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Tissue Characterization in Reperfused Myocardial Infarction with Cardiac Magnetic Resonance Imaging
No full textCardiovascular disease (CAD) is still the most prevalent disease although there are extensive improvements in mortality and healthcare. More patients who received initial treatment for heart failure suffer greatly from reperfusion injury, resulting in myocardial infarction (MI). Hemorrhagic MI is proven to be the severest form of MI, and there is the calling for comprehensively characterize MI for patient’s long-term survival and quality of life. Cardiac magnetic resonance (CMR) imaging has been developed as first-line imaging modality for tissue characterization: fibrosis, edema, microvascular obstruction (MVO), intramyocardial hemorrhage (IMH) and its residual iron, and fat deposition. Those substrates are independent predictors of major adverse cardiac events (MACE) and manifests as different severity of MIs. Thus, being able to characterize MVO, IMH, MVO and its fat deposition is of great significance. Current practice of MI characterization continues to demand strong needs and technical challenges. Three needs were identified: a fast-imaging protocol to identifying MI, non-contrast technique to characterize multiple substrates underlying MI, and overlooked influence of spatial resolution on IMH detection.First, the lengthy CMR protocol in multiple tissue characterization may have impeded its implementation. A fast, comprehensive acquisition to characterize MI, MVO, IMH, cardiac function is on demand. In Chapter 2, we developed a free-breathing, non-ECG gating 3D T1, T2* imaging approach based on low-rank tensor (LRT) framework to shorten the imaging protocol of the same conventional acquisition by factor of 3-4. This framework also overcomes critical image artifacts from undesirable cardiac and respiratory motion and provides additional information in MVO characterization. Second, native T1 mapping has been extensively studied to provide diagnostic values in identifying acute and chronic MIs by characterizing edema or fibrotic tissue with elevated their T1 values. However, we realized that the co-existence of fibrosis, IMH and/or its induced fat deposition are causing inhomogeneity of T1 values within MI. Instead of treating them as confounding factors, in Chapter 3, we demonstrated native T1 heterogeneity within MIs as a new look for MI characterization and theorized it as a potential application for MI patient risk stratification. Specifically, we probed the heterogeneity of MIs in T1 mapping using entropy analysis, known as T1 entropy. We have shown that T1 entropy is capable of distinguishing MI from remote myocardium in both acute and chronic MI. We found T1 entropy is strongly associated with fat fraction and R2* (iron content) in the high fat fraction and high R2* group. The results were also validated in patient studies. In conclusion, T1 entropy is a promising predictor for heterogeneity of MI, and it is a reliable biomarker for analysis of severity of chronic MI.Third, the current imaging protocol in T2* mapping for IMH and iron remnants detection is derived from iron overload from thalassemia. However, for iron deposits from chronic MI with wall thinning (< 6 mm), the long-overlooked influence of spatial resolution may play a significant role in its detection. The primary goal of Chapter 4 in this dissertation is to address the limitations by investigating the influence of spatial infarction on T2* mapping in the competing effect of partial volume and SNR with simulation phantoms, ex-vivo heart scans and in-vivo scans in detecting iron residuals from thinned myocardial wall. We found that the spatial resolution can be optimized given SNR greater than 10. However, the current in-vivo CMR protocol may be limited in detecting thinned narrowed iron band (< 1 mm) due to insufficient SNR level.
In general, this dissertation contributed MI tissue characterization with CMR by addressing the spatial, temporal, and contrast challenges. It paves the way for MRI to characterize MI for prognosis and therapeutic care of patients with the capability to characterize severe form of MI such as IMH. These challenges have been addressed in this dissertation.
In future work, our developed fully ungated free-breathing 3D LRT T1, T2* will be investigated for patients for MI characterization. And we will further specialize the technique due to its advantages in MVO characterization for delayed enhancement. The T1 entropy will be validated in post-contrast T1 mapping. We would also employ the free-breathing nature of LRT framework to improve the SNR profile for iron remnants detection in T2* mapping
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Technological Advances and New Physiological Insights for Reliably Probing Myocardial Oxygenation with Magnetic Resonance Imaging
Full text linkCoronary artery disease (CAD) is the leading cause of death in the developed world. Evaluation of coronary function is critically important in the course of CAD management. Myocardial perfusion imaging (MPI) is the most popular noninvasive means of probing coronary function. While various imaging modalities have been used to image myocardial perfusion, the current clinical standards usually require the use of ionizing radiation or the exogenous contrast agent. The requirements increase the potential risks and render MPI infeeasible in a large segment of patients with CAD. Blood oxygenation level dependent (BOLD) cardiac MRI (CMR) is a newer approach for imaging myocardial perfusion. BOLD CMR utilizes the intrinsic contrast of the deoxygenated blood to probe myocardial oxygenation without ionizing radiation and contrast agent. Developments in the past twenty years have made significant advance in BOLD CMR and recent studies have shown promising results for the clinical application of the approach. However, BOLD CMR still suffer from multiple challenges, such as inadequate accuracy, imaging confounders, limited imaging speed, and sub optimal stress imaging protocols, all which significantly limit its reliability and clinical applicability. In this dissertation, we propose to overcome these limitations from the technical and physiological vantage points to enable a reliable BOLD CMR exam, which can rapidly accelerate the clinical translation and adoption of the approach. The first objective of this dissertation is to develop, test and validate a cardiac MRI technique that is robust, reliable and fast. To overcome the challenging cardiac imaging condition at 3T and provide reliable and sensitive BOLD signal, this dissertation utilized multiple techniques, such as motion correction, SR preparation, adiabatic pulses and novel reconstruction methods, to realize a confounder-corrected, free-breathing 3D T2 mapping technique at 3T that can be completed within the period of adenosine stress. The technique was tested and validated with simultaneously acquired 13N-ammonia PET perfusion in a whole-body PET/MR system. Ex-vivo studies demonstrated the proposed approach could be used to overcome the heart-rate dependent changes in T2 between rest and stress. In canines without coronary stenosis, T2 under adenosine stress was significantly greater than at rest, which was consistent with the observed increase in PET perfusion measurements. The changes in BOLD signal between rest and stress was highly correlated to myocardial perfusion reserve. In animals with coronary stenosis, perfusion anomalies were consistently detected between the developed technique and PET. These results demonstrate the proposed approach has the capability to enable rapid and reliable measurements of whole heart perfusion. The second objective of the dissertation is to explore innovative vasodilation strategies to improve the reliability and applicability of BOLD CMR exams. Two novel ways of inducing vasodilation (Regadenoson and hypercapnia) for BOLD CMR were studied. Regadenoson is a new pharmacological vasodilator that has a prolonged vasodilation effect compared to the standard stress agent (adenosine). Utilizing the longer vasodilation period, we found that a significantly improved stress image quality and reliability can be achieved by imaging at a delayed time point (10 mins after the regadenoson administration). For validation purpose, BOLD and PET images were acquired simultaneously in healthy animals. The delayed acquisitions showed markedly increased myocardial T2 from the BOLD images and increased myocardial blood flow from 13N-ammonia PET perfusion. To further improve the sensitivity and reliability of regadenoson BOLD exam, a repeated BOLD image acquisition strategy was proposed to continuously monitor the dynamics of BOLD signal after regadenoson injection. The BOLD signal changes were used to investigate the coronary dynamics after the peak vasodilation in healthy and diseased subjects. The coronary dynamic parameters (CDPs) were derived and were used to compare to the conventional single time point approach. CDPs showed the capability of extracting greater BOLD response in the healthy subjects and improved performance in disease identification in the animals with impaired coronary arteries. This preliminary study showed the potential of improving BOLD CMR performance with existing stress agents and better-designed strategies to assess coronary vasodilatation. Hypercapnia (elevated arterial CO2 (PaCO2)) is a known mediator of carotid vasodilation, but its effects on the coronary arteries had been unclear given the lack of tools to accurately and rapidly alter arterial CO2. By prospectively and independently controlling PaCO2, this dissertation first investigated whether a physiologically tolerable hypercapnic stimulus can increase MBF in healthy and diseased animals. The extent of effect on MBF due to hypercapnia was compared to adenosine using quantitative 13N-ammonia PET measurements. In the healthy animals, MBF under hypercapnia and adenosine were positively correlated; and were not different. Under LAD stenosis, MBF increased under hypercapnia and adenosine but the effect was significantly lower in the affected territories. Mean perfusion defect volumes measured with adenosine and hypercapnia were significantly correlated and were not different. The BOLD MR signal response to the controlled hypercapnia was also investigated under similar setup. In intact canines, changes in myocardial BOLD MR signal were equivalent to changes with adenosine. In addition, BOLD response under repeat hypercapnic stimulations were also tested. Reproducible BOLD responses were observed following repeat stimulation between baseline and equivalent hypercapnic states. In the dogs with coronary artery stenosis, BOLD MR signal changes during hypercapnia and adenosine infusion were also not different. The results demonstrate arterial blood CO2 tension is an independent variable of MBF, which can induce MBF and BOLD signal to the same level as standard dose of adenosine. In summary, this dissertation culminates in key advancements which have the capacity to reliably advance cardiac BOLD in the clinical arena in the assessment of myocardial perfusion in the setting of ischemic heart disease. The technical and physiological advances direly address the key obstacles present with in the current BOLD techniques and build the foundation for a reliable, robust and practical myocardial BOLD exam
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Noninvasive Imaging of Hemorrhagic Myocardial infarction with Confounder-Corrected T2* Cardiac MRI
Full text linkThe current gold-standard approach for detection and quantification of intramyocardial hemorrhage (IMH) is T2* cardiovascular magnetic resonance imaging (CMR). T2*-based imaging techniques have been demonstrated to have high sensitivity for detecting hemorrhage and residual iron. The conventional T2*-based imaging employed for IMH imaging is based on a 2D breath-held, ECG-triggered, segmented, multi-gradient-echo sequence. More recently, a dark-blood cardiac T2* MRI technique has emerged for imaging of global iron overload such as thalassemia. It has been interchangeably used with bright-blood T2* MRI for imaging of local iron overload such as intramyocardial hemorrhage. To date however, dark-blood T2* techniques for intramyocardial hemorrhage characterization has not been validated. In Chapters 2 and 3, we investigated the diagnostic capacity of dark-blood T2* MRI against bright-blood T2* MRI for intramyocardial hemorrhage characterization in both clinical and preclinical settings. We found that double-inversion-recovery prepared dark-blood T2* images provide lower signal-to-noise ratio and lower contrast-to-noise ratio between hemorrhage and remote myocardium, consequently underestimating the hemorrhage extent. Dark-blood T2* MRI also demonstrated weaker sensitivity, specificity, accuracy, and inter-observer variability compared to bright-blood T2*-weighted MRI. Our studies also showed that the loss in SNR and CNR in dark-blood T2* imaging emerges from the signal loss following double-inversion-recovery preparation and insufficient recovery time between double-inversion-recovery preparation and readout. Hence, we conclude that dark-blood T2* MRI does not have the same diagnostic capacity for assessment of intramyocardial hemorrhage and bright-blood T2* MRI should be the preferred choice for clinical use.
Studies have shown that fat infiltration is a common phenomenon in chronic myocardial infarction. However, signal from fat protons can confound the T2* assessment of intramyocardial hemorrhage. To address this issue, in Chapter 4, we studied the influence of fat infiltration on iron quantification in T2* mapping using a widely accepted water-fat separation algorithm. Specifically, we evaluated the temporal dependence of fat infiltration in hemorrhagic myocardial infarctions. We found that fat infiltration was observed in early and late chronic phases of myocardial infarctions, which if not corrected for, can underestimate the extent of iron content within the infarct zone. Notably, we also found that the amount of fat infiltration in chronic phase of MI was closely correlated with the amount of iron.
Another major confounder in conventional 2D breath-held ECG-gated T2* imaging is motion artifacts. In clinical settings, patients with acute myocardial infarctions often find it difficult to hold their breath during cardiac MRI exams. Some patients may even suffer from arrhythmia (irregular heartbeat). Both situations can lead to unsuccessful gating during data acquisition leading to motion artifacts on T2* images especially with long echo times. To address this issue, in Chapter 5, we developed a motion-resolved fully ungated free-breathing 3D cardiac T2* imaging technique using a low-rank tensor framework to accommodate clinical needs and to mitigate motion artifacts due to unsuccessful breath-holds or ECG gating. We tested our 3D LRT technique in healthy volunteers and animal models for image quality, SNR and T2*. We found that the proposed 3D LRT technique can provide superior image quality compared to conventional T2* techniques at the same level of signal-to-noise ratio. T2* measured from proposed 3D LRT data showed excellent agreement with T2* from conventional 2D approach. We also found that a key benefit of 3D acquisition is that it permits the reconstruction of high-resolution T2* images using the proposed 3D LRT T2* approach. High-resolution T2* images from proposed 3D LRT approach showed superior image quality and diagnostic capacity for assessment of intramyocardial hemorrhage. In Chapter 6, the proposed 3D LRT T2* imaging approach was validated on an animal model for feasibility and capability for characterization of intramyocardial hemorrhage. We found that our 3D LRT approach had excellent image quality and diagnostic accuracy in the assessment of intramyocardial hemorrhage compared to the 2D breath-held and gated acquisitions.
Broadly, this dissertation identified and corrected a number of critical confounders affecting the accuracy of T2* MRI in assessment of intramyocardial hemorrhage. By identifying and solving these confounders in T2* imaging, we aim to improve the diagnostic capability of MRI for prognosis and therapeutic care of patients with hemorrhagic myocardial infarctions.
In future work, feasibility of the newly developed fully ungated free-breathing 3D LRT T2* imaging technique will be investigated on patients for imaging of intramyocardial hemorrhage. And the potential of high-resolution T2* imaging which greatly improved intravoxel dephasing due to off-resonance will be explored
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Non-Contrast Enhanced Cardiovascular Magnetic Resonance Imaging for Characterizing Chronic Myocardial Infarctions
Full text linkMyocardial infarction (MI) is the leading cause of morbidity and death globally. Non-invasive characterization of chronic MIs is of significant clinical importance due to its association with adverse cardiac outcomes such as cardiac arrhythmias, heart failure, and sudden cardiac death. Late Gadolinium Enhancement (LGE) MRI has evolved into a robust non-invasive imaging technique for characterizing chronic MIs and identifying new pathophysiological substrates of adverse cardiac outcomes within chronic MIs. However, the requisite Gadolinium administration in LGE MRI is contra-indicated in nearly 25% of the MI patients due to co-morbidity of chronic kidney disease. In this light, there has been a growing interest to develop non-contrast enhanced MRI techniques for robust characterization of chronic MIs. This dissertation focuses on the development of novel non-Gadolinium based MRI techniques for robust characterization of chronic MIs and pathological substrates of adverse cardiac outcomes. Using extensive histopathology in an animal model and validation studies in chronic MI patients, native T1 mapping at 3T was shown to characterize chronic MIs with high diagnostic accuracy. The second part of the dissertation focuses on detecting post-reperfusion intramyocardial hemorrhage using non-contrast enhanced MRI techniques, and its role as a potential pathological substrate of adverse cardiac outcomes in chronic MIs. Using histopathology and mass spectrometry analysis, T2* MRI was shown to be a highly sensitive technique for detecting hemorrhage and its degradation byproducts. Hemorrhage was found to persist within chronic MIs for several months post-MI in the form of localized iron deposits, which in turn was found to be associated with prolonged inflammatory burden and adverse left-ventricular remodeling. Using high-resolution electroanatomical maps co-registered with T2*-weighted images, localized iron deposition within chronic MIs was found to be a potential arrhythmogenic substrate. The prognostic value of cardiac T2* MRI for risk-stratifying patients susceptible to malignant ventricular arrhythmias was evaluated
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Cardiac Magnetic Resonance Imaging-Guided Therapies for Chronic Hemorrhagic Myocardial Infarction
Full text linkThis dissertation aims to evaluate therapies that have the potential to improve the recovery of the left ventricle (LV) following myocardial infarction (MI) burdened with intramyocardial hemorrhage (IMH). Prior studies have shown that hemorrhagic MI results in the deposition of chronic iron in the myocardium, which induces cytotoxic effects as well as impacts the normal function of the microvasculature. In order to characterize the content of intramyocardial iron, T2* magnetic resonance imaging (MRI) was used as the gold standard in non-invasive detection of cardiac iron, and therefore acts as a diagnostic guidance tool informing the efficacy of the therapies. The dissertation may be broken down into three phases, all performed with MRI guidance to elucidate: 1) mechanistic understanding of the microvascular environment in chronic MI subjects; 2) effects of iron chelation therapy via Deferiprone (DFP) administration; and 3) effects of therapeutic hypothermia (TH) induced post reperfusion. The first phase investigated the long-term changes in myocardial perfusion assessed via MRI, in patients with reperfused myocardial infarction and an animal model of ischemia reperfusion (I/R) injury. From animal studies, histology, immunohistochemistry (IHC), and western blotting analysis were performed to elucidate the mechanistic underpinnings of MRI observations. The outcomes of this study led to the discovery that hemorrhagic MI results in reduced myocardial perfusion within hemorrhagic, but not non-hemorrhagic, MI territories. Further, the protein expression investigations enabled the proposal of a mechanistic pathway to examine the role chronic iron deposition plays in the perfusion defects observed in hemorrhagic MI.
The subsequent study in a canine model of hemorrhagic MI to remove iron from within chronic infarction regions using the small-molecule iron chelator deferiprone (DFP), is the first to show the potential to abrogate resting perfusion defects observed in the hemorrhagic MI setting. Furthermore, the study showed that the recovery of rest perfusion did not persist following termination of the DFP therapy, indicating the potential need for continuous, or extended, iron chelation in this population to maintain persistent benefits. Lastly, the study showed the potential beneficial impact of DFP therapy on LV remodeling by resulting in reduced end-diastolic mass, suggesting a possible role of iron in LV hypertrophy and diastolic dysfunction.
Finally, a study of post-reperfusion localized therapeutic hypothermia was conducted in a pig model to evaluate the potential impact of hypothermia therapy on IMH and chronic iron deposition. This is the first study to show the capability of therapeutic hypothermia to reduce chronic iron deposition in hemorrhagic MI. The results of this study showed that post-reperfusion hypothermia did not impact acute infarct size and did not affect hemorrhage in the acute phase (day 3 post-MI). However, by 1 month hypothermia-treated animals showed significantly reduced T2*-derived iron deposition volume, which held when normalized by infarct size. By 2 months post-MI, absolute T2* values were also indicative of decreased myocardial iron content, with significantly increased T2* values (lower iron content) in hypothermia-treated animals. Furthermore, LV ejection fraction (LVEF) was significantly elevated at 2 months in the hypothermia group, suggesting a positive effect of therapeutic hypothermia on chronic LV function.
In summary, this dissertation used animal models of hemorrhagic MI to investigate two promising therapeutic methods for alleviating the adverse remodeling in hemorrhagic MI subjects, showing promising results that will aid the future development of adjunctive clinical therapies for advancing treatment in MI and ischemia reperfusion injury
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Susceptibility-based Magnetic Resonance Imaging in Ischemic Heart Disease
No full textIschemic heart disease (IHD) remains the leading cause of mortality worldwide, driven by its progressive nature and wide-ranging clinical manifestations. Among these, myocardial infarction (MI) represents a critical event in the IHD spectrum, resulting from prolonged myocardial ischemia and irreversible tissue injury. Beyond the acute insult, complications following MI, particularly intramyocardial hemorrhage (IMH), a severe form of reperfusion injury, are increasingly recognized as key contributors to adverse ventricular remodeling, chronic heart failure, and long-term morbidity. Therefore, comprehensive detection and characterization across the entire spectrum of ischemic heart disease, from early-stage perfusion and oxygenation deficits to detailed tissue characterization of myocardial infarction and its complications, are essential for effective risk stratification and personalized therapeutic intervention. This holistic approach is critical to capturing both the functional and structural consequences of IHD, enabling timely diagnosis, guiding clinical decision-making, and improving long-term outcomes.Despite significant advances in non-invasive cardiac imaging, current techniques still fall short in fully capturing the spatial heterogeneity, physiological dynamics, and compositional complexity caused by IHD. Although recent developments in cardiac magnetic resonance imaging (CMR) have improved IHD characterization, conventional protocols still underutilize susceptibility-sensitive information embedded across multiple sequences (such as T2, T2* and quantitative susceptibility mapping (QSM)). These parameters reflect underlying variations in perfusion, oxygenation, and tissue iron, yet their potential remains largely untapped in routine clinical practice. By systematically integrating these susceptibility-related signals, susceptibility-based MRI emerges as a powerful framework for enhancing IHD assessment and enabling more accurate, physiologically meaningful evaluation. This dissertation establishes susceptibility-based MRI as a robust and non-contrast technique to capture tissue-specific markers such as perfusion and iron deposition, critical indicators of IHD progression.Chapter 2 develops a gas-modulated dynamic T2-based imaging method for endogenous-contrast myocardial perfusion mapping, demonstrating its sensitivity to oxygenation changes in both myocardium and blood pool under controlled oxygen tension modulation and provide an alternative method for myocardial perfusion measurement. Chapter 3 introduces a free-breathing, non-ECG-gated high-dynamic-range quantitative susceptibility mapping (HDR-QSM) framework, validated in iron phantom, preclinical ex-vivo and in-vivo animal studies, and histology, that demonstrates superior accuracy and artifact suppression in detecting hemorrhagic MI and quantifying focal iron concentration. Chapter 4 translates HDR-QSM into a clinical setting in patients with ST-elevation myocardial infarction (STEMI), demonstrating reduced image artifacts and superior diagnostic performance compared to conventional T2*-based methods. Notably, HDR-QSM provides more accurate iron quantification even during the acute phase of MI, where the presence of edema typically confounds standard susceptibility imaging techniques. Chapter 5 investigates respiratory motion-induced B0 field variations in the heart and introduces a motion-adaptive B0 shimming strategy that significantly enhances field homogeneity and improves the quality of susceptibility-sensitive imaging at 3T.Collectively, this dissertation overcome critical limitations of existing susceptibility-based cardiac MRI techniques by enhancing robustness to motion and susceptibility artifacts while enabling quantitative, physiology-driven biomarker characterization. These contributions establish a foundation for more accurate risk assessment and monitoring in IHD.Looking forward, the future of susceptibility-based MRI lies in integrating physiologically targeted contrast mechanisms, motion-resilient acquisition strategies, and AI-powered real-time reconstruction. Techniques such as gas-modulated dynamic T2-based imaging offers a contrast-free alternative to traditional perfusion imaging, expanding accessibility and safety. Motion-resolved T2* mapping and HDR-QSM are poised to become clinically relevant biomarkers of oxygenation and iron deposition. Future efforts will prioritize automation of image reconstruction, optimization of motion correction, and implementation of real-time B0 shimming across diverse clinical populations. Multi-center validation, outcome correlation, and integration into streamlined multiparametric MRI protocols will be key to clinical translation. Ultimately, this work advances susceptibility-based imaging toward becoming a powerful tool for precision diagnosis and personalized management of IHD
Building a Unified Mechanistic Insight Into the Bimodal Pattern of Edema in Reperfused Acute Myocardial Infarctions Observations, Interpretations, and Outlook∗
No full textMagnetic-susceptibility-based functional MRI for heart disease
Full text linkHeart disease is the primary cause of mortality in the western world. A common feature among several cardiac pathologies is the disruption of hemodynamic and/or oxygen metabolism/delivery homeostasis. The major hemodynamic variables of interest in the clinical assessment of heart disease are blood pressure and flow. While the noninvasive assessment of flow and systemic pressures are easily obtained, the measurement of pulmonary arterial pressure (PAP) is challenging. Since a small change in PAP (5mmHg) defines pulmonary hypertension (PH), for early detection of PH, a highly sensitive technique is needed. Since PH is progressive in nature, in time, right ventricular failure will cause death. Currently existing diagnostic techniques are limited either by their invasiveness to the body or by their inability to provide a quantitative measure of PAP, even for moderate PH. Further, impairments in oxygen metabolism/delivery mechanisms are also critical in many serious heart conditions. Magnetic resonance imaging (MRI) is being developed around the world as a potential methodology for the assessment of oxygen-related functional changes in the cardiovascular system. However, the scan times associated with commonly employed MRI measurement methods are prohibitively long for some cardiac applications. This dissertation focuses on using MRI to develop noninvasive methods that can provide accurate measurements of pressure and fast measurements of blood oxygen saturations. Both techniques were developed by exploiting the unique ability of MRI to detect changes in field perturbation due to magnetic susceptibility differences in the vicinity of different probing media---a novel pressure-sensitive contrast agent for manometry and deoxygenated red blood cells for oximetry. The first two contributions are theoretical studies aimed at improving the microbubble-based manometry technique. The first of these works explores the parameter space of microbubble-based MR manometry. Based on the conclusions derived, the second work proposes a novel microbubble construct and shows theoretically how such a construct may be useful in improving the sensitivity. The following chapter forms the basis for improving the temporal sensitivity of the oximetry technique. The final chapter concludes with the discussion of future directions on how the magnetic-susceptibility-based functional measures need to be developed further to become clinically useful.Ph.D
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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