Readable, practical and concise, this self-contained guide to nuclear cardiology provides a foundation of essential knowledge for practitioners from any background. Including technical and clinical aspects of the subspecialty this fully updated handbook offers a core knowledge of nuclear cardiology ideal for use in a clinical setting.
Prevailing physiological concepts (PPC) of blood circulation consider the cardiovascular system (CVS) an autonomous system that has its own goal and mechanisms for achieving it. Physiologists agreed that complex neural and humoral controllers of a mean arterial pressure (MAP) indirectly alter the blood flows for satisfying cellular needs. However, PPCs are incapable of explaining the causes of long-term shifts of an MAP’s rest level. In particular, this affects current understanding and cure technologies of arterial hypertension (AH). Considering AH as a disease, physicians seek a cure that effectively decreases the elevated pressure. This gave rise to the palliative cure softening of AH symptoms without an understanding of AH’s primary causes. But this strategy, working until the patient intakes antihypertensive drugs, often leads to AH’s further development, and in extreme cases current antihypertensive drugs are helpless. These limitations of PPC are forced to seek a circulation’s extended physiological theory (EPT), explaining the mechanisms of both normal and altered MAPs. In the EPT presented in the book, CVS is considered a constituent part of a more complex functional super-system (FSS) that appeared in a multi-cellular animal organism during the co-evolution of specialized cells. The general goal of the FSS is to provide optimal physiochemical and energy states of the cell cytoplasm. To achieve this goal under a stochastic total and local variations of cells’ activity, FSS should control: i) The cardiac output; ii) the regional and local blood flows; and iii) the chemical composition of both arterial and venous blood. Under chronic energy shortage, FSS should also provide an adequate increasing of ATP-synthesis in mitochondria of stagnated cells. So, under the ineffectiveness of current mitochondria, FSS must enrich the arterial blood by chemicals providing the biogenesis of mitochondria. However, neither the energy providers nor the providers of blood chemistry are properly involved in PC of the blood circulation. The EPT for the first time integrates the hemodynamic and metabolic aspects of cell life at the organism scale. It is proved that the CVS activity is inversely associated with the activity mechanisms controlling the rates of both pulmonary ventilation and erythropoiesis. Under significant and chronic energy deficiency, the cells activate additional FSS mechanisms, materially supporting the biogenesis of mitochondria. The activity of FSS mechanisms forming the chemical composition of arterial and venous blood is in reciprocal relationships with the function of CVS. So, the EPT associates the function of CVS with energy and metabolic problems in cells.The EPT concerns both traditional and additional determinants of the MAP level. It is proved that stochastic combinations of these determinants force the MAP level to “float”. In particular, both the mitochondrial insufficiency and the chemical contamination of cytoplasm are capable of causing AH. The normal arterial pressure is always individual. Before correcting the altered arterial pressure, a complex medical examination for ascertaining the mitochondrial function, the status of the FSS mechanisms is recommended. The diagnosis of AH should be reoriented for detecting cellular abnormalities. The therapy of AH should be targeted at finding strategies for the optimizing the entire FSS function.
Cellular and Molecular Pathobiology of Cardiovascular Disease focuses on the pathophysiology of common cardiovascular disease in the context of its underlying mechanisms and molecular biology. This book has been developed from the editors' experiences teaching an advanced cardiovascular pathology course for PhD trainees in the biomedical sciences, and trainees in cardiology, pathology, public health, and veterinary medicine. No other single text-reference combines clinical cardiology and cardiovascular pathology with enough molecular content for graduate students in both biomedical research and clinical departments. The text is complemented and supported by a rich variety of photomicrographs, diagrams of molecular relationships, and tables. It is uniquely useful to a wide audience of graduate students and post-doctoral fellows in areas from pathology to physiology, genetics, pharmacology, and more, as well as medical residents in pathology, laboratory medicine, internal medicine, cardiovascular surgery, and cardiology. Explains how to identify cardiovascular pathologies and compare with normal physiology to aid research Gives concise explanations of key issues and background reading suggestions Covers molecular bases of diseases for better understanding of molecular events that precede or accompany the development of pathology
This special issue of Cells Tissues Organs contains a collection of state-of-the-art papers on cardiovascular regenerative medicine. Diseases of the cardiovascular system are the most frequent cause of death, a problem which will further increase due to aging demographics. Therefore, approaches to tissue engineering and regenerative medicine that have the ability to reconstruct functional healthy cardiovascular structures could have a major impact on health care delivery. Current concepts and approaches which have the potential to be critical components of the next generation of therapy to create or repair blood vessels and heart tissues are discussed in this issue. The focus is on cell sources for cardiovascular tissues, niche scaffolds, blood vessels and vascular networks, as well as engineered heart tissues. This publication is of special importance for scientist and physicians who are interested in vascular tissue engineering, artificial grafting, developmental biology, cardiovascular regenerative medicine, and surgery.
Injured mammalian hearts do not regenerate but scar. This is a major medical problem, as ischemic heart disease is among the leading causes of morbidity and mortality worldwide. Essential clues for human heart repair are uncovered when zebrafish and newt are found to regenerate cardiac muscle after injury.This book presents the major advances of the last decade in the field of cardiac regeneration. These recent advances include: demonstration that zebrafish, a genetically tractable system, can regenerate heart; the identification of several new stem cell populations in the heart; demonstration that stem cells can be used to improve heart function; and demonstration that induction of cardiomyocyte proliferation is a realistic future option to repair injured hearts. This book also provides detailed reviews of the research on model organisms capable of heart regeneration as well as innovative translational research to achieve regeneration in mammals, that comprises work on blood born stem cells, endogenous cardiac stem cells, paracrine factors, reawakening of cardiomyocyte proliferation, and bioengineering. More importantly, the book, in the concluding chapter, dovetails the studies with a comprehensive overview of clinical trials.
This conference had as its focus the phrase 'From the Cell to the Body Surface'. It comprised five minisymposia, which concentrated on some of the major issues of the day for basic scientists and clinicians. In addition to the invited papers, the proceedings contain volume presentations and posters selected from among abstracts sent in by some of the most important investigators in electrocardiology worldwide.
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