Abstract
Systolic wall stress is the main determinant of myocardial O2 consumption in chronic clinical heart disease as well as following acute inotropic pharmacological interventions. The fundamental relationship between stress and O2 consumption may be modified by alterations in myocardial contractility and/or left ventricular function parameters; these, however, contribute to the overall energy demand by a maximum 10-15%. The therapeutic consequences in chronic heart disease--with regard to left ventricular function and myocardial energy demand--has implications for the degree of left ventricular hypertrophy and dilatation.
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