Abstract
The clinical demonstration that contractile function is depressed in failing human hearts resulted in several logical corollaries to explain the pathophysiology of heart failure. Only recently have investigators been able to study human myocardium as opposed to making extrapolations from animal studies. As a result of these studies several hypotheses have been dispelled and the inappropriateness of certain animal models eluded to. However, there are limitations to human studies. When studying human myocardium one is often left with studying only one point in time. Further, one is left with the question of whether one is studying a mechanism of the disease, an adaptive response to the disease, or changes in response to the varied pharmacological treatments. Therefore mechanisms involved in the pathogenesis or natural history of the disease process cannot be easily investigated. Furthermore, one is often left studying an end-stage process that may or may not be reflective of the disease process. Nevertheless, despite these limitations studies involving human myocardium have yielded important information regarding pathophysiology as well as markers of the disease state.
Keywords
- Human Myocardium
- Myofibrillar ATPase Activity
- Human Ventricular Myocardium
- Abnormal Calcium Metabolism
- Thin Myofilament
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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Gwathmey, J.K., Hajjar, R.J. (1993). Abnormal Calcium Metabolism in Heart Muscle Dysfunction. In: Figulla, HR., Kandolf, R., McManus, B. (eds) Idiopathic Dilated Cardiomyopathy. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77891-9_13
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DOI: https://doi.org/10.1007/978-3-642-77891-9_13
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