Inotropic Stimulation and Myocardial Energetics
Published on 1. January 1989
Book
Hardback
IX, 273 pages
978-3-7985-0815-6 (ISBN)
Description
Inotropic stimulation of the myocardium, as well as vasodilation and diuresis as essential principles in the treatment of congestive heart failure have recently met with considerable criticism and reevaluation. It is generally agreed that unloading of the heart, either through vasodilation and/or diuresis, improves the working conditions of the dilated, failing heart. It reduces myocar dial oxygen consumption through reduction of chamber radius and, thereby, wall tension as the major determinants of myocardial oxygen consumption. Inotropic stimulation, quite in contrast, does not conserve oxygen. It rather consumes energy and that may be disadvantageous in situations of compromised oxygen supply and energy metabolism of the working myocardium. However, under conditions of suf ficient oxygen supply and metabolic support inotropic stimulation may bring about in creased pumping and subsequent improvement of myocardial failure. In recent years it could convincingly be demonstrated that vasodilation leads to symp tomatic improvement of congestive heart failure, improvement of exercise tolerance, and it prolongs life - especially in the case of ACE-inhibitors and the combination of hydra lazine with long-acting nitrates. Quite in contrast, equally beneficial effects could not be demonstrated for inotropic agents in congestive heart failure. Only for the cardiac glyco sides has it been shown that beneficial effects can be achieved, especially if atrial fibril lation with absolute arrhythmia is present. The influence of the cardiac glycosides on the latter represents an effect which is independent of the inotropic action.
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Content
Introduction: Mechanisms of positive inotropic effects.- Adrenoceptors in myocardial regulation: concomitant contribution from both Alpha- and betaadrenoceptor stimulation to the inotropic response.- Studies on the cellular mechanisms of action of positive and negative inotropic agents.- On the mechanism of positive inotropic effects of alpha-adrenoceptor agonists.- Cytosolic sodium concentration regulates contractility of cardiac muscle.- Energy requirements of contraction and relaxation: implications for inotropic stimulation of the failing heart.- Genetic and non-genetic control of myocardial calcium.- Regulation of force and intracellular calcium transients by cyclic AMP generated by forskolin, MDL 17,043 and isoprenaline, and its modulation by muscarinic receptor agents: a novel mechanism for accentuated antagonism.- Studies on the mechanism of action of the bipyridine milrinone on the heart.- Ca-Agonists: a new class of inotropic drugs.- Myofibrillar Ca++ activation and heart failure - Ca++ sensitization by the cardiotonic agent APP 201-533.- Positive inotropic stimulation in the normal and insufficient human myocardium.- Do human cardiac beta-2 adrenoceptors play a (patho)physiological role in regulation of heart rate and/or contractility?.- Influence of isoproterenol on myocardial energetics. Experimental and clinical investigations.- Effects of long-term xamoterol therapy on the left ventricular mechanical efficiency in patients with ischemic heart disease.- Modulation of the autonomic control of the failing heart.- Dopexamine in congestive heart failure: how do the pharmacological activities translate into the clinical situation?.- The use of levodopa, an oral dopamine precursor, in congestive heart failure.- Clinical relevance of long-term therapy with levodopa and orally active dopamine analogues in patients with chronic congestive heart failure.- Cardiovascular effects of forskolin and phosphodiesterase-III inhibitors.- Phosphodiesterase inhibitors: alterations in systemic and coronary hemodynamics.- Influence of the calcium-sensitizer UDCG-115 on hemodynamics and myocardial energetics in patients with idiopathic dilated cardiomyopathy. Comparison with nitroprusside.- Myocardial energetics: experimental and clinical studies to address its determinants and aerobic limit.- Use of a conductance catheter to detect increased left ventricular inotropic state by end-systolic pressure-volume analysis.- Separation between vasodilation and positive inotropism by assessment of myocardial energetics in patients with dilated cardiomyopathy.