Abstract:
The large amount of data in the Karlsruhe 3D Ultrasound Computed Tomography (USCT) has to be reduced. For compression of ultrasound signals, cascading bit-wise run length method and adjacent A-scans or samples based method as new lossless methods were developed. Lossy compression methods are evaluated with an image quality based scheme using the newly designed optical flow based and committee model based estimators. Finally, an optimal method with a feasible compression ratio was suggested
Abstract:
Atrial fibrillation (AF) is the most common arrhythmia in the human heart. Its prevalence increases with rising age, with about 8 % of people over 80 having AF. AF is usually characterized by symptoms of rapid and irregular heart rate. The human heart normally contracts at a rate of 60 to 80 BPM in nomal sinus rhythm. During AF, the atrial rate could rise to between 400 and 600 BPM. AF is normally not as fatal as ventricular fibrillation, but it can cause not only palpitation, fainting, chest pain or congestive heart failure, but also a higher chance of stroke (about 2 to 7 times of the regular population) [1]. AF is a self perpetuating disease, because AF can lead to electrophysiological and anatomical changes in the atria, prolonging the AF episodes or initiate new AF. Thats why paroxysmal AF often progresses to chronic AF. About 18 % of patients with lone paroxysmal atrial fibrillation also developed sustained fibrillation [2]. The success rate of electrical atrial defibrillation is related to the duration of the AF. Terminating AF using cardioversion by patients with chronic AF is often not successful. A better understanding of fundamental mechanism underlying AF is of great benefit to the therapeutic approaches [3]. The ionic channel properties of the atrial myocytes play an important role in the heart rhythm. As revealed by recent researches, AF can occur on a familial basis, pointing to a genetic cause of arrhythmia in some individuals [4]. Study on the influences of genetic defects to the ionic channels could help understanding the mechanisms of AF better and contribute to the prevention and treatment of AF. Three different genetic mutations are incorporated in this work with a mathematical model which describes the cellular mechanisms. To realize an accurate simulation of exciation in atria it is necessary to consider different anatomy structures . Because of the different electrophysiological properties of these structures they must be incorporated properly. In this work, new anatomical structures such as the fossa ovalis (FO) and the cardiac opening areas (ostia) are incorporated