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Decompensation of chronic heart failure (CHF) is associated with high morbidity, mortality, and immense treatment costs. According to the American Heart Association (AHA) approximately 5 million people in the United States have heart failure, with >500,000 new cases each year. Approximately $30 billion was spent in the United States on the direct and indirect costs of managing CHF in 2006. In developed countries, 70% of these medical costs are directly related to (re)hospitalization. Pulmonary congestion, resulting from elevated left atrial and left ventricular filling pressures, is the most common cause of acute heart failure hospitalization. Appropriate tools for monitoring patients with CHF are absent. Instead physicians rely on the subjective assessment of clinical examinations. Although regular monitoring of CHF patients is recommended in management programs, none of these measures have shown conclusive impact on heart failure morbidity. Additionally, symptoms leading to CHF hospitalization usually occur late in the course of decompensation. In one study, dyspnea was noted on average only 3 days before admission. Careful monitoring of fluid status in ambulatory patients (possibly within their domestic environment) with CHF, therefore, may permit an early warning of impending decompensation, and assist in reducing hearth failure-related hospital admissions. Established clinical methods, however, can detect cardiogenic pulmonary edema only when its clinical signs have already appeared. Pulmonary capillary wedge pressure measurement can be used for early detection of cardiogenic pulmonary edema, but this is an invasive and expensive method, marked by serious complications. Radiography, instead cannot be applied for monitoring patients at risk of cardiogenic pulmonary edema because of their inconvenience, the associated cost, the unacceptable accumulated radiation dose, and its inappropriateness for ambulatory applications. One potential method of detecting developing pulmonary congestion as a sign of impending acute CHF decompensation is to measure thoracic impedance. For those patients scheduled to receive an implantable cardioverter defibrillator (ICD) or cardiac resynchronization therapy/defibrillator (CRT-D) implant, intrathoracic impedance measurement became available as the newest device-based diagnostic tool for continuous monitoring of thoracic fluid status. The operating principle underlying intrathoracic impedance measurement is rather straightforward. Measurements are made between the device case, typically implanted in the left pectorial region, and the defibrillator lead introduced into the right ventricle of the heart. This vector encompasses much of the left thoracic cavity. When an electrical current is passed across the lung, accumulation of intrathoracic fluid as a result of worsening heart failure will cause a corresponding decrease in electrical impedance. Major advantages of this technique are its high sensitivity and the relative fixed position between the measurement electrodes, which ensures consistent and reliable measurements. Yu et al. investigated the feasibility of intrathoracic impedance monitoring to identify potential fluid overload as an early indicator of impending CHF decompensation in ambulatory patients. In this study, daily intrathoracic impedance was found to be consistently below the reference impedance over an average of 18 days predating hospital admission for acute CHF decompensation. During this time, impedance decreased by 12% from its reference baseline to the impedance measured on the day before hospitalization. The reduction in impedance occurred an average of 15 days before the onset of clinical signs leading up to CHF related hospitalization a significant improvement over the late and subjective occurrence of fluid overload symptoms. In this way, the development of worsening heart failure might be detected early in the preclinical stage, when appropriate therapy could be initiated early enough to reduce hospital admissions. Similar results were obtained in several other publications. The potential advantages of ambulatory intrathoracic impedance monitoring, however, remain restricted to those CHF patients with ICD or CRT-D implants. A related method to monitor pulmonary congestion is to noninvasively measure transthoracic impedance across the chest by means of a surface electrode system. A series of studies, involving both animal models and humans, have been conducted to validate and confirm the feasibility of measuring transthoracic impedance by means of surface electrodes. Non-invasive monitoring of transthoracic impedance was found useful in several studies in which clearing of cardiogenic pulmonary congestion was associated with an increase in transthoracic impedance as measured by the Minnesota Impedance Cardiograph (aka. Kubicek monitor). More recently, the accuracy of transthoracic impedance measurement to detect early signs of progressing pulmonary fluid accumulation during acute CHF decompensation, has been questioned. Because the transcutaneous and skin-to-electrode contact impedances are the dominant contributions to noninvasively measured transthoracic impedance, with values several times higher than the actual lung related impedance, sensitivity generally is low. This also makes that even the smallest drift of the skin-to-electrode impedance during the monitoring period may completely obfuscate the minute changes in lung impedance accompanying the initiation of pulmonary congestion. In an early study, induction of pulmonary edema was reported to result in changes in transthoracic impedance as small as 2 to 5 ohm. These values are to be compared with the noninvasively measured transthoracic impedance in humans, which was found to be in the range between 1050-1280 ohm. Although there is no practical way to measure the transcutaneous and skin-electrode contact impedances, a recent study by Shochat et al. has shown that good estimates of these contributions can be obtained from reference measurements between a set of guard electrodes. Subtracting these estimates from the transthoracic impedance, a corrected value for the transthoracic impedance is obtained, that most closely matches the actual intrathoracic impedance. This procedure is claimed to remove the detrimental effects caused by drift of the skin-to-electrode impedance, and to result in a 3-fold increase in sensitivity over conventional measurement of transthoracic impedance to detect pulmonary fluid accumulation. Influence of cardiac cycles, respiration, and other incidental factors are eliminated by repeating the measurements several times over a 1 minute interval, and calculating the average values. After correction, individual transthoracic impedance in this study varied between 40 and 100 ohm. For all 37 patients in the study cohort who developed cardiogenic pulmonary congestion, a decrease in the corrected transthoracic impedance of more than 12% from baseline was observed in a time span of 30-60 minutes before the actual onset of clinical signs. Instead, corrected transthoracic impedance fell by less than 10% for all 228 patient that did not develop pulmonary congestion. Though, there are several factors that may affect the reliability and specificity of thoracic impedance monitoring. Intrathoracic processes, pneumonia, or pleural effusion, all may affect thoracic impedance measurements. Similarly, the air volume in the lung can affect thoracic impedance. For example, in patients with chronic obstructive pulmonary disease, the functional residual volume in the lungs may change over time, such as to affect thoracic impedance readings over the long term. Tomographic imaging of the fluid retention processes, is suggested in this project as a innovative approach to improve both clinical reliability, as well as to enhance diagnostic power of the method.