Author + information
- Arnold M. Katz, MD, FACC*
- ↵*Address for reprints: Arnold M. Katz, MD, Cardiology Division, Department of Medicine, University of Connecticut Health Center, Farming-ton, Connecticut 06032.
The past 25 years have seen an unprecedented growth in our understanding of the mechanisms responsible for the regulation of myocardial contractility. Beginning with a demonstration that myocardial contractility represents an important determinant of cardiac function, this quarter century has witnessed a series of attempts to explain length-independent changes in myocardial contractile function. Alterations in the properties of the cardiac contractile proteins and changes in the amount of calcium (Ca2+) available for binding to the contractile proteins during excitation-contraction coupling are now recognized as important biochemical bases for physiologic, pharmacologic and pathologic changes in myocardial contractility. Identification of the central role of Ca2+ in the initiation of the cardiac contractile process has made possible the analysis of the mechanisms by which several drugs alter myocardial contractile function, including the biochemical processes that allow beta-adrenergic agonists to enhance contractility. The rapid developments in this field since 1958 promise an even greater flow of new knowledge regarding the causes, prevention and treatment of heart failure provided that there is given adequate support for such research activities.
Supported by Research Grants HL-21812 and HL-22135 from the National Institutes of Health, Bethesda, Maryland.
- American College of Cardiology Foundation