Spectral Analysis of Electrophysiological & Metabolic Function in Healthy and Diseased Perfused Hearts
Open Access DepositedHeart disease is the leading cause of death in the US, with more than half of those deaths due to coronary artery disease (CAD), where plaque buildup narrows the arteries and may cause myocardial ischemia due to impaired blood flow. Complete arterial blockage will cause a myocardial infarction (MI). If not treated within a few hours, MI tissue will die and will subsequently be replaced with non-contracting fibrotic scar tissue. In the aftermath of an MI, patients can eventually deteriorate into heart failure, and have an increased prevalence of deadly arrhythmias. The overall goal of this dissertation was to study how myocardial hypoxia and MI scar formation alter cardiac function, and increase the incidence of arrhythmias. This was accomplished by developing new instrumentation that incorporated novel spectral analysis and panoramic imaging to study healthy and infarcted rodent hearts.A panoramic imaging system was built to image the scar tissue, and electrophysiology of hearts with an MI. The system included a camera to image the geometry of the heart, a line scan hyperspectral camera, four cameras equally spaced around the heart to record cellular depolarizations, and hardware to facilitate the vertical and radial positioning of perfused hearts. Using the system, we were able to construct a 3D model of the heart, and texture map the recorded data to it in order to directly correlate the underlying electrophysiology with the scarred regions of the heart. Using this system a study was performed to investigate the changes in electrophysiology after 1-, 2-, and 4-weeks of recovery from an MI. Using the collected, and processed data, regions were identified using the spectral data to discern between healthy, border, and scar tissue. Within these regions the action potential durations (APD) were measured and compared. After analysis we found continued conduction through the scar, significant changes in the spectral characteristics of scar tissue, changes in arrhythmia incidence, and changes in APD between regions, and through time. In our last experiment we investigated demand hypoxia during sudden increases in cardiac demand induced by rapid pacing. In healthy hearts we recorded coronary flow, left ventricular developed pressure, and NADH fluorescence as an analog for metabolic demand to see how an increased oxygenation delivery by higher coronary flow alters this response. Panoramic hyperspectral imaging of tissue type and electrophysiology provided new insights into the location of infarcted tissue and tissue-specific alterations of APD and conduction, enabling function and tissue type to be correlated and analyzed at high spatiotemporal resolution. Future work will investigate the electrophysiology of patchy fibrotic areas in failing myocardium, temporal changes in electrophysiology as heart failure progresses, and other molecular signatures that can be identified using hyperspectral imaging.
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