most schools, there is likely to be zero tolerance for not being able to screen for potentially lethal cardiac pathology.

No description available.

No description available.

Thesis (M.S.)--University of Wisconsin--Madison, 1970. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--Ohio State University, 2005. / Available online via OhioLINK's ETD Center; full text release delayed at author's request until 2006 September 15.

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Inflammation is important in both the pathogenesis and outcome of atherosclerosis. Plaques containing numerous inflammatory cells, particularly macrophages, have a high risk of rupture, whereas those with fewer inflammatory cells are at lower risk. The current ‘gold standard’ technique for imaging atherosclerosis is x-ray contrast angiography, which provides high-resolution definition of the site and severity of luminal stenoses, but no information about plaque inflammation. Quantification of plaque inflammation is desirable both to predict risk of plaque rupture and to monitor the effects of atheroma-modifying therapies. This is important since recent studies strongly suggest that HMG Co-A reductase inhibitors promote plaque stability by decreasing plaque macrophage content and activity without substantially reducing plaque size and therefore angiographic appearance. FDG is a glucose analogue that is taken up by cells in proportion to their metabolic activity. In this work, the central hypothesis was that plaque inflammation could be visualised and quantified non-invasively using FDG-PET. Initially, THP-1 monocytes and buffy-coat macrophages were stimulated with cellular activators, and the effect on deoxyglucose uptake was observed. It was demonstrated that both types of cell accumulated deoxyglucose in proportion to their metabolic activity. Next, FDG uptake was assessed in endarterectomy specimens from patients with symptomatic carotid disease. Autoradiography of excised plaques confirmed accumulation of deoxyglucose in macrophage-rich areas. Subsequently, co-registered FDG-PET imaging was performed in patients with transient ischaemic attack. FDG accumulated within carotid plaques, with significantly more FDG being taken up into symptomatic plaques than contralateral asymptomatic lesions. Finally, a rabbit model of atherosclerosis was established to investigate two related questions: firstly, whether an animal PET scanner (MicroPet) might detect atheroma, and secondly whether FDG-PET could image and perhaps quantify both atheroma progression and regression. Aortic atheroma was identified by FDG-PET, but full quantification was not possible, because the microPet system is currently unable to perform studies with attenuation correction. In summary, it has been shown, both in vitro and in vivo, that inflammation within atherosclerotic plaques can be successfully imaged by FDG-PET. In addition, pilot data from an experimental study of atherosclerosis in rabbits suggested that serial imaging with this technique might be useful for monitoring the effects of anti-atheroma drugs.